PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33799951-9	2021	We found that alisertib effectively inhibited breast cancer cell lines with high KDM1A expression.	MLN 8237	14-23	lysine demethylase 1A	Homo sapiens	81-86
34896433-0	2022	Alisertib shows negligible potential for perpetrating pharmacokinetic drug-drug interactions on ABCB1, ABCG2 and cytochromes P450, but acts as dual-activity resistance modulator through the inhibition of ABCC1 transporter.	MLN 8237	0-9	ATP binding cassette subfamily C member 1	Homo sapiens	204-209
34896433-3	2022	In accumulation assays, alisertib potently inhibited ABCC1 transporter, but not ABCB1 or ABCG2.	MLN 8237	24-33	ATP binding cassette subfamily C member 1	Homo sapiens	53-58
34896433-5	2022	In addition, alisertib was characterized as a low- to moderate-affinity inhibitor of recombinant CYP3A4, CYP2C8, CYP2C9, CYP2C19, and CYP2D6 isoenzymes, but without potential clinical relevance.	MLN 8237	13-22	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	97-103
34896433-5	2022	In addition, alisertib was characterized as a low- to moderate-affinity inhibitor of recombinant CYP3A4, CYP2C8, CYP2C9, CYP2C19, and CYP2D6 isoenzymes, but without potential clinical relevance.	MLN 8237	13-22	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	105-111
34896433-5	2022	In addition, alisertib was characterized as a low- to moderate-affinity inhibitor of recombinant CYP3A4, CYP2C8, CYP2C9, CYP2C19, and CYP2D6 isoenzymes, but without potential clinical relevance.	MLN 8237	13-22	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	113-119
34896433-5	2022	In addition, alisertib was characterized as a low- to moderate-affinity inhibitor of recombinant CYP3A4, CYP2C8, CYP2C9, CYP2C19, and CYP2D6 isoenzymes, but without potential clinical relevance.	MLN 8237	13-22	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	121-128
34896433-5	2022	In addition, alisertib was characterized as a low- to moderate-affinity inhibitor of recombinant CYP3A4, CYP2C8, CYP2C9, CYP2C19, and CYP2D6 isoenzymes, but without potential clinical relevance.	MLN 8237	13-22	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	134-140
34896433-6	2022	Drug combination studies revealed the capability of alisertib to synergistically antagonize ABCC1-mediated resistance to daunorubicin.	MLN 8237	52-61	ATP binding cassette subfamily C member 1	Homo sapiens	92-97
34896433-7	2022	Although alisertib exhibited substrate characteristics toward ABCB1 transporter in monolayer transport assays, comparative proliferation studies showed lack of its MDR-victim behavior in cells overexpressing ABCB1 as well as ABCG2 and ABCC1.	MLN 8237	9-18	ATP binding cassette subfamily B member 1	Homo sapiens	62-67
34582773-10	2021	In contrast, the Aurora-A inhibitor MLN8237 exerted a synergistic anti-cell proliferation effect when combined with either inhibitor.	MLN 8237	36-43	aurora kinase A	Homo sapiens	17-25
34692693-6	2021	The Aurora A inhibitor alisertib decreased ER stress.	MLN 8237	23-32	aurora kinase A	Homo sapiens	4-12
34593753-3	2021	Alisertib (MLN8237) is a promising oral mitotic aurora kinase A (AURKA, Aurora-A) selective inhibitor, which is currently under several clinical evaluations but has failed in its first Phase III trial due to inadequate efficacy.	MLN 8237	0-9	aurora kinase A	Homo sapiens	48-63
34593753-3	2021	Alisertib (MLN8237) is a promising oral mitotic aurora kinase A (AURKA, Aurora-A) selective inhibitor, which is currently under several clinical evaluations but has failed in its first Phase III trial due to inadequate efficacy.	MLN 8237	0-9	aurora kinase A	Homo sapiens	65-70
34593753-3	2021	Alisertib (MLN8237) is a promising oral mitotic aurora kinase A (AURKA, Aurora-A) selective inhibitor, which is currently under several clinical evaluations but has failed in its first Phase III trial due to inadequate efficacy.	MLN 8237	0-9	aurora kinase A	Homo sapiens	72-80
34593753-3	2021	Alisertib (MLN8237) is a promising oral mitotic aurora kinase A (AURKA, Aurora-A) selective inhibitor, which is currently under several clinical evaluations but has failed in its first Phase III trial due to inadequate efficacy.	MLN 8237	11-18	aurora kinase A	Homo sapiens	48-63
34593753-3	2021	Alisertib (MLN8237) is a promising oral mitotic aurora kinase A (AURKA, Aurora-A) selective inhibitor, which is currently under several clinical evaluations but has failed in its first Phase III trial due to inadequate efficacy.	MLN 8237	11-18	aurora kinase A	Homo sapiens	65-70
34593753-3	2021	Alisertib (MLN8237) is a promising oral mitotic aurora kinase A (AURKA, Aurora-A) selective inhibitor, which is currently under several clinical evaluations but has failed in its first Phase III trial due to inadequate efficacy.	MLN 8237	11-18	aurora kinase A	Homo sapiens	72-80
34256279-3	2021	The combination of AURKA inhibitor (alisertib) plus paclitaxel may be synergistic in rapidly proliferative cancers.	MLN 8237	36-45	aurora kinase A	Homo sapiens	19-24
34522170-3	2021	Here, we found that signal transducer and activator of transcription 1 (STAT1) was highly expressed in colorectal cancer (CRC) xenograft mouse models that were resistant to alisertib, an Aurora-A inhibitor.	MLN 8237	173-182	signal transducer and activator of transcription 1	Mus musculus	20-70
34522170-3	2021	Here, we found that signal transducer and activator of transcription 1 (STAT1) was highly expressed in colorectal cancer (CRC) xenograft mouse models that were resistant to alisertib, an Aurora-A inhibitor.	MLN 8237	173-182	signal transducer and activator of transcription 1	Mus musculus	72-77
34522170-3	2021	Here, we found that signal transducer and activator of transcription 1 (STAT1) was highly expressed in colorectal cancer (CRC) xenograft mouse models that were resistant to alisertib, an Aurora-A inhibitor.	MLN 8237	173-182	aurora kinase A	Mus musculus	187-195
34522170-4	2021	Unexpectedly, we found that alisertib disrupted Aurora-A binding with ubiquitin-like with plant homeodomain and ring finger domain 1 (UHRF1), leading to UHRF1 mediated ubiquitination and degradation of DNA methyltransferase 1 (DNMT1), which in turn resulted in demethylation of CpG islands of STAT1 promoter and STAT1 overexpression.	MLN 8237	28-37	aurora kinase A	Mus musculus	48-56
34522170-4	2021	Unexpectedly, we found that alisertib disrupted Aurora-A binding with ubiquitin-like with plant homeodomain and ring finger domain 1 (UHRF1), leading to UHRF1 mediated ubiquitination and degradation of DNA methyltransferase 1 (DNMT1), which in turn resulted in demethylation of CpG islands of STAT1 promoter and STAT1 overexpression.	MLN 8237	28-37	ubiquitin like with PHD and ring finger domains 1	Homo sapiens	134-139
34522170-4	2021	Unexpectedly, we found that alisertib disrupted Aurora-A binding with ubiquitin-like with plant homeodomain and ring finger domain 1 (UHRF1), leading to UHRF1 mediated ubiquitination and degradation of DNA methyltransferase 1 (DNMT1), which in turn resulted in demethylation of CpG islands of STAT1 promoter and STAT1 overexpression.	MLN 8237	28-37	ubiquitin like with PHD and ring finger domains 1	Homo sapiens	153-158
34522170-4	2021	Unexpectedly, we found that alisertib disrupted Aurora-A binding with ubiquitin-like with plant homeodomain and ring finger domain 1 (UHRF1), leading to UHRF1 mediated ubiquitination and degradation of DNA methyltransferase 1 (DNMT1), which in turn resulted in demethylation of CpG islands of STAT1 promoter and STAT1 overexpression.	MLN 8237	28-37	DNA methyltransferase 1	Homo sapiens	202-225
34522170-4	2021	Unexpectedly, we found that alisertib disrupted Aurora-A binding with ubiquitin-like with plant homeodomain and ring finger domain 1 (UHRF1), leading to UHRF1 mediated ubiquitination and degradation of DNA methyltransferase 1 (DNMT1), which in turn resulted in demethylation of CpG islands of STAT1 promoter and STAT1 overexpression.	MLN 8237	28-37	DNA methyltransferase 1	Homo sapiens	227-232
34522170-4	2021	Unexpectedly, we found that alisertib disrupted Aurora-A binding with ubiquitin-like with plant homeodomain and ring finger domain 1 (UHRF1), leading to UHRF1 mediated ubiquitination and degradation of DNA methyltransferase 1 (DNMT1), which in turn resulted in demethylation of CpG islands of STAT1 promoter and STAT1 overexpression.	MLN 8237	28-37	signal transducer and activator of transcription 1	Mus musculus	293-298
34522170-4	2021	Unexpectedly, we found that alisertib disrupted Aurora-A binding with ubiquitin-like with plant homeodomain and ring finger domain 1 (UHRF1), leading to UHRF1 mediated ubiquitination and degradation of DNA methyltransferase 1 (DNMT1), which in turn resulted in demethylation of CpG islands of STAT1 promoter and STAT1 overexpression.	MLN 8237	28-37	signal transducer and activator of transcription 1	Mus musculus	312-317
34107377-10	2021	JQ1+Alisertib combination treatment of a MYCN-amplified, TP53-null or TP53-restored genetically engineered mouse model of NBL prolonged survival better than either single agent.	MLN 8237	4-13	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	41-45
34107377-10	2021	JQ1+Alisertib combination treatment of a MYCN-amplified, TP53-null or TP53-restored genetically engineered mouse model of NBL prolonged survival better than either single agent.	MLN 8237	4-13	transformation related protein 53	Mus musculus	57-61
34107377-10	2021	JQ1+Alisertib combination treatment of a MYCN-amplified, TP53-null or TP53-restored genetically engineered mouse model of NBL prolonged survival better than either single agent.	MLN 8237	4-13	transformation related protein 53	Mus musculus	70-74
34107377-11	2021	This was most profound with TP53 restored, with marked tumor shrinkage and apoptosis induction in response to combination JQ1+Alisertib.	MLN 8237	126-135	transformation related protein 53	Mus musculus	28-32
35550115-0	2022	Aurora kinase a inhibitor MLN8237 suppresses pancreatic cancer growth.	MLN 8237	26-33	aurora kinase A	Homo sapiens	0-15
35550115-3	2022	MLN8237, an inhibitor of Aurora kinase-A, efficiently reduced the proliferation and motility of PDAC cells in vitro as well as tumor growth in orthotropic xenograft model and genetic pancreatic cancer animal models (p53/LSL/Pdx-Cre mice) in vivo.	MLN 8237	0-7	aurora kinase A	Mus musculus	25-40
35550115-3	2022	MLN8237, an inhibitor of Aurora kinase-A, efficiently reduced the proliferation and motility of PDAC cells in vitro as well as tumor growth in orthotropic xenograft model and genetic pancreatic cancer animal models (p53/LSL/Pdx-Cre mice) in vivo.	MLN 8237	0-7	transformation related protein 53, pseudogene	Mus musculus	216-219
35466883-8	2022	RESULTS: Aurora A inhibitor Alisertib and AKT inhibitor MK2206 displayed consistent and synergistic antiproliferation and proapoptotic effects.	MLN 8237	28-37	aurora kinase A	Mus musculus	9-17
35466883-13	2022	CONCLUSION: Combined administration of Aurora A inhibitor Alisertib and AKT inhibitor MK2206 can inhibit the proliferation of colon cancer cells and induce apoptosis, while inhibiting tumor growth in vivo.	MLN 8237	58-67	aurora kinase A	Mus musculus	39-47
35389552-6	2022	RESULTS: We identified an Aurora kinase A inhibitor (MLN8237) possessed a significant synergistic effect with BTZ on t(4;14) positive MM cells.	MLN 8237	53-60	aurora kinase A	Homo sapiens	26-41
35217309-0	2022	Combining selinexor with alisertib to target the p53 pathway in neuroblastoma.	MLN 8237	25-34	tumor protein p53	Homo sapiens	49-52
35217309-7	2022	Since this phosphorylation step is undertaken mostly by aurora kinase A (AURKA), we used the clinically available AURKA inhibitor, alisertib, and found p53-mediated lethality could be further augmented in three orthotopic xenograft mouse models.	MLN 8237	131-140	aurora kinase A	Mus musculus	56-71
35217309-7	2022	Since this phosphorylation step is undertaken mostly by aurora kinase A (AURKA), we used the clinically available AURKA inhibitor, alisertib, and found p53-mediated lethality could be further augmented in three orthotopic xenograft mouse models.	MLN 8237	131-140	aurora kinase A	Mus musculus	114-119
35217309-7	2022	Since this phosphorylation step is undertaken mostly by aurora kinase A (AURKA), we used the clinically available AURKA inhibitor, alisertib, and found p53-mediated lethality could be further augmented in three orthotopic xenograft mouse models.	MLN 8237	131-140	transformation related protein 53, pseudogene	Mus musculus	152-155
35217309-8	2022	These findings suggest a potential therapeutic benefit using selinexor and alisertib to synergistically increase p53-mediated cytotoxicity of high-risk neuroblastoma.	MLN 8237	75-84	transformation related protein 53, pseudogene	Mus musculus	113-116
35309907-4	2022	In this study, we established an in vitro senescence model using neuroblastoma cells subjected to low-dose Chemotherapeutic drug doxorubicin or the Aurora A inhibitor MLN8237.	MLN 8237	167-174	aurora kinase A	Homo sapiens	148-156
35054947-4	2022	The AURKA-selective inhibitor Aurora-A inhibitor I and novel derivatives as well as a structurally different inhibitor, Alisertib, prevented the cAMP-induced redistribution of AQP2.	MLN 8237	120-129	aquaporin 2	Rattus norvegicus	176-180
35059393-9	2021	Treatment with an AURKA inhibitor (alisertib) and an EZH2 inhibitor (gambogenic) inhibited HCC cell proliferation, migration, and invasion.	MLN 8237	35-44	aurora kinase A	Homo sapiens	18-23
34050235-3	2021	Here we describe the functional characterization of a PROTAC derived from AURKA inhibitor MLN8237 (alisertib).	MLN 8237	90-97	aurora kinase A	Homo sapiens	74-79
34050235-3	2021	Here we describe the functional characterization of a PROTAC derived from AURKA inhibitor MLN8237 (alisertib).	MLN 8237	99-108	aurora kinase A	Homo sapiens	74-79
33744274-0	2021	Alisertib inhibits migration and invasion of EGFR-TKI resistant cells by partially reversing the epithelial-mesenchymal transition.	MLN 8237	0-9	epidermal growth factor receptor	Homo sapiens	45-49
33744274-7	2021	Interestingly, the AURKA inhibitor, alisertib treatment restored the susceptibility of resistant cells to EGFR-TKIs and partially reversed the EMT process, thereby reducing migration and invasion in EGFR-TKI-resistant cells.	MLN 8237	36-45	aurora kinase A	Homo sapiens	19-24
33744274-7	2021	Interestingly, the AURKA inhibitor, alisertib treatment restored the susceptibility of resistant cells to EGFR-TKIs and partially reversed the EMT process, thereby reducing migration and invasion in EGFR-TKI-resistant cells.	MLN 8237	36-45	epidermal growth factor receptor	Homo sapiens	106-110
33744274-7	2021	Interestingly, the AURKA inhibitor, alisertib treatment restored the susceptibility of resistant cells to EGFR-TKIs and partially reversed the EMT process, thereby reducing migration and invasion in EGFR-TKI-resistant cells.	MLN 8237	36-45	epidermal growth factor receptor	Homo sapiens	199-203
33744274-8	2021	This study provides evidence that targeting AURKA signaling pathway by alisertib may be a novel approach for overcoming EGFR-TKI resistance and for the treatment of metastatic EGFR-TKIs in NSCLC patients.	MLN 8237	71-80	aurora kinase A	Homo sapiens	44-49
33744274-8	2021	This study provides evidence that targeting AURKA signaling pathway by alisertib may be a novel approach for overcoming EGFR-TKI resistance and for the treatment of metastatic EGFR-TKIs in NSCLC patients.	MLN 8237	71-80	epidermal growth factor receptor	Homo sapiens	120-124
33744274-8	2021	This study provides evidence that targeting AURKA signaling pathway by alisertib may be a novel approach for overcoming EGFR-TKI resistance and for the treatment of metastatic EGFR-TKIs in NSCLC patients.	MLN 8237	71-80	epidermal growth factor receptor	Homo sapiens	176-180
32978717-6	2021	In the present study, based on virtual drug screening of more than 48,000 natural compounds, the antibiotic deschloro-chlorotricin (DCCT) has been identified to bind to AURKA with even higher binding affinity (free bindung energy: -12.25 kcal/mol) than the known AURKA inhibitor, alisertib (free binding energy: -11.25 kcal/mol).	MLN 8237	280-289	aurora kinase A	Homo sapiens	169-174
33877311-2	2021	Objective: To compare paclitaxel alone vs paclitaxel plus alisertib in patients with ER-positive and ERBB2-negative or triple-negative metastatic breast cancer (MBC).	MLN 8237	58-67	estrogen receptor 1	Homo sapiens	85-87
33877311-2	2021	Objective: To compare paclitaxel alone vs paclitaxel plus alisertib in patients with ER-positive and ERBB2-negative or triple-negative metastatic breast cancer (MBC).	MLN 8237	58-67	erb-b2 receptor tyrosine kinase 2	Homo sapiens	101-106
33877311-17	2021	These data support further evaluation of alisertib in patients with ER-positive, ERBB2-negative MBC.	MLN 8237	41-50	estrogen receptor 1	Homo sapiens	68-70
33877311-17	2021	These data support further evaluation of alisertib in patients with ER-positive, ERBB2-negative MBC.	MLN 8237	41-50	erb-b2 receptor tyrosine kinase 2	Homo sapiens	81-86
33471959-2	2021	The selective Aurora-A inhibitor alisertib (MLN8237) has recently demonstrated promising antitumor responses as a single agent in various cancer types but its phase III clinical trial was reported as a failure since MLN8237 did not show an apparent effect in prolonging the survival of patients.	MLN 8237	33-42	aurora kinase A	Homo sapiens	14-22
33471959-2	2021	The selective Aurora-A inhibitor alisertib (MLN8237) has recently demonstrated promising antitumor responses as a single agent in various cancer types but its phase III clinical trial was reported as a failure since MLN8237 did not show an apparent effect in prolonging the survival of patients.	MLN 8237	44-51	aurora kinase A	Homo sapiens	14-22
33471959-7	2021	RESULTS: Among the hits, we observed that Haspin depletion or inhibition marginally inhibited breast cancer cell growth but could substantially enhance the killing effects of MLN8237.	MLN 8237	175-182	histone H3 associated protein kinase	Mus musculus	42-48
33163279-6	2020	Enhanced and rapid cervical cancer cell killing was observed when Alisertib was combined with inhibitors of either Bcl-2 (Venetoclax), Bcl-XL (A1331852) or Mcl-1 (A1210477) proteins, likely by accelerating apoptosis during mitotic delay due to the loss of functional Bcl-2, Mcl-1, or Bcl-XL.	MLN 8237	66-75	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	156-171
33163279-6	2020	Enhanced and rapid cervical cancer cell killing was observed when Alisertib was combined with inhibitors of either Bcl-2 (Venetoclax), Bcl-XL (A1331852) or Mcl-1 (A1210477) proteins, likely by accelerating apoptosis during mitotic delay due to the loss of functional Bcl-2, Mcl-1, or Bcl-XL.	MLN 8237	66-75	BCL2 apoptosis regulator	Homo sapiens	267-272
33163279-6	2020	Enhanced and rapid cervical cancer cell killing was observed when Alisertib was combined with inhibitors of either Bcl-2 (Venetoclax), Bcl-XL (A1331852) or Mcl-1 (A1210477) proteins, likely by accelerating apoptosis during mitotic delay due to the loss of functional Bcl-2, Mcl-1, or Bcl-XL.	MLN 8237	66-75	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	156-161
33163279-6	2020	Enhanced and rapid cervical cancer cell killing was observed when Alisertib was combined with inhibitors of either Bcl-2 (Venetoclax), Bcl-XL (A1331852) or Mcl-1 (A1210477) proteins, likely by accelerating apoptosis during mitotic delay due to the loss of functional Bcl-2, Mcl-1, or Bcl-XL.	MLN 8237	66-75	BCL2 like 1	Homo sapiens	284-290
32591441-3	2020	Interestingly, inhibition of Aurora kinase A (Aurora-A) by its selective inhibitor alisertib obviously induced infiltration of CD8+ T cells.	MLN 8237	83-92	aurora kinase A	Homo sapiens	29-44
32591441-3	2020	Interestingly, inhibition of Aurora kinase A (Aurora-A) by its selective inhibitor alisertib obviously induced infiltration of CD8+ T cells.	MLN 8237	83-92	aurora kinase A	Homo sapiens	46-54
32591441-3	2020	Interestingly, inhibition of Aurora kinase A (Aurora-A) by its selective inhibitor alisertib obviously induced infiltration of CD8+ T cells.	MLN 8237	83-92	CD8a molecule	Homo sapiens	127-130
32591441-5	2020	Our recent results demonstrated that conditional deletion of the AURKA gene or blockade of Aurora-A by alisertib slowed tumor growth in association with an increase in the infiltration of intratumoral CD8+ T cells as well as the mRNA levels of their interleukin-10 receptor a (IL-10Ra).	MLN 8237	103-112	aurora kinase A	Homo sapiens	91-99
32608142-2	2020	In a limited sample size, MYC copy-number gain or gene amplification, a candidate predictive biomarker for alisertib, did not correlate with improved response numbers or patient outcomes.	MLN 8237	107-116	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	26-29
32440158-0	2020	Inhibition of Aurora Kinase A by Alisertib Reduces Cell Proliferation and Induces Apoptosis and Autophagy in HuH-6 Human Hepatoblastoma Cells.	MLN 8237	33-42	aurora kinase A	Homo sapiens	14-29
32440158-9	2020	In vitro, AURKA knockdown significantly reduced the viability of HuH-6 cells, while ALS treatment significantly suppressed HuH-6 cell proliferation and induced G1-phase cell cycle arrest by reducing cyclin-D1 expression.	MLN 8237	84-87	cyclin D1	Homo sapiens	199-208
31911485-7	2020	In vitro, oxidative metabolism of alisertib was primarily mediated by CYP3A.	MLN 8237	34-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	70-75
32127951-5	2020	Afterwards, cell number counting, CCK-8 assay, and Caspase 3/7 assay were used to explore the antitumor effect of AURKA inhibitor Alisertib in vitro.	MLN 8237	130-139	aurora kinase A	Homo sapiens	114-119
32127951-10	2020	AURKA specific inhibitor Alisertib, inhibited cell growth, induced cell cycle arrest in G2/M phase, and promoted apoptosis in cholangiocarcinoma cell lines.	MLN 8237	25-34	aurora kinase A	Homo sapiens	0-5
32127951-12	2020	Furthermore, AURKA knockdown by siRNA recapitulated the antitumor effect of Alisertib.	MLN 8237	76-85	aurora kinase A	Mus musculus	13-18
31655296-8	2020	A subset of patients with c-Myc expression showed significantly improved PFS with alisertib/paclitaxel.	MLN 8237	82-91	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	26-31
31655296-12	2020	c-Myc expression and mutations in cell cycle regulators may be potential predictive biomarkers of alisertib efficacy; further prospective validations are warranted.	MLN 8237	98-107	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-5
31920463-0	2020	Silencing of AURKA augments the antitumor efficacy of the AURKA inhibitor MLN8237 on neuroblastoma cells.	MLN 8237	74-81	aurora kinase A	Homo sapiens	13-18
31920463-0	2020	Silencing of AURKA augments the antitumor efficacy of the AURKA inhibitor MLN8237 on neuroblastoma cells.	MLN 8237	74-81	aurora kinase A	Homo sapiens	58-63
31920463-4	2020	Here, we evaluated the inhibitory effects of AURKA inhibitor MLN8237 on neuroblastoma cells to understand the potential mechanisms responsible for tumor therapy.	MLN 8237	61-68	aurora kinase A	Homo sapiens	45-50
31920463-12	2020	Results: We demonstrate that MLN8237, an inhibitor of AURKA, induces the neuroblastoma cell line IMR32 into cellular senescence and G2/M cell phase arrest.	MLN 8237	29-36	aurora kinase A	Homo sapiens	54-59
31920463-14	2020	Although MLN8237 inhibits AURKA kinase activity, it has almost no inhibitory effect on the AURKA protein level.	MLN 8237	9-16	aurora kinase A	Homo sapiens	26-31
31920463-15	2020	By contrast, MLN8237 treatment leads to abnormal high expression of AURKA in vitro and in vivo.	MLN 8237	13-20	aurora kinase A	Homo sapiens	68-73
31920463-18	2020	Moreover, MLN8237 treatment followed by AURKA siRNA forces senescent cells into apoptosis via suppression of the Akt/Stat3 pathway.	MLN 8237	10-17	AKT serine/threonine kinase 1	Homo sapiens	113-116
31774882-0	2019	Development of an intravaginal ring for the topical delivery of Aurora kinase A inhibitor, MLN8237.	MLN 8237	91-98	aurora kinase A	Homo sapiens	64-79
31647033-7	2019	AURKA inhibition using 100 nM MLN8237 for 48 h decreases cell growth in a partially P53-dependent manner, and the survival rates of H460, HCC2429, and H1299 cells were 56, 50, and 77%, respectively.	MLN 8237	30-37	aurora kinase A	Homo sapiens	0-5
31647033-7	2019	AURKA inhibition using 100 nM MLN8237 for 48 h decreases cell growth in a partially P53-dependent manner, and the survival rates of H460, HCC2429, and H1299 cells were 56, 50, and 77%, respectively.	MLN 8237	30-37	tumor protein p53	Homo sapiens	84-87
31647033-11	2019	Modulation of P53 function could provide a new option for reversing cell resistance to the AURKA inhibitor MLN8237, which deserves further investigation.	MLN 8237	107-114	tumor protein p53	Homo sapiens	14-17
31647033-11	2019	Modulation of P53 function could provide a new option for reversing cell resistance to the AURKA inhibitor MLN8237, which deserves further investigation.	MLN 8237	107-114	aurora kinase A	Homo sapiens	91-96
31485600-10	2019	In an in vitro model, MLN8237, an AURKA inhibitor, could inhibit AURKA in LPS cell lines with a resultant G2/M arrest.	MLN 8237	22-29	aurora kinase A	Homo sapiens	34-39
31485600-10	2019	In an in vitro model, MLN8237, an AURKA inhibitor, could inhibit AURKA in LPS cell lines with a resultant G2/M arrest.	MLN 8237	22-29	aurora kinase A	Homo sapiens	65-70
31429028-12	2019	The combination of MLN8237 and conventional chemotherapy showed promising safety and anti-tumor activities in preclinical models of Myc-positive NHL.	MLN 8237	19-26	myelocytomatosis oncogene	Mus musculus	132-135
31207577-4	2019	We found that AURK-A inhibitor Alisertib and AURK-B inhibitor Barasertib strongly inhibited the growth and proliferation of t(8;21) AML cells.	MLN 8237	31-40	aurora kinase A	Homo sapiens	14-20
31254157-4	2019	Here, for the first time, we evaluated the effect of combining the AURKA inhibitor alisertib and the PAK inhibitor FRAX1036 in preclinical models of breast cancer.	MLN 8237	83-92	aurora kinase A	Homo sapiens	67-72
31063779-10	2019	LCCLs with inactivating mutations in TSC1 and TSC2 were sensitive to the mammalian target of rapamycin inhibitor rapamycin, and cells with inactivating mutations in TP53 were sensitive to the Aurora kinase A inhibitor alisertib.	MLN 8237	218-227	tumor protein p53	Homo sapiens	165-169
30902796-1	2019	The Aurora A inhibitor alisertib shows encouraging activities in clinical trials against advanced breast cancer.	MLN 8237	23-32	aurora kinase A	Mus musculus	4-12
30902796-5	2019	Furthermore, alisertib treatment disrupted the immunosuppressive functions of MDSC by inhibiting Stat3-mediated ROS production.	MLN 8237	13-22	signal transducer and activator of transcription 3	Mus musculus	97-102
31262832-3	2019	In this issue of Cancer Research, Yin and colleagues demonstrate unequivocally that the Aurora A kinase inhibitor, alisertib, specifically neutralizes MDSCs and triggers the rapid accrual of cytotoxic T cells, with consequent tumor clearance potentiated by PD-L1 blockade.	MLN 8237	115-124	CD274 molecule	Homo sapiens	257-262
30755439-5	2019	We evaluated treatment with the AURKA inhibitor alisertib (MLN8237) and the WEE1 inhibitor adavosertib (AZD1775), alone or in combination, using in vitro and in vivo HNSCC models.	MLN 8237	48-57	aurora kinase A	Homo sapiens	32-37
30755439-7	2019	Alisertib caused spindle defects, G2-M arrest and inhibitory CDK1 phosphorylation, and cytostasis in TP53 mutant HNSCC FaDu and UNC7 cells.	MLN 8237	0-9	cyclin dependent kinase 1	Homo sapiens	61-65
30755439-7	2019	Alisertib caused spindle defects, G2-M arrest and inhibitory CDK1 phosphorylation, and cytostasis in TP53 mutant HNSCC FaDu and UNC7 cells.	MLN 8237	0-9	tumor protein p53	Homo sapiens	101-105
31011934-0	2019	Cytotoxic synergy between alisertib and carboplatin versus alisertib and irinotecan are inversely dependent on MGMT levels in glioblastoma cells.	MLN 8237	26-35	O-6-methylguanine-DNA methyltransferase	Homo sapiens	111-115
31011934-0	2019	Cytotoxic synergy between alisertib and carboplatin versus alisertib and irinotecan are inversely dependent on MGMT levels in glioblastoma cells.	MLN 8237	59-68	O-6-methylguanine-DNA methyltransferase	Homo sapiens	111-115
31011934-2	2019	We have previously shown that the selective AURKA inhibitor alisertib potently inhibits growth of glioblastoma cells.	MLN 8237	60-69	aurora kinase A	Homo sapiens	44-49
31011934-5	2019	Western blotting showed that high MGMT expression in cell lines correlated with more pronounced potentiation of carboplatin"s growth inhibitory effects by alisertib, while low MGMT expression correlated with stronger potentiation of irinotecan by alisertib.	MLN 8237	155-164	O-6-methylguanine-DNA methyltransferase	Homo sapiens	34-38
31011934-7	2019	MGMT knockdown increased apoptosis caused by combined alisertib and irinotecan, while exogenous MGMT overexpression increased apoptosis from alisertib and carboplatin combination treatment.	MLN 8237	54-63	O-6-methylguanine-DNA methyltransferase	Homo sapiens	0-4
31011934-7	2019	MGMT knockdown increased apoptosis caused by combined alisertib and irinotecan, while exogenous MGMT overexpression increased apoptosis from alisertib and carboplatin combination treatment.	MLN 8237	141-150	O-6-methylguanine-DNA methyltransferase	Homo sapiens	96-100
31011934-8	2019	CONCLUSIONS: These results suggest that tumor MGMT expression levels may be predictive of patient response to these drug combinations, and importantly that the combination of alisertib and carboplatin may be selectively effective in glioblastoma patients with high tumor MGMT who are resistant to standard therapy.	MLN 8237	175-184	O-6-methylguanine-DNA methyltransferase	Homo sapiens	46-50
31011934-8	2019	CONCLUSIONS: These results suggest that tumor MGMT expression levels may be predictive of patient response to these drug combinations, and importantly that the combination of alisertib and carboplatin may be selectively effective in glioblastoma patients with high tumor MGMT who are resistant to standard therapy.	MLN 8237	175-184	O-6-methylguanine-DNA methyltransferase	Homo sapiens	271-275
30877245-10	2019	MLN8237, a Food and Drug Administration-approved AURKA inhibitor, selectively killed temozolomide-resistant primary glioma cells in vitro and prolonged the survival of a patient-derived xenograft mouse model with a high-CDC20-M signature.	MLN 8237	0-7	aurora kinase A	Homo sapiens	49-54
30877245-10	2019	MLN8237, a Food and Drug Administration-approved AURKA inhibitor, selectively killed temozolomide-resistant primary glioma cells in vitro and prolonged the survival of a patient-derived xenograft mouse model with a high-CDC20-M signature.	MLN 8237	0-7	cell division cycle 20	Mus musculus	220-225
30596512-4	2019	In support of these findings, we showed that alisertib, a pharmacological inhibitor of AURKA, causes primary cilia formation and cellular senescence by irreversibly arresting cell growth.	MLN 8237	45-54	aurora kinase A	Homo sapiens	87-92
30191522-0	2019	Phase I study combining the aurora kinase a inhibitor alisertib with mFOLFOX in gastrointestinal cancer.	MLN 8237	54-63	aurora kinase A	Homo sapiens	28-43
30191522-3	2019	Our preclinical data showed cooperative activity with the AURKA inhibitor alisertib and platinum agents in cell lines and xenografts, and suggested an optimal treatment window.	MLN 8237	74-83	aurora kinase A	Homo sapiens	58-63
30342037-9	2019	AURKA knockdown or inhibition with alisertib reduced levels of phosphorylated RPS6KB1 (at T389) and increased levels of proteins that induce apoptosis, including BIM, cleaved PARP, and cleaved caspase 3.	MLN 8237	35-44	aurora kinase A	Homo sapiens	0-5
30342037-9	2019	AURKA knockdown or inhibition with alisertib reduced levels of phosphorylated RPS6KB1 (at T389) and increased levels of proteins that induce apoptosis, including BIM, cleaved PARP, and cleaved caspase 3.	MLN 8237	35-44	ribosomal protein S6 kinase B1	Homo sapiens	78-85
30342037-9	2019	AURKA knockdown or inhibition with alisertib reduced levels of phosphorylated RPS6KB1 (at T389) and increased levels of proteins that induce apoptosis, including BIM, cleaved PARP, and cleaved caspase 3.	MLN 8237	35-44	poly(ADP-ribose) polymerase 1	Homo sapiens	175-179
30342037-13	2019	Alisertib reduced phosphorylation of RPS6KB1 and Ki-67 and increased levels of cleaved caspase 3 in tumor tissues.	MLN 8237	0-9	ribosomal protein S6 kinase B1	Homo sapiens	37-44
30177840-10	2019	In line with these findings, BRCA2-depleted and BRCA2-mutant human cell lines, or tumor cell lines derived from Brca2-/-;p53-/- mice showed increased sensitivity to the Aurora-A kinase inhibitor alisertib, with delayed mitotic progression and frequent mitotic failure.	MLN 8237	195-204	BRCA2 DNA repair associated	Homo sapiens	29-34
30177840-10	2019	In line with these findings, BRCA2-depleted and BRCA2-mutant human cell lines, or tumor cell lines derived from Brca2-/-;p53-/- mice showed increased sensitivity to the Aurora-A kinase inhibitor alisertib, with delayed mitotic progression and frequent mitotic failure.	MLN 8237	195-204	BRCA2 DNA repair associated	Homo sapiens	48-53
30177840-10	2019	In line with these findings, BRCA2-depleted and BRCA2-mutant human cell lines, or tumor cell lines derived from Brca2-/-;p53-/- mice showed increased sensitivity to the Aurora-A kinase inhibitor alisertib, with delayed mitotic progression and frequent mitotic failure.	MLN 8237	195-204	BRCA2 DNA repair associated	Homo sapiens	112-117
30177840-10	2019	In line with these findings, BRCA2-depleted and BRCA2-mutant human cell lines, or tumor cell lines derived from Brca2-/-;p53-/- mice showed increased sensitivity to the Aurora-A kinase inhibitor alisertib, with delayed mitotic progression and frequent mitotic failure.	MLN 8237	195-204	tumor protein p53	Homo sapiens	121-124
30177840-10	2019	In line with these findings, BRCA2-depleted and BRCA2-mutant human cell lines, or tumor cell lines derived from Brca2-/-;p53-/- mice showed increased sensitivity to the Aurora-A kinase inhibitor alisertib, with delayed mitotic progression and frequent mitotic failure.	MLN 8237	195-204	aurora kinase A	Mus musculus	169-177
30297384-5	2019	After discussion at the molecular tumor board, she was offered alisertib, an aurora A kinase inhibitor, on a single-patient expanded-use program and achieved prolonged disease stabilization.	MLN 8237	63-72	aurora kinase A	Homo sapiens	77-92
30297384-7	2019	KEY POINTS: Loss of the SWItch/Sucrose Non-Fermentable-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 gene (SMARCB1), which encodes integrase interactor 1 (INI-1), is associated with various mesenchymal malignancies, but a few carcinomas with rhabdoid features have been recently described as a distinct entity.INI-1-deficient carcinoma can be very aggressive, and there is no known treatment option available.There are encouraging preliminary data with an enhancer of zeste homolog 2 inhibitor, tazematostat, in INI-1-deficient malignancies, including INI-1-deficient carcinomas.Loss of INI-1 can activate aurora A kinase (AurkA), and inhibition of AurkA by alisertib could be a viable option and warrants further investigation in this cancer.Clinical genomic profiling can confirm diagnosis of molecularly defined malignancy and provide insights on therapeutic options.	MLN 8237	698-707	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1	Homo sapiens	147-154
30297384-7	2019	KEY POINTS: Loss of the SWItch/Sucrose Non-Fermentable-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 gene (SMARCB1), which encodes integrase interactor 1 (INI-1), is associated with various mesenchymal malignancies, but a few carcinomas with rhabdoid features have been recently described as a distinct entity.INI-1-deficient carcinoma can be very aggressive, and there is no known treatment option available.There are encouraging preliminary data with an enhancer of zeste homolog 2 inhibitor, tazematostat, in INI-1-deficient malignancies, including INI-1-deficient carcinomas.Loss of INI-1 can activate aurora A kinase (AurkA), and inhibition of AurkA by alisertib could be a viable option and warrants further investigation in this cancer.Clinical genomic profiling can confirm diagnosis of molecularly defined malignancy and provide insights on therapeutic options.	MLN 8237	698-707	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1	Homo sapiens	171-193
30297384-7	2019	KEY POINTS: Loss of the SWItch/Sucrose Non-Fermentable-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 gene (SMARCB1), which encodes integrase interactor 1 (INI-1), is associated with various mesenchymal malignancies, but a few carcinomas with rhabdoid features have been recently described as a distinct entity.INI-1-deficient carcinoma can be very aggressive, and there is no known treatment option available.There are encouraging preliminary data with an enhancer of zeste homolog 2 inhibitor, tazematostat, in INI-1-deficient malignancies, including INI-1-deficient carcinomas.Loss of INI-1 can activate aurora A kinase (AurkA), and inhibition of AurkA by alisertib could be a viable option and warrants further investigation in this cancer.Clinical genomic profiling can confirm diagnosis of molecularly defined malignancy and provide insights on therapeutic options.	MLN 8237	698-707	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1	Homo sapiens	195-200
30297384-7	2019	KEY POINTS: Loss of the SWItch/Sucrose Non-Fermentable-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 gene (SMARCB1), which encodes integrase interactor 1 (INI-1), is associated with various mesenchymal malignancies, but a few carcinomas with rhabdoid features have been recently described as a distinct entity.INI-1-deficient carcinoma can be very aggressive, and there is no known treatment option available.There are encouraging preliminary data with an enhancer of zeste homolog 2 inhibitor, tazematostat, in INI-1-deficient malignancies, including INI-1-deficient carcinomas.Loss of INI-1 can activate aurora A kinase (AurkA), and inhibition of AurkA by alisertib could be a viable option and warrants further investigation in this cancer.Clinical genomic profiling can confirm diagnosis of molecularly defined malignancy and provide insights on therapeutic options.	MLN 8237	698-707	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	496-523
30297384-7	2019	KEY POINTS: Loss of the SWItch/Sucrose Non-Fermentable-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 gene (SMARCB1), which encodes integrase interactor 1 (INI-1), is associated with various mesenchymal malignancies, but a few carcinomas with rhabdoid features have been recently described as a distinct entity.INI-1-deficient carcinoma can be very aggressive, and there is no known treatment option available.There are encouraging preliminary data with an enhancer of zeste homolog 2 inhibitor, tazematostat, in INI-1-deficient malignancies, including INI-1-deficient carcinomas.Loss of INI-1 can activate aurora A kinase (AurkA), and inhibition of AurkA by alisertib could be a viable option and warrants further investigation in this cancer.Clinical genomic profiling can confirm diagnosis of molecularly defined malignancy and provide insights on therapeutic options.	MLN 8237	698-707	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1	Homo sapiens	350-355
30297384-7	2019	KEY POINTS: Loss of the SWItch/Sucrose Non-Fermentable-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 gene (SMARCB1), which encodes integrase interactor 1 (INI-1), is associated with various mesenchymal malignancies, but a few carcinomas with rhabdoid features have been recently described as a distinct entity.INI-1-deficient carcinoma can be very aggressive, and there is no known treatment option available.There are encouraging preliminary data with an enhancer of zeste homolog 2 inhibitor, tazematostat, in INI-1-deficient malignancies, including INI-1-deficient carcinomas.Loss of INI-1 can activate aurora A kinase (AurkA), and inhibition of AurkA by alisertib could be a viable option and warrants further investigation in this cancer.Clinical genomic profiling can confirm diagnosis of molecularly defined malignancy and provide insights on therapeutic options.	MLN 8237	698-707	aurora kinase A	Homo sapiens	646-661
30297384-7	2019	KEY POINTS: Loss of the SWItch/Sucrose Non-Fermentable-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 gene (SMARCB1), which encodes integrase interactor 1 (INI-1), is associated with various mesenchymal malignancies, but a few carcinomas with rhabdoid features have been recently described as a distinct entity.INI-1-deficient carcinoma can be very aggressive, and there is no known treatment option available.There are encouraging preliminary data with an enhancer of zeste homolog 2 inhibitor, tazematostat, in INI-1-deficient malignancies, including INI-1-deficient carcinomas.Loss of INI-1 can activate aurora A kinase (AurkA), and inhibition of AurkA by alisertib could be a viable option and warrants further investigation in this cancer.Clinical genomic profiling can confirm diagnosis of molecularly defined malignancy and provide insights on therapeutic options.	MLN 8237	698-707	aurora kinase A	Homo sapiens	663-668
30297384-7	2019	KEY POINTS: Loss of the SWItch/Sucrose Non-Fermentable-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1 gene (SMARCB1), which encodes integrase interactor 1 (INI-1), is associated with various mesenchymal malignancies, but a few carcinomas with rhabdoid features have been recently described as a distinct entity.INI-1-deficient carcinoma can be very aggressive, and there is no known treatment option available.There are encouraging preliminary data with an enhancer of zeste homolog 2 inhibitor, tazematostat, in INI-1-deficient malignancies, including INI-1-deficient carcinomas.Loss of INI-1 can activate aurora A kinase (AurkA), and inhibition of AurkA by alisertib could be a viable option and warrants further investigation in this cancer.Clinical genomic profiling can confirm diagnosis of molecularly defined malignancy and provide insights on therapeutic options.	MLN 8237	698-707	aurora kinase A	Homo sapiens	689-694
30232224-3	2019	Alisertib inhibits the interaction between N-myc and its stabilizing factor Aurora-A, inhibiting N-myc signaling, and suppressing tumor growth.	MLN 8237	0-9	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	43-48
30232224-3	2019	Alisertib inhibits the interaction between N-myc and its stabilizing factor Aurora-A, inhibiting N-myc signaling, and suppressing tumor growth.	MLN 8237	0-9	aurora kinase A	Homo sapiens	76-84
30232224-3	2019	Alisertib inhibits the interaction between N-myc and its stabilizing factor Aurora-A, inhibiting N-myc signaling, and suppressing tumor growth.	MLN 8237	0-9	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	97-102
30547784-7	2018	Furthermore, we proved that AURKA inhibitor MLN8237 arrested BC cell growth and induced apoptosis.	MLN 8237	44-51	aurora kinase A	Homo sapiens	28-33
30292139-0	2018	A Novel Aurora-A Inhibitor (MLN8237) Synergistically Enhances the Antitumor Activity of Sorafenib in Hepatocellular Carcinoma.	MLN 8237	28-35	aurora kinase A	Homo sapiens	8-16
30292139-5	2018	Mechanism dissection suggests that the combination of MLN8237 and sorafenib led to significant inhibition of the activation of phospho-Akt (p-Akt) and phospho-p38 mitogen-activated protein kinase (p-p38 MAPK) and their downstream genes including CDK4, cyclinD1, and VEGFA.	MLN 8237	54-61	AKT serine/threonine kinase 1	Homo sapiens	135-138
30292139-5	2018	Mechanism dissection suggests that the combination of MLN8237 and sorafenib led to significant inhibition of the activation of phospho-Akt (p-Akt) and phospho-p38 mitogen-activated protein kinase (p-p38 MAPK) and their downstream genes including CDK4, cyclinD1, and VEGFA.	MLN 8237	54-61	AKT serine/threonine kinase 1	Homo sapiens	142-145
30292139-5	2018	Mechanism dissection suggests that the combination of MLN8237 and sorafenib led to significant inhibition of the activation of phospho-Akt (p-Akt) and phospho-p38 mitogen-activated protein kinase (p-p38 MAPK) and their downstream genes including CDK4, cyclinD1, and VEGFA.	MLN 8237	54-61	cyclin dependent kinase 4	Homo sapiens	246-250
30292139-5	2018	Mechanism dissection suggests that the combination of MLN8237 and sorafenib led to significant inhibition of the activation of phospho-Akt (p-Akt) and phospho-p38 mitogen-activated protein kinase (p-p38 MAPK) and their downstream genes including CDK4, cyclinD1, and VEGFA.	MLN 8237	54-61	cyclin D1	Homo sapiens	252-260
30292139-5	2018	Mechanism dissection suggests that the combination of MLN8237 and sorafenib led to significant inhibition of the activation of phospho-Akt (p-Akt) and phospho-p38 mitogen-activated protein kinase (p-p38 MAPK) and their downstream genes including CDK4, cyclinD1, and VEGFA.	MLN 8237	54-61	vascular endothelial growth factor A	Homo sapiens	266-271
30292139-6	2018	The activators of p-Akt and p-p38 MAPK signaling partially reversed the synergistic inhibitory effects of sorafenib and MLN8237 on HCC progression.	MLN 8237	120-127	AKT serine/threonine kinase 1	Homo sapiens	20-23
30226440-0	2018	c-Myc Is a Major Determinant for Antitumor Activity of Aurora A Kinase Inhibitor MLN8237 in Thyroid Cancer.	MLN 8237	81-88	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-5
30226440-0	2018	c-Myc Is a Major Determinant for Antitumor Activity of Aurora A Kinase Inhibitor MLN8237 in Thyroid Cancer.	MLN 8237	81-88	aurora kinase A	Homo sapiens	55-70
30013191-5	2018	Furthermore, knockdown of MMSET potently inhibits tumorigenic cells and renders them sensitive to growth inhibition by the therapeutic drug, alisertib (AURKA inhibitor).	MLN 8237	141-150	nuclear receptor binding SET domain protein 2	Homo sapiens	26-31
30013191-5	2018	Furthermore, knockdown of MMSET potently inhibits tumorigenic cells and renders them sensitive to growth inhibition by the therapeutic drug, alisertib (AURKA inhibitor).	MLN 8237	141-150	aurora kinase A	Homo sapiens	152-157
30153557-4	2018	We report our studies on the concomitant use of the BRD4 inhibitor I-BET151 and AURKA inhibitor alisertib.	MLN 8237	96-105	aurora kinase A	Homo sapiens	80-85
30197758-5	2018	Treatment with the Aurora kinase A inhibitor alisertib blocked Ph+ leukemia cell proliferation and Aurora kinase A phosphorylation; it also induced G2/M-phase arrest and increased the intracellular levels of reactive oxygen species.	MLN 8237	45-54	aurora kinase A	Mus musculus	19-34
30197758-5	2018	Treatment with the Aurora kinase A inhibitor alisertib blocked Ph+ leukemia cell proliferation and Aurora kinase A phosphorylation; it also induced G2/M-phase arrest and increased the intracellular levels of reactive oxygen species.	MLN 8237	45-54	aurora kinase A	Mus musculus	99-114
29863884-3	2018	MLN8237 (alisertib) is a known inhibitor of aurora kinases; its specificity for AURKA, however, is compromised by its poor solubility and transport across the cell membrane.	MLN 8237	0-7	aurora kinase A	Homo sapiens	80-85
29863884-3	2018	MLN8237 (alisertib) is a known inhibitor of aurora kinases; its specificity for AURKA, however, is compromised by its poor solubility and transport across the cell membrane.	MLN 8237	9-18	aurora kinase A	Homo sapiens	80-85
29942081-5	2018	Incomplete inhibition of AURKA was a common source of therapy failure, and combinations of PI3K, AKT or mTOR inhibitors with the AURKA inhibitor MLN8237 were highly synergistic and durably suppressed mTOR signaling, resulting in apoptosis and tumor regression in vivo.	MLN 8237	145-152	aurora kinase A	Homo sapiens	25-30
29942081-5	2018	Incomplete inhibition of AURKA was a common source of therapy failure, and combinations of PI3K, AKT or mTOR inhibitors with the AURKA inhibitor MLN8237 were highly synergistic and durably suppressed mTOR signaling, resulting in apoptosis and tumor regression in vivo.	MLN 8237	145-152	AKT serine/threonine kinase 1	Homo sapiens	97-100
29942081-5	2018	Incomplete inhibition of AURKA was a common source of therapy failure, and combinations of PI3K, AKT or mTOR inhibitors with the AURKA inhibitor MLN8237 were highly synergistic and durably suppressed mTOR signaling, resulting in apoptosis and tumor regression in vivo.	MLN 8237	145-152	mechanistic target of rapamycin kinase	Homo sapiens	104-108
29942081-5	2018	Incomplete inhibition of AURKA was a common source of therapy failure, and combinations of PI3K, AKT or mTOR inhibitors with the AURKA inhibitor MLN8237 were highly synergistic and durably suppressed mTOR signaling, resulting in apoptosis and tumor regression in vivo.	MLN 8237	145-152	aurora kinase A	Homo sapiens	129-134
29942081-5	2018	Incomplete inhibition of AURKA was a common source of therapy failure, and combinations of PI3K, AKT or mTOR inhibitors with the AURKA inhibitor MLN8237 were highly synergistic and durably suppressed mTOR signaling, resulting in apoptosis and tumor regression in vivo.	MLN 8237	145-152	mechanistic target of rapamycin kinase	Homo sapiens	200-204
29845253-4	2018	The anti-tumor activities of alisertib, an AURKA-specific chemical inhibitor, were detected by Cell Counting Kit-8 assay in vitro and mouse xenograft model in vivo.	MLN 8237	29-38	aurora kinase A	Mus musculus	43-48
29845253-7	2018	By contrast, alisertib-resistant CAKI and ACHN cells expressed the wild type VHL gene.	MLN 8237	13-22	von Hippel-Lindau tumor suppressor	Homo sapiens	77-80
29845253-8	2018	In addition, rescue or knockdown of VHL was observed to increase or decrease alisertib anti-proliferation activity, respectively, in RCC cells.	MLN 8237	77-86	von Hippel-Lindau tumor suppressor	Homo sapiens	36-39
29571950-5	2018	Golgi dispersal was also induced by a selective Aurora A inhibitor, MLN8237.	MLN 8237	68-75	aurora kinase A	Homo sapiens	48-56
29477140-4	2018	We revealed that the AURKA inhibitor alisertib accelerates the expression of the H3K27 demethylase KDM6B, thereby dissociating AURKA and YY1 from the KDM6B promoter region.	MLN 8237	37-46	aurora kinase A	Homo sapiens	21-26
29477140-4	2018	We revealed that the AURKA inhibitor alisertib accelerates the expression of the H3K27 demethylase KDM6B, thereby dissociating AURKA and YY1 from the KDM6B promoter region.	MLN 8237	37-46	lysine demethylase 6B	Homo sapiens	99-104
29477140-4	2018	We revealed that the AURKA inhibitor alisertib accelerates the expression of the H3K27 demethylase KDM6B, thereby dissociating AURKA and YY1 from the KDM6B promoter region.	MLN 8237	37-46	aurora kinase A	Homo sapiens	127-132
29477140-4	2018	We revealed that the AURKA inhibitor alisertib accelerates the expression of the H3K27 demethylase KDM6B, thereby dissociating AURKA and YY1 from the KDM6B promoter region.	MLN 8237	37-46	YY1 transcription factor	Homo sapiens	137-140
29477140-4	2018	We revealed that the AURKA inhibitor alisertib accelerates the expression of the H3K27 demethylase KDM6B, thereby dissociating AURKA and YY1 from the KDM6B promoter region.	MLN 8237	37-46	lysine demethylase 6B	Homo sapiens	150-155
29477140-5	2018	Using Flow cytometry, we found that alisertib induces THP-1 differentiation into monocytes.	MLN 8237	36-45	GLI family zinc finger 2	Homo sapiens	54-59
29396807-0	2018	The CNS penetrating taxane TPI 287 and the AURKA inhibitor alisertib induce synergistic apoptosis in glioblastoma cells.	MLN 8237	59-68	aurora kinase A	Homo sapiens	43-48
29396807-2	2018	The AURKA inhibitor alisertib exhibits antiproliferative activity against glioblastoma in vitro and in vivo.	MLN 8237	20-29	aurora kinase A	Homo sapiens	4-9
29396807-7	2018	TPI 287 not only potentiated the cytotoxicity of the AURKA inhibitors alisertib, MLN8054 and TC-A2317, but was often potently synergistic.	MLN 8237	70-79	triosephosphate isomerase 1	Homo sapiens	0-3
29396807-7	2018	TPI 287 not only potentiated the cytotoxicity of the AURKA inhibitors alisertib, MLN8054 and TC-A2317, but was often potently synergistic.	MLN 8237	70-79	aurora kinase A	Homo sapiens	53-58
29289986-2	2018	Alisertib is an oral selective inhibitor of AURKA.	MLN 8237	0-9	aurora kinase A	Homo sapiens	44-49
28852909-1	2018	Aim Two studies investigated the effect of gastric acid reducing agents and strong inducers/inhibitors of CYP3A4 on the pharmacokinetics of alisertib, an investigational Aurora A kinase inhibitor, in patients with advanced malignancies.	MLN 8237	140-149	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	106-112
29269934-7	2017	The growth of the cells was also significantly inhibited by an AURKA specific inhibitor, alisertib (MLN8237).	MLN 8237	89-98	aurora kinase A	Homo sapiens	63-68
29269934-7	2017	The growth of the cells was also significantly inhibited by an AURKA specific inhibitor, alisertib (MLN8237).	MLN 8237	100-107	aurora kinase A	Homo sapiens	63-68
28482026-6	2017	Results: BT183 cells are very sensitive to the topoisomerase inhibitors topotecan and doxorubicin, to the epigenetic agents decitabine and panobinostat, to actinomycin D, and to targeted drugs such as the polo-like kinase 1 (PLK1) inhibitor volasertib, the aurora kinase A inhibitor alisertib, and the mammalian target of rapamycin (mTOR) inhibitor MLN0128.	MLN 8237	283-292	polo like kinase 1	Homo sapiens	205-223
29291012-0	2017	Alisertib promotes apoptosis and autophagy in melanoma through p38 MAPK-mediated aurora a signaling.	MLN 8237	0-9	mitogen-activated protein kinase 14	Homo sapiens	63-66
29291012-1	2017	We investigated the efficacy of Alisertib (ALS), a selective Aurora kinase A (AURKA) inhibitor, in melanoma.	MLN 8237	32-41	aurora kinase A	Homo sapiens	61-76
29291012-1	2017	We investigated the efficacy of Alisertib (ALS), a selective Aurora kinase A (AURKA) inhibitor, in melanoma.	MLN 8237	32-41	aurora kinase A	Homo sapiens	78-83
29122619-0	2017	Aurora A Functional Single Nucleotide Polymorphism (SNP) Correlates With Clinical Outcome in Patients With Advanced Solid Tumors Treated With Alisertib, an Investigational Aurora A Kinase Inhibitor.	MLN 8237	142-151	aurora kinase A	Homo sapiens	0-8
29122619-0	2017	Aurora A Functional Single Nucleotide Polymorphism (SNP) Correlates With Clinical Outcome in Patients With Advanced Solid Tumors Treated With Alisertib, an Investigational Aurora A Kinase Inhibitor.	MLN 8237	142-151	aurora kinase A	Homo sapiens	172-180
29122619-1	2017	BACKGROUND: Alisertib (MLN8237) is an investigational, oral, selective Aurora A kinase inhibitor.	MLN 8237	12-21	aurora kinase A	Homo sapiens	71-79
29122619-1	2017	BACKGROUND: Alisertib (MLN8237) is an investigational, oral, selective Aurora A kinase inhibitor.	MLN 8237	23-30	aurora kinase A	Homo sapiens	71-79
29122619-13	2017	INTERPRETATION: These findings suggest that Aurora A SNP at codon 57 may predict disease outcome and response to alisertib in patients with solid tumors.	MLN 8237	113-122	aurora kinase A	Homo sapiens	44-52
28847989-6	2017	Alisertib was tested as AURKA inhibitor and LY2603618 as CHEK1 inhibitor.	MLN 8237	0-9	aurora kinase A	Homo sapiens	24-29
29245981-7	2017	Combination of alisertib with pan-PI3K inhibition or VCR significantly reduced PD-L1, NF-kappaB expression and inhibited phosphorylation of AKT, ERK1/2 and AK with enhanced apoptosis.	MLN 8237	15-24	CD274 antigen	Mus musculus	79-84
29245981-7	2017	Combination of alisertib with pan-PI3K inhibition or VCR significantly reduced PD-L1, NF-kappaB expression and inhibited phosphorylation of AKT, ERK1/2 and AK with enhanced apoptosis.	MLN 8237	15-24	thymoma viral proto-oncogene 1	Mus musculus	140-143
29245981-7	2017	Combination of alisertib with pan-PI3K inhibition or VCR significantly reduced PD-L1, NF-kappaB expression and inhibited phosphorylation of AKT, ERK1/2 and AK with enhanced apoptosis.	MLN 8237	15-24	mitogen-activated protein kinase 3	Mus musculus	145-151
29022893-10	2017	In addition, Aurora inhibitor MLN8237 inhibited the proliferation of erythroleukemia cells through repression of MYCN/EZH2 axis, whereas it minimally affected the normal hematopoietic cells.	MLN 8237	30-37	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	113-117
29022893-10	2017	In addition, Aurora inhibitor MLN8237 inhibited the proliferation of erythroleukemia cells through repression of MYCN/EZH2 axis, whereas it minimally affected the normal hematopoietic cells.	MLN 8237	30-37	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	118-122
28602975-10	2017	Furthermore, combinations of YK-4-279 with vincristine, paclitaxel or the Aurora kinase A inhibitor MLN8237/Alisertib show strong synergy, particularly at low doses.	MLN 8237	100-107	aurora kinase A	Homo sapiens	74-89
28602975-10	2017	Furthermore, combinations of YK-4-279 with vincristine, paclitaxel or the Aurora kinase A inhibitor MLN8237/Alisertib show strong synergy, particularly at low doses.	MLN 8237	108-117	aurora kinase A	Homo sapiens	74-89
28522591-3	2017	Alisertib has inhibitory activity against both Aurora A and B, although it is considered to be primarily an Aurora A inhibitor in vivo Here, we show that alisertib inhibits both Aurora A and B in vivo in preclinical models of HPV-driven cervical cancer, and that it is the inhibition of Aurora A and B that provides the selectivity and efficacy of this drug in vivo in this disease setting.	MLN 8237	0-9	aurora kinase A	Homo sapiens	47-61
28522591-3	2017	Alisertib has inhibitory activity against both Aurora A and B, although it is considered to be primarily an Aurora A inhibitor in vivo Here, we show that alisertib inhibits both Aurora A and B in vivo in preclinical models of HPV-driven cervical cancer, and that it is the inhibition of Aurora A and B that provides the selectivity and efficacy of this drug in vivo in this disease setting.	MLN 8237	0-9	aurora kinase A	Homo sapiens	47-55
28522591-3	2017	Alisertib has inhibitory activity against both Aurora A and B, although it is considered to be primarily an Aurora A inhibitor in vivo Here, we show that alisertib inhibits both Aurora A and B in vivo in preclinical models of HPV-driven cervical cancer, and that it is the inhibition of Aurora A and B that provides the selectivity and efficacy of this drug in vivo in this disease setting.	MLN 8237	154-163	aurora kinase A	Homo sapiens	47-55
28522591-3	2017	Alisertib has inhibitory activity against both Aurora A and B, although it is considered to be primarily an Aurora A inhibitor in vivo Here, we show that alisertib inhibits both Aurora A and B in vivo in preclinical models of HPV-driven cervical cancer, and that it is the inhibition of Aurora A and B that provides the selectivity and efficacy of this drug in vivo in this disease setting.	MLN 8237	154-163	aurora kinase A	Homo sapiens	108-116
28522591-3	2017	Alisertib has inhibitory activity against both Aurora A and B, although it is considered to be primarily an Aurora A inhibitor in vivo Here, we show that alisertib inhibits both Aurora A and B in vivo in preclinical models of HPV-driven cervical cancer, and that it is the inhibition of Aurora A and B that provides the selectivity and efficacy of this drug in vivo in this disease setting.	MLN 8237	154-163	aurora kinase A	Homo sapiens	108-116
29207686-5	2017	Breast cancer cells overexpressing Aurora-A showed resistance to conventional chemotherapeutic agents, while treatment with alisertib, a selective Aurora-A kinase inhibitor, restored chemosensitivity.	MLN 8237	124-133	aurora kinase A	Homo sapiens	147-155
28155045-0	2017	Association of an aurora kinase a (AURKA) gene polymorphism with progression-free survival in patients with advanced urothelial carcinoma treated with the selective aurora kinase a inhibitor alisertib.	MLN 8237	191-200	aurora kinase A	Homo sapiens	18-33
28155045-0	2017	Association of an aurora kinase a (AURKA) gene polymorphism with progression-free survival in patients with advanced urothelial carcinoma treated with the selective aurora kinase a inhibitor alisertib.	MLN 8237	191-200	aurora kinase A	Homo sapiens	35-40
28155045-0	2017	Association of an aurora kinase a (AURKA) gene polymorphism with progression-free survival in patients with advanced urothelial carcinoma treated with the selective aurora kinase a inhibitor alisertib.	MLN 8237	191-200	aurora kinase A	Homo sapiens	165-180
28155045-2	2017	A single-arm trial in patients with advanced or metastatic urothelial carcinoma refractive to other therapies found that alisertib, a selective inhibitor of aurora kinase A, maintained stable disease in a few cases, despite a low objective response rate.	MLN 8237	121-130	aurora kinase A	Homo sapiens	157-172
28155045-3	2017	To better understand why some patients benefited from alisertib, we genotyped the 22 patients of this pilot trial for two single nucleotide polymorphisms (rs2273535 and rs1047972) in AURKA, the gene encoding aurora kinase A, and looked for associations with survival and treatment response.	MLN 8237	54-63	aurora kinase A	Homo sapiens	183-188
28155045-8	2017	Conclusion In patients who received alisertib for advanced or metastatic urothelial carcinoma, longer progression-free survival was observed in carriers of the minor allele A of rs2273535 in AURKA than in patients who were homozygous for the major allele T. This finding, based on a small pilot trial, warrants further investigation.	MLN 8237	36-45	aurora kinase A	Homo sapiens	191-196
28073841-6	2017	Targeting AURKA using genetic knockdown or a small-molecule inhibitor, alisertib, reversed these molecular events, leading to a decrease in cancer cell survival in acquired and intrinsic resistant cell models.	MLN 8237	71-80	aurora kinase A	Mus musculus	10-15
28073841-8	2017	Data from tumor xenograft mouse models confirmed that everolimus-resistant cancer cells are sensitive to alisertib.Conclusions: Our results indicate that AURKA plays an important role in the activation of EIF4E and cap-dependent translation.	MLN 8237	105-114	aurora kinase A	Mus musculus	154-159
28073841-8	2017	Data from tumor xenograft mouse models confirmed that everolimus-resistant cancer cells are sensitive to alisertib.Conclusions: Our results indicate that AURKA plays an important role in the activation of EIF4E and cap-dependent translation.	MLN 8237	105-114	eukaryotic translation initiation factor 4E	Mus musculus	205-210
28073841-9	2017	Targeting the AURKA-EIF4E-c-MYC axis using alisertib is a novel therapeutic strategy that can be applicable for everolimus-resistant tumors and/or subgroups of cancers that show overexpression of AURKA and activation of EIF4E and c-MYC.	MLN 8237	43-52	aurora kinase A	Mus musculus	14-19
28073841-9	2017	Targeting the AURKA-EIF4E-c-MYC axis using alisertib is a novel therapeutic strategy that can be applicable for everolimus-resistant tumors and/or subgroups of cancers that show overexpression of AURKA and activation of EIF4E and c-MYC.	MLN 8237	43-52	eukaryotic translation initiation factor 4E	Mus musculus	20-25
28073841-9	2017	Targeting the AURKA-EIF4E-c-MYC axis using alisertib is a novel therapeutic strategy that can be applicable for everolimus-resistant tumors and/or subgroups of cancers that show overexpression of AURKA and activation of EIF4E and c-MYC.	MLN 8237	43-52	aurora kinase A	Mus musculus	196-201
28073841-9	2017	Targeting the AURKA-EIF4E-c-MYC axis using alisertib is a novel therapeutic strategy that can be applicable for everolimus-resistant tumors and/or subgroups of cancers that show overexpression of AURKA and activation of EIF4E and c-MYC.	MLN 8237	43-52	eukaryotic translation initiation factor 4E	Mus musculus	220-225
28881569-6	2017	Further, specific inhibition of AURKA activity with the small molecule inhibitor, alisertib, stimulated the non-homologous end-joining (NHEJ) repair pathway by elevating DNA-PKcs activity, a catalytic subunit required for double-strand break (DSB) repair, as well as decreased the expression of PARP and BRCA1/2, which are required for high-fidelity homologous recombination-based DNA repair.	MLN 8237	82-91	aurora kinase A	Homo sapiens	32-37
28881569-6	2017	Further, specific inhibition of AURKA activity with the small molecule inhibitor, alisertib, stimulated the non-homologous end-joining (NHEJ) repair pathway by elevating DNA-PKcs activity, a catalytic subunit required for double-strand break (DSB) repair, as well as decreased the expression of PARP and BRCA1/2, which are required for high-fidelity homologous recombination-based DNA repair.	MLN 8237	82-91	poly(ADP-ribose) polymerase 1	Homo sapiens	295-299
28881569-6	2017	Further, specific inhibition of AURKA activity with the small molecule inhibitor, alisertib, stimulated the non-homologous end-joining (NHEJ) repair pathway by elevating DNA-PKcs activity, a catalytic subunit required for double-strand break (DSB) repair, as well as decreased the expression of PARP and BRCA1/2, which are required for high-fidelity homologous recombination-based DNA repair.	MLN 8237	82-91	BRCA1 DNA repair associated	Homo sapiens	304-311
28881569-8	2017	Consistent with in vitro findings, alisertib treatment increased phosphorylated DNA-PKcs(pDNA-PKcsT2609) and decreased PARP levels in vivo.	MLN 8237	35-44	poly(ADP-ribose) polymerase 1	Homo sapiens	119-123
28386317-0	2017	Alisertib induces G2/M arrest, apoptosis, and autophagy via PI3K/Akt/mTOR- and p38 MAPK-mediated pathways in human glioblastoma cells.	MLN 8237	0-9	AKT serine/threonine kinase 1	Homo sapiens	65-68
28386317-0	2017	Alisertib induces G2/M arrest, apoptosis, and autophagy via PI3K/Akt/mTOR- and p38 MAPK-mediated pathways in human glioblastoma cells.	MLN 8237	0-9	mechanistic target of rapamycin kinase	Homo sapiens	69-73
28386317-0	2017	Alisertib induces G2/M arrest, apoptosis, and autophagy via PI3K/Akt/mTOR- and p38 MAPK-mediated pathways in human glioblastoma cells.	MLN 8237	0-9	mitogen-activated protein kinase 14	Homo sapiens	79-82
28386317-2	2017	Alisertib (ALS), a second-generation selective Aurora kinase A (AURKA) inhibitor, has shown potent anticancer effects on solid tumors in animal studies.	MLN 8237	0-9	aurora kinase A	Homo sapiens	47-62
28386317-2	2017	Alisertib (ALS), a second-generation selective Aurora kinase A (AURKA) inhibitor, has shown potent anticancer effects on solid tumors in animal studies.	MLN 8237	0-9	aurora kinase A	Homo sapiens	64-69
27797168-4	2017	Herein, the cross-talk between these pathways was investigated, using the single-target reference compounds MP7 (PDK1 inhibitor) and Alisertib (AurA inhibitor).	MLN 8237	133-142	aurora kinase A	Homo sapiens	144-148
27816996-2	2017	Alisertib (MLN8237) is an orally administered selective AURKA inhibitor with potent antiproliferative activity, currently undergoing clinical testing in different tumor types.	MLN 8237	0-9	aurora kinase A	Homo sapiens	56-61
27816996-2	2017	Alisertib (MLN8237) is an orally administered selective AURKA inhibitor with potent antiproliferative activity, currently undergoing clinical testing in different tumor types.	MLN 8237	11-18	aurora kinase A	Homo sapiens	56-61
28178640-2	2016	BACKGROUND: We hypothesized that Aurora A kinase (AK) contributes to castrate resistance in prostate cancer (PCa) and that inhibiting AK with alisertib can resensitize PCa cells to androgen receptor (AR) inhibitor abiraterone.	MLN 8237	142-151	androgen receptor	Homo sapiens	181-198
28178640-2	2016	BACKGROUND: We hypothesized that Aurora A kinase (AK) contributes to castrate resistance in prostate cancer (PCa) and that inhibiting AK with alisertib can resensitize PCa cells to androgen receptor (AR) inhibitor abiraterone.	MLN 8237	142-151	androgen receptor	Homo sapiens	200-202
27502708-3	2016	MLN8237 (alisertib) is a novel oral adenosine triphosphate-competitive AURKA inhibitor.	MLN 8237	0-7	aurora kinase A	Homo sapiens	71-76
27502708-3	2016	MLN8237 (alisertib) is a novel oral adenosine triphosphate-competitive AURKA inhibitor.	MLN 8237	9-18	aurora kinase A	Homo sapiens	71-76
27385211-0	2016	Antitumor activity of the aurora a selective kinase inhibitor, alisertib, against preclinical models of colorectal cancer.	MLN 8237	63-72	aurora kinase A	Homo sapiens	26-34
27385211-2	2016	Alisertib (MLN8237) is an investigational Aurora A selective inhibitor that has demonstrated activity against a wide variety of tumor types in vitro and in vivo, including CRC.	MLN 8237	0-9	aurora kinase A	Homo sapiens	42-50
27385211-2	2016	Alisertib (MLN8237) is an investigational Aurora A selective inhibitor that has demonstrated activity against a wide variety of tumor types in vitro and in vivo, including CRC.	MLN 8237	11-18	aurora kinase A	Homo sapiens	42-50
27235164-0	2016	Combination of Eribulin and Aurora A Inhibitor MLN8237 Prevents Metastatic Colonization and Induces Cytotoxic Autophagy in Breast Cancer.	MLN 8237	47-54	aurora kinase A	Homo sapiens	28-36
27235164-2	2016	In the current study, we determined the effects of AURKA inhibition by the small molecule inhibitor MLN8237 both as a monotherapy and in combination with the microtubule-targeting drug eribulin on different stages of metastasis in triple-negative breast cancer (TNBC) and defined the potential mechanism of its action.	MLN 8237	100-107	aurora kinase A	Homo sapiens	51-56
27446393-10	2016	In addition, the transfection of a NEAT1 overexpression plasmid into K562 and THP-1 leukemia cell lines alleviated MDR induced by cytotoxic agents, such as Alisertib and Bortezomib, through inhibition of ATP-binding cassette G2.	MLN 8237	156-165	nuclear paraspeckle assembly transcript 1	Homo sapiens	35-40
27177156-0	2016	Alisertib induces apoptosis and autophagy through targeting the AKT/mTOR/AMPK/p38 pathway in leukemic cells.	MLN 8237	0-9	AKT serine/threonine kinase 1	Homo sapiens	64-67
27177156-0	2016	Alisertib induces apoptosis and autophagy through targeting the AKT/mTOR/AMPK/p38 pathway in leukemic cells.	MLN 8237	0-9	mechanistic target of rapamycin kinase	Homo sapiens	68-72
27177156-0	2016	Alisertib induces apoptosis and autophagy through targeting the AKT/mTOR/AMPK/p38 pathway in leukemic cells.	MLN 8237	0-9	mitogen-activated protein kinase 14	Homo sapiens	78-81
27177156-4	2016	Acid phosphatase, MTT and Annexin V/propidium iodide staining assays as well as immunostaining for light chain 3B showed that treatment of the REH leukemia cell line with alisertib exerted potent growth inhibitory effects, and induced apoptosis and autophagy in a dose-dependent manner.	MLN 8237	171-180	annexin A5	Homo sapiens	26-35
26999067-0	2016	An update on the pharmacokinetics and pharmacodynamics of alisertib, a selective Aurora kinase A inhibitor.	MLN 8237	58-67	aurora kinase A	Homo sapiens	81-96
26999067-6	2016	MLN8237, also known as alisertib, is one selective AURKA inhibitor that has shown remarkable anticancer effects in preclinical studies.	MLN 8237	0-7	aurora kinase A	Homo sapiens	51-56
26999067-6	2016	MLN8237, also known as alisertib, is one selective AURKA inhibitor that has shown remarkable anticancer effects in preclinical studies.	MLN 8237	23-32	aurora kinase A	Homo sapiens	51-56
27121204-6	2016	We observed that MLN8237, which is a specific inhibitor of AURKA, decreased the beta-catenin and the phosphorylation of Akt1 and GSK-3beta, as well as blocked the Akt and Wnt signaling pathways.	MLN 8237	17-24	aurora kinase A	Homo sapiens	59-64
27121204-6	2016	We observed that MLN8237, which is a specific inhibitor of AURKA, decreased the beta-catenin and the phosphorylation of Akt1 and GSK-3beta, as well as blocked the Akt and Wnt signaling pathways.	MLN 8237	17-24	catenin beta 1	Homo sapiens	80-92
27121204-6	2016	We observed that MLN8237, which is a specific inhibitor of AURKA, decreased the beta-catenin and the phosphorylation of Akt1 and GSK-3beta, as well as blocked the Akt and Wnt signaling pathways.	MLN 8237	17-24	AKT serine/threonine kinase 1	Homo sapiens	120-124
27121204-6	2016	We observed that MLN8237, which is a specific inhibitor of AURKA, decreased the beta-catenin and the phosphorylation of Akt1 and GSK-3beta, as well as blocked the Akt and Wnt signaling pathways.	MLN 8237	17-24	glycogen synthase kinase 3 beta	Homo sapiens	129-138
27121204-6	2016	We observed that MLN8237, which is a specific inhibitor of AURKA, decreased the beta-catenin and the phosphorylation of Akt1 and GSK-3beta, as well as blocked the Akt and Wnt signaling pathways.	MLN 8237	17-24	AKT serine/threonine kinase 1	Homo sapiens	120-123
26873642-0	2016	An open-label, single-arm, phase 2 study of the Aurora kinase A inhibitor alisertib in patients with advanced urothelial cancer.	MLN 8237	74-83	aurora kinase A	Homo sapiens	48-63
26873642-2	2016	Alisertib is an orally available, selective inhibitor of the aurora kinase A.	MLN 8237	0-9	aurora kinase A	Homo sapiens	61-76
26887042-0	2016	MLN-8237: A dual inhibitor of aurora A and B in soft tissue sarcomas.	MLN 8237	0-8	aurora kinase A	Homo sapiens	30-44
26887042-9	2016	However, micromolar dose of MLN-8237 induced polyploidy, a hallmark effect of Aurora B inhibition.	MLN 8237	28-36	aurora kinase B	Homo sapiens	78-86
26859456-5	2016	Screening for enhancers of ABT-199 sensitivity in MYCN-amplified neuroblastomas, we demonstrate that the Aurora Kinase A inhibitor MLN8237 combines with ABT-199 to induce widespread apoptosis.	MLN 8237	131-138	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	50-54
26859456-5	2016	Screening for enhancers of ABT-199 sensitivity in MYCN-amplified neuroblastomas, we demonstrate that the Aurora Kinase A inhibitor MLN8237 combines with ABT-199 to induce widespread apoptosis.	MLN 8237	131-138	aurora kinase A	Homo sapiens	105-120
26432753-0	2016	Molecular imaging of aurora kinase A (AURKA) expression: Synthesis and preclinical evaluation of radiolabeled alisertib (MLN8237).	MLN 8237	110-119	aurora kinase A	Homo sapiens	21-36
26432753-0	2016	Molecular imaging of aurora kinase A (AURKA) expression: Synthesis and preclinical evaluation of radiolabeled alisertib (MLN8237).	MLN 8237	110-119	aurora kinase A	Homo sapiens	38-43
26432753-13	2016	In brains of P-gp knockout mice [(11)C]alisertib uptake was increased compared to uptake in wild-type mice (P<.01) CONCLUSIONS: Radiolabeled alisertib can be synthesized and may have potential for the imaging of AURKA, particularly when AURKA expression is high.	MLN 8237	39-48	phosphoglycolate phosphatase	Mus musculus	13-17
26432753-13	2016	In brains of P-gp knockout mice [(11)C]alisertib uptake was increased compared to uptake in wild-type mice (P<.01) CONCLUSIONS: Radiolabeled alisertib can be synthesized and may have potential for the imaging of AURKA, particularly when AURKA expression is high.	MLN 8237	144-153	phosphoglycolate phosphatase	Mus musculus	13-17
26432753-13	2016	In brains of P-gp knockout mice [(11)C]alisertib uptake was increased compared to uptake in wild-type mice (P<.01) CONCLUSIONS: Radiolabeled alisertib can be synthesized and may have potential for the imaging of AURKA, particularly when AURKA expression is high.	MLN 8237	144-153	aurora kinase A	Mus musculus	215-220
26432753-13	2016	In brains of P-gp knockout mice [(11)C]alisertib uptake was increased compared to uptake in wild-type mice (P<.01) CONCLUSIONS: Radiolabeled alisertib can be synthesized and may have potential for the imaging of AURKA, particularly when AURKA expression is high.	MLN 8237	144-153	aurora kinase A	Mus musculus	240-245
26729093-2	2015	Alisertib (ALS) is a selective Aurora kinase A (AURKA) inhibitor with unclear effect and molecular interactome on CRC.	MLN 8237	0-9	aurora kinase A	Homo sapiens	31-46
26729093-2	2015	Alisertib (ALS) is a selective Aurora kinase A (AURKA) inhibitor with unclear effect and molecular interactome on CRC.	MLN 8237	0-9	aurora kinase A	Homo sapiens	48-53
26516156-4	2015	The investigational AURKA inhibitor MLN8237/Alisertib selectively promoted apoptosis in the HPV cancers.	MLN 8237	36-43	aurora kinase A	Homo sapiens	20-25
26516156-4	2015	The investigational AURKA inhibitor MLN8237/Alisertib selectively promoted apoptosis in the HPV cancers.	MLN 8237	44-53	aurora kinase A	Homo sapiens	20-25
26516156-12	2015	Here, we show for the first time that targeting of the Aurora A kinase in mice using drugs such as Alisertib results in a curative sterilizing therapy that may be useful in treating HPV-driven cancers.	MLN 8237	99-108	aurora kinase A	Homo sapiens	55-63
26569382-5	2015	Treatment with MLN8237, a selective AURKA inhibitor, promoted polyploidization and differentiation of megakaryocytes with PMF-associated mutations and had potent antifibrotic and antitumor activity in vivo in mouse models of PMF.	MLN 8237	15-22	aurora kinase A	Mus musculus	36-41
26567366-0	2015	Correction: Aurora A Inhibitor (MLN8237) plus Vincristine plus Rituximab Is Synthetic Lethal and a Potential Curative Therapy in Aggressive B-cell Non-Hodgkin Lymphoma.	MLN 8237	32-39	aurora kinase A	Homo sapiens	12-20
26807190-1	2015	Alisertib (MLN8237, ALS), an Aurora kinase A (AURKA) inhibitor, exerts potent anti-tumor effects in the treatment of solid tumor and hematologic malignancies in preclinical and clinical studies.	MLN 8237	0-9	aurora kinase A	Homo sapiens	29-44
26807190-1	2015	Alisertib (MLN8237, ALS), an Aurora kinase A (AURKA) inhibitor, exerts potent anti-tumor effects in the treatment of solid tumor and hematologic malignancies in preclinical and clinical studies.	MLN 8237	0-9	aurora kinase A	Homo sapiens	46-51
26528438-2	2015	Alisertib and other small-molecule inhibitors targeting AURKA are effective in some patients as monotherapies or combination therapies.	MLN 8237	0-9	aurora kinase A	Homo sapiens	56-61
26528438-7	2015	Interestingly, alisertib exacerbates the disease phenotype in mouse models for autosomal-dominant polycystic kidney disease (ADPKD), a common inherited syndrome induced by aberrant signaling from PKD1 and PKD2, cilia-localized proteins that have calcium channel activity.	MLN 8237	15-24	polycystin 1, transient receptor potential channel interacting	Mus musculus	196-200
26528438-7	2015	Interestingly, alisertib exacerbates the disease phenotype in mouse models for autosomal-dominant polycystic kidney disease (ADPKD), a common inherited syndrome induced by aberrant signaling from PKD1 and PKD2, cilia-localized proteins that have calcium channel activity.	MLN 8237	15-24	polycystin 2, transient receptor potential cation channel	Mus musculus	205-209
26415506-1	2015	BACKGROUND: Recently, we have shown that the ATP-binding cassette (ABC) transporter ABCB1 interferes with the anti-cancer activity of the pan-aurora kinase inhibitor tozasertib (VX680, MK-0457) but not of the aurora kinase A and B inhibitor alisertib (MLN8237).	MLN 8237	241-250	ATP binding cassette subfamily B member 1	Homo sapiens	84-89
26415506-1	2015	BACKGROUND: Recently, we have shown that the ATP-binding cassette (ABC) transporter ABCB1 interferes with the anti-cancer activity of the pan-aurora kinase inhibitor tozasertib (VX680, MK-0457) but not of the aurora kinase A and B inhibitor alisertib (MLN8237).	MLN 8237	241-250	aurora kinase A	Homo sapiens	209-230
26415506-1	2015	BACKGROUND: Recently, we have shown that the ATP-binding cassette (ABC) transporter ABCB1 interferes with the anti-cancer activity of the pan-aurora kinase inhibitor tozasertib (VX680, MK-0457) but not of the aurora kinase A and B inhibitor alisertib (MLN8237).	MLN 8237	252-259	ATP binding cassette subfamily B member 1	Homo sapiens	84-89
26415506-1	2015	BACKGROUND: Recently, we have shown that the ATP-binding cassette (ABC) transporter ABCB1 interferes with the anti-cancer activity of the pan-aurora kinase inhibitor tozasertib (VX680, MK-0457) but not of the aurora kinase A and B inhibitor alisertib (MLN8237).	MLN 8237	252-259	aurora kinase A	Homo sapiens	209-230
26415506-3	2015	Here, we studied the effect of ABCG2 on the activity of tozasertib and alisertib.	MLN 8237	71-80	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	31-36
26380220-0	2015	Scientific Rationale Supporting the Clinical Development Strategy for the Investigational Aurora A Kinase Inhibitor Alisertib in Cancer.	MLN 8237	116-125	aurora kinase A	Homo sapiens	90-98
26380220-1	2015	Alisertib (MLN8237) is a selective small molecule inhibitor of Aurora A kinase that is being developed in multiple cancer indications as a single agent and in combination with other therapies.	MLN 8237	0-9	aurora kinase A	Homo sapiens	63-71
26380220-1	2015	Alisertib (MLN8237) is a selective small molecule inhibitor of Aurora A kinase that is being developed in multiple cancer indications as a single agent and in combination with other therapies.	MLN 8237	11-18	aurora kinase A	Homo sapiens	63-71
26380220-4	2015	Several key facets of Aurora A biology as well as empirical data collected in experimental systems and early clinical trials have directed the development of alisertib toward certain cancer types, including neuroblastoma, small cell lung cancer, neuroendocrine prostate cancer, atypical teratoid/rhabdoid tumors, and breast cancer among others.	MLN 8237	158-167	aurora kinase A	Homo sapiens	22-30
26084989-2	2015	PATIENTS AND METHODS: Patients received alisertib twice-daily (BID) for 7 days in 21-day cycles.	MLN 8237	40-49	BH3 interacting domain death agonist	Homo sapiens	63-66
25688119-2	2015	Alisertib (MLN8237) inhibits AURKA in vitro and in vivo.	MLN 8237	0-9	aurora kinase A	Homo sapiens	29-34
25688119-2	2015	Alisertib (MLN8237) inhibits AURKA in vitro and in vivo.	MLN 8237	11-18	aurora kinase A	Homo sapiens	29-34
25758253-4	2015	A secondary objective was to determine the role of the p53 family of transcriptional regulators, commonly mutated in TNBC, in determining the phenotypic response to the AurA inhibitor alisertib (MLN8237).	MLN 8237	184-193	tumor protein p53	Homo sapiens	55-58
25758253-4	2015	A secondary objective was to determine the role of the p53 family of transcriptional regulators, commonly mutated in TNBC, in determining the phenotypic response to the AurA inhibitor alisertib (MLN8237).	MLN 8237	184-193	aurora kinase A	Homo sapiens	169-173
25758253-6	2015	The induction of apoptosis in response to alisertib exposure was dependent on p53 and p73 activity.	MLN 8237	42-51	tumor protein p53	Homo sapiens	78-81
25758253-6	2015	The induction of apoptosis in response to alisertib exposure was dependent on p53 and p73 activity.	MLN 8237	42-51	tumor protein p73	Homo sapiens	86-89
25758253-7	2015	In the absence of functional p53 or p73, there was a shift in the phenotypic response following alisertib exposure from apoptosis to cellular senescence.	MLN 8237	96-105	tumor protein p53	Homo sapiens	29-32
25758253-7	2015	In the absence of functional p53 or p73, there was a shift in the phenotypic response following alisertib exposure from apoptosis to cellular senescence.	MLN 8237	96-105	tumor protein p73	Homo sapiens	36-39
25777964-7	2015	These broad classes of E-cadherin synthetic lethal hits were validated using both lentiviral-mediated shRNA knockdown and specific antagonists, including the JAK inhibitor LY2784544, Pertussis toxin, and the aurora kinase inhibitors alisertib and danusertib.	MLN 8237	233-242	cadherin 1	Homo sapiens	23-33
26101564-0	2015	MLN8054 and Alisertib (MLN8237): Discovery of Selective Oral Aurora A Inhibitors.	MLN 8237	12-21	aurora kinase A	Homo sapiens	61-69
26101564-0	2015	MLN8054 and Alisertib (MLN8237): Discovery of Selective Oral Aurora A Inhibitors.	MLN 8237	23-30	aurora kinase A	Homo sapiens	61-69
26101564-2	2015	Investigational agents MLN8054 (8) and alisertib (MLN8237, 10) have been identified as high affinity, selective, orally bioavailable inhibitors of Aurora A that have advanced into human clinical trials.	MLN 8237	39-48	aurora kinase A	Homo sapiens	147-155
25785590-6	2015	Principal component analyzes using single cell RNA assay data suggested that the clinical candidate aurora-A kinase inhibitor MLN8237 converts GTML neurospheres to resemble non-MYCN expressors.	MLN 8237	126-133	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	177-181
25834401-0	2015	The investigational Aurora kinase A inhibitor alisertib (MLN8237) induces cell cycle G2/M arrest, apoptosis, and autophagy via p38 MAPK and Akt/mTOR signaling pathways in human breast cancer cells.	MLN 8237	46-55	mitogen-activated protein kinase 14	Homo sapiens	127-130
25834401-0	2015	The investigational Aurora kinase A inhibitor alisertib (MLN8237) induces cell cycle G2/M arrest, apoptosis, and autophagy via p38 MAPK and Akt/mTOR signaling pathways in human breast cancer cells.	MLN 8237	46-55	AKT serine/threonine kinase 1	Homo sapiens	140-143
25834401-0	2015	The investigational Aurora kinase A inhibitor alisertib (MLN8237) induces cell cycle G2/M arrest, apoptosis, and autophagy via p38 MAPK and Akt/mTOR signaling pathways in human breast cancer cells.	MLN 8237	46-55	mechanistic target of rapamycin kinase	Homo sapiens	144-148
25834401-0	2015	The investigational Aurora kinase A inhibitor alisertib (MLN8237) induces cell cycle G2/M arrest, apoptosis, and autophagy via p38 MAPK and Akt/mTOR signaling pathways in human breast cancer cells.	MLN 8237	57-64	mitogen-activated protein kinase 14	Homo sapiens	127-130
25834401-0	2015	The investigational Aurora kinase A inhibitor alisertib (MLN8237) induces cell cycle G2/M arrest, apoptosis, and autophagy via p38 MAPK and Akt/mTOR signaling pathways in human breast cancer cells.	MLN 8237	57-64	AKT serine/threonine kinase 1	Homo sapiens	140-143
25834401-0	2015	The investigational Aurora kinase A inhibitor alisertib (MLN8237) induces cell cycle G2/M arrest, apoptosis, and autophagy via p38 MAPK and Akt/mTOR signaling pathways in human breast cancer cells.	MLN 8237	57-64	mechanistic target of rapamycin kinase	Homo sapiens	144-148
25792811-0	2015	Pro-apoptotic and pro-autophagic effects of the Aurora kinase A inhibitor alisertib (MLN8237) on human osteosarcoma U-2 OS and MG-63 cells through the activation of mitochondria-mediated pathway and inhibition of p38 MAPK/PI3K/Akt/mTOR signaling pathway.	MLN 8237	74-83	mitogen-activated protein kinase 14	Homo sapiens	213-221
25792811-0	2015	Pro-apoptotic and pro-autophagic effects of the Aurora kinase A inhibitor alisertib (MLN8237) on human osteosarcoma U-2 OS and MG-63 cells through the activation of mitochondria-mediated pathway and inhibition of p38 MAPK/PI3K/Akt/mTOR signaling pathway.	MLN 8237	74-83	AKT serine/threonine kinase 1	Homo sapiens	227-230
25792811-0	2015	Pro-apoptotic and pro-autophagic effects of the Aurora kinase A inhibitor alisertib (MLN8237) on human osteosarcoma U-2 OS and MG-63 cells through the activation of mitochondria-mediated pathway and inhibition of p38 MAPK/PI3K/Akt/mTOR signaling pathway.	MLN 8237	74-83	mechanistic target of rapamycin kinase	Homo sapiens	231-235
25792811-0	2015	Pro-apoptotic and pro-autophagic effects of the Aurora kinase A inhibitor alisertib (MLN8237) on human osteosarcoma U-2 OS and MG-63 cells through the activation of mitochondria-mediated pathway and inhibition of p38 MAPK/PI3K/Akt/mTOR signaling pathway.	MLN 8237	85-92	mitogen-activated protein kinase 14	Homo sapiens	213-221
25792811-0	2015	Pro-apoptotic and pro-autophagic effects of the Aurora kinase A inhibitor alisertib (MLN8237) on human osteosarcoma U-2 OS and MG-63 cells through the activation of mitochondria-mediated pathway and inhibition of p38 MAPK/PI3K/Akt/mTOR signaling pathway.	MLN 8237	85-92	AKT serine/threonine kinase 1	Homo sapiens	227-230
25792811-0	2015	Pro-apoptotic and pro-autophagic effects of the Aurora kinase A inhibitor alisertib (MLN8237) on human osteosarcoma U-2 OS and MG-63 cells through the activation of mitochondria-mediated pathway and inhibition of p38 MAPK/PI3K/Akt/mTOR signaling pathway.	MLN 8237	85-92	mechanistic target of rapamycin kinase	Homo sapiens	231-235
25366143-0	2015	Alisertib (MLN8237), a selective Aurora-A kinase inhibitor, induces apoptosis in human tongue squamous cell carcinoma cell both in vitro and in vivo.	MLN 8237	0-9	aurora kinase A	Mus musculus	33-41
25366143-0	2015	Alisertib (MLN8237), a selective Aurora-A kinase inhibitor, induces apoptosis in human tongue squamous cell carcinoma cell both in vitro and in vivo.	MLN 8237	11-18	aurora kinase A	Mus musculus	33-41
25366143-2	2015	Alisertib is an investigational, orally administered, selective, small-molecule Aurora-A kinase inhibitor with preclinical activity against a broad range of tumors.	MLN 8237	0-9	aurora kinase A	Mus musculus	80-88
25366143-4	2015	Treatment of a human tongue squamous cell carcinoma cell line, HSC-3, with alisertib to inhibition of Aurora-A kinases reduced proliferation and induced apoptosis, which was accompanied by activation of the ATM/Chk2/p53 pathway.	MLN 8237	75-84	aurora kinase A	Homo sapiens	102-110
25366143-4	2015	Treatment of a human tongue squamous cell carcinoma cell line, HSC-3, with alisertib to inhibition of Aurora-A kinases reduced proliferation and induced apoptosis, which was accompanied by activation of the ATM/Chk2/p53 pathway.	MLN 8237	75-84	ATM serine/threonine kinase	Homo sapiens	207-210
25366143-4	2015	Treatment of a human tongue squamous cell carcinoma cell line, HSC-3, with alisertib to inhibition of Aurora-A kinases reduced proliferation and induced apoptosis, which was accompanied by activation of the ATM/Chk2/p53 pathway.	MLN 8237	75-84	checkpoint kinase 2	Homo sapiens	211-215
25366143-4	2015	Treatment of a human tongue squamous cell carcinoma cell line, HSC-3, with alisertib to inhibition of Aurora-A kinases reduced proliferation and induced apoptosis, which was accompanied by activation of the ATM/Chk2/p53 pathway.	MLN 8237	75-84	tumor protein p53	Homo sapiens	216-219
25632225-0	2015	Alisertib induces cell cycle arrest and autophagy and suppresses epithelial-to-mesenchymal transition involving PI3K/Akt/mTOR and sirtuin 1-mediated signaling pathways in human pancreatic cancer cells.	MLN 8237	0-9	AKT serine/threonine kinase 1	Homo sapiens	117-120
25632225-0	2015	Alisertib induces cell cycle arrest and autophagy and suppresses epithelial-to-mesenchymal transition involving PI3K/Akt/mTOR and sirtuin 1-mediated signaling pathways in human pancreatic cancer cells.	MLN 8237	0-9	mechanistic target of rapamycin kinase	Homo sapiens	121-125
25632225-0	2015	Alisertib induces cell cycle arrest and autophagy and suppresses epithelial-to-mesenchymal transition involving PI3K/Akt/mTOR and sirtuin 1-mediated signaling pathways in human pancreatic cancer cells.	MLN 8237	0-9	sirtuin 1	Homo sapiens	130-139
25632225-2	2015	Alisertib (ALS), a potent and selective Aurora kinase A inhibitor, exhibits potent anticancer effects in preclinical and clinical studies; however, the effect and underlying mechanism of ALS in the pancreatic cancer treatment remain elusive.	MLN 8237	0-9	aurora kinase A	Homo sapiens	40-55
25609923-0	2015	Inhibition of mitotic Aurora kinase A by alisertib induces apoptosis and autophagy of human gastric cancer AGS and NCI-N78 cells.	MLN 8237	41-50	aurora kinase A	Homo sapiens	22-37
25609923-2	2015	Alisertib (ALS) is a second-generation, orally bioavailable, highly selective small-molecule inhibitor of the serine/threonine protein kinase Aurora kinase A (AURKA).	MLN 8237	0-9	aurora kinase A	Homo sapiens	142-157
25609923-2	2015	Alisertib (ALS) is a second-generation, orally bioavailable, highly selective small-molecule inhibitor of the serine/threonine protein kinase Aurora kinase A (AURKA).	MLN 8237	0-9	aurora kinase A	Homo sapiens	159-164
25579846-1	2015	MLN8237 is a highly potent and presumably selective inhibitor of Aurora kinase A (AKA) and has shown promising antitumor activities.	MLN 8237	0-7	aurora kinase A	Homo sapiens	65-80
25579846-1	2015	MLN8237 is a highly potent and presumably selective inhibitor of Aurora kinase A (AKA) and has shown promising antitumor activities.	MLN 8237	0-7	aurora kinase A	Homo sapiens	82-85
25624750-0	2015	Alisertib, an Aurora kinase A inhibitor, induces apoptosis and autophagy but inhibits epithelial to mesenchymal transition in human epithelial ovarian cancer cells.	MLN 8237	0-9	aurora kinase A	Homo sapiens	14-29
25624750-2	2015	Alisertib (ALS), a selective Aurora kinase A (AURKA) inhibitor, has shown potent anticancer effects, and is under clinical investigation for the treatment of advanced solid tumor and hematologic malignancies.	MLN 8237	0-9	aurora kinase A	Homo sapiens	29-44
25624750-2	2015	Alisertib (ALS), a selective Aurora kinase A (AURKA) inhibitor, has shown potent anticancer effects, and is under clinical investigation for the treatment of advanced solid tumor and hematologic malignancies.	MLN 8237	0-9	aurora kinase A	Homo sapiens	46-51
25789545-7	2015	Surprisingly, an Aurora A inhibitor, Alisertib (MLN8237), also disrupted centrosomal localization of Tpr and induced mitotic catastrophe and cell death in a time- and dose-dependent manner.	MLN 8237	37-46	aurora kinase A	Homo sapiens	17-25
25789545-7	2015	Surprisingly, an Aurora A inhibitor, Alisertib (MLN8237), also disrupted centrosomal localization of Tpr and induced mitotic catastrophe and cell death in a time- and dose-dependent manner.	MLN 8237	37-46	translocated promoter region, nuclear basket protein	Homo sapiens	101-104
25200357-6	2014	We pay special attention to Alisertib, a potent and selective Aurora A inhibitor currently in Phase III.	MLN 8237	28-37	aurora kinase A	Homo sapiens	62-70
24879333-2	2014	METHODS: Patients with advanced, non-hematologic malignancies received oral alisertib ECT for 7 d BID followed by 14 d treatment-free (21-day cycles; 3 + 3 dose escalation schema).	MLN 8237	76-85	BH3 interacting domain death agonist	Homo sapiens	98-101
24166501-5	2014	Notably, Aurora-A inhibitor MLN8237, which is currently in clinical trial, synergizes with tamoxifen and overcomes tamoxifen resistance.	MLN 8237	28-35	aurora kinase A	Homo sapiens	9-17
25106428-2	2014	Here, we report that the Aurora-A kinase inhibitor alisertib exhibits potent efficacy against glioblastoma neurosphere tumor stem-like cells in vitro and in vivo.	MLN 8237	51-60	aurora kinase A	Homo sapiens	25-33
25268132-2	2014	Here, we studied the effects of the pan-aurora kinase inhibitor tozasertib (VX680, MK-0457) and the aurora kinase inhibitor alisertib (MLN8237) that shows some specificity for aurora kinase A over aurora kinase B in a panel of neuroblastoma cell lines with acquired drug resistance.	MLN 8237	135-142	aurora kinase A	Homo sapiens	176-191
25268132-5	2014	The activity of alisertib but not of tozasertib was affected by ABCB1 expression.	MLN 8237	16-25	ATP binding cassette subfamily B member 1	Homo sapiens	64-69
24980948-0	2014	Translational exposure-efficacy modeling to optimize the dose and schedule of taxanes combined with the investigational Aurora A kinase inhibitor MLN8237 (alisertib).	MLN 8237	146-153	aurora kinase A	Homo sapiens	120-128
24980948-0	2014	Translational exposure-efficacy modeling to optimize the dose and schedule of taxanes combined with the investigational Aurora A kinase inhibitor MLN8237 (alisertib).	MLN 8237	155-164	aurora kinase A	Homo sapiens	120-128
24980948-2	2014	MLN8237 (alisertib) is a selective Aurora A inhibitor that is being evaluated as an anticancer agent in multiple solid tumors and heme-lymphatic malignancies.	MLN 8237	0-7	aurora kinase A	Homo sapiens	35-43
24980948-2	2014	MLN8237 (alisertib) is a selective Aurora A inhibitor that is being evaluated as an anticancer agent in multiple solid tumors and heme-lymphatic malignancies.	MLN 8237	9-18	aurora kinase A	Homo sapiens	35-43
25153724-0	2014	The Aurora-A inhibitor MLN8237 affects multiple mitotic processes and induces dose-dependent mitotic abnormalities and aneuploidy.	MLN 8237	23-30	aurora kinase A	Homo sapiens	4-12
25153724-3	2014	Here we have used the Aurora-A inhibitor MLN8237, currently under phase-I/III clinical trials, in dose-response assays in U2OS human cancer cells synchronously proceeding towards mitosis.	MLN 8237	41-48	aurora kinase A	Homo sapiens	22-30
24901229-8	2014	In an in vitro study, MLN8237, an AURKA inhibitor, inhibited growth of both IM-sensitive and IM-resistant GIST cells in a concentration-dependent manner, and exhibited synergistic cytotoxicity with IM in GIST cells.	MLN 8237	22-29	aurora kinase A	Homo sapiens	34-39
24893165-0	2014	Alisertib added to rituximab and vincristine is synthetic lethal and potentially curative in mice with aggressive DLBCL co-overexpressing MYC and BCL2.	MLN 8237	0-9	myelocytomatosis oncogene	Mus musculus	138-141
24893165-0	2014	Alisertib added to rituximab and vincristine is synthetic lethal and potentially curative in mice with aggressive DLBCL co-overexpressing MYC and BCL2.	MLN 8237	0-9	B cell leukemia/lymphoma 2	Mus musculus	146-150
24893165-4	2014	Alisertib [MLN8237 or M], a highly selective small molecule inhibitor of Aurora A kinase, was synergistic with vincristine [VCR] and rituximab [R] for inhibition of cell proliferation, abrogation of cell cycle checkpoints and enhanced apoptosis versus single agent or doublet therapy.	MLN 8237	0-9	aurora kinase A	Homo sapiens	73-81
24893165-4	2014	Alisertib [MLN8237 or M], a highly selective small molecule inhibitor of Aurora A kinase, was synergistic with vincristine [VCR] and rituximab [R] for inhibition of cell proliferation, abrogation of cell cycle checkpoints and enhanced apoptosis versus single agent or doublet therapy.	MLN 8237	11-18	aurora kinase A	Homo sapiens	73-81
24893165-9	2014	Together, our data suggest that the interaction between alisertib plus VCR plus rituximab is synergistic and synthetic lethal in Myc and Bcl-2 co-expressing DLBCL.	MLN 8237	56-65	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	129-132
24893165-9	2014	Together, our data suggest that the interaction between alisertib plus VCR plus rituximab is synergistic and synthetic lethal in Myc and Bcl-2 co-expressing DLBCL.	MLN 8237	56-65	BCL2 apoptosis regulator	Homo sapiens	137-142
24930769-3	2014	Furthermore, siRNA silencing or pharmacological inhibition of Aurora A and JAK2 with Alisertib and Ruxolitinib, respectively, is more effective than blocking each kinase alone at suppressing anchorage-dependent and -independent growth and invasion as well as at inducing apoptosis.	MLN 8237	85-94	aurora kinase A	Homo sapiens	62-70
24930769-3	2014	Furthermore, siRNA silencing or pharmacological inhibition of Aurora A and JAK2 with Alisertib and Ruxolitinib, respectively, is more effective than blocking each kinase alone at suppressing anchorage-dependent and -independent growth and invasion as well as at inducing apoptosis.	MLN 8237	85-94	Janus kinase 2	Homo sapiens	75-79
24627220-0	2014	The selective Aurora-A kinase inhibitor MLN8237 (alisertib) potently inhibits proliferation of glioblastoma neurosphere tumor stem-like cells and potentiates the effects of temozolomide and ionizing radiation.	MLN 8237	40-47	aurora kinase A	Homo sapiens	14-22
24627220-1	2014	The selective Aurora-A kinase inhibitor MLN8237 is in clinical trials for hematologic malignancies, ovarian cancer and other solid tumors.	MLN 8237	40-47	aurora kinase A	Homo sapiens	14-22
24627220-8	2014	We also found that Aurora-A inhibition by MLN8237 was synergistic with temozolomide and potentiated the effects of ionizing radiation on colony formation in neurosphere glioblastoma tumor stem-like cells.	MLN 8237	42-49	aurora kinase A	Homo sapiens	19-27
24574519-8	2014	Inhibition of AURKA and HDAC6 activity by alisertib and Tubastatin A in xenograft models of breast cancer leads to a decrease in the number of pulmonary metastases.	MLN 8237	42-51	aurora kinase A	Homo sapiens	14-19
24574519-8	2014	Inhibition of AURKA and HDAC6 activity by alisertib and Tubastatin A in xenograft models of breast cancer leads to a decrease in the number of pulmonary metastases.	MLN 8237	42-51	histone deacetylase 6	Homo sapiens	24-29
23334327-3	2014	In the current study, we identified a novel role for AURKA in regulating ovarian cancer cell dissemination and evaluated the efficacy of an AURKA-selective small molecule inhibitor, alisertib (MLN8237), as a single agent and combined with paclitaxel using an orthotopic xenograft model of epithelial ovarian cancer (EOC).	MLN 8237	182-191	aurora kinase A	Homo sapiens	140-145
24240108-10	2014	Inhibition of AURKA using an investigational small-molecule specific inhibitor, alisertib, decreased the HDM2 protein level and induced P53 transcriptional activity.	MLN 8237	80-89	aurora kinase A	Homo sapiens	14-19
24240108-10	2014	Inhibition of AURKA using an investigational small-molecule specific inhibitor, alisertib, decreased the HDM2 protein level and induced P53 transcriptional activity.	MLN 8237	80-89	MDM2 proto-oncogene	Homo sapiens	105-109
24240108-10	2014	Inhibition of AURKA using an investigational small-molecule specific inhibitor, alisertib, decreased the HDM2 protein level and induced P53 transcriptional activity.	MLN 8237	80-89	tumor protein p53	Homo sapiens	136-139
24222664-3	2014	We sought to evaluate the AAK-selective inhibitor MLN8237 as a potential indirect anti-RalA-targeted therapy for PDAC.	MLN 8237	50-57	RAS like proto-oncogene A	Homo sapiens	87-91
24101146-0	2013	Preclinical pharmacokinetic/pharmacodynamic/efficacy relationships for alisertib, an investigational small-molecule inhibitor of Aurora A kinase.	MLN 8237	71-80	aurora kinase A	Homo sapiens	129-137
24101146-1	2013	PURPOSE: Alisertib (MLN8237) is an investigational inhibitor of Aurora A kinase (AAK).	MLN 8237	9-18	aurora kinase A	Homo sapiens	64-72
24101146-1	2013	PURPOSE: Alisertib (MLN8237) is an investigational inhibitor of Aurora A kinase (AAK).	MLN 8237	20-27	aurora kinase A	Homo sapiens	64-72
24101146-3	2013	Inhibition of Aurora A by alisertib in tissue culture has previously been demonstrated to lead to improper chromosomal alignment and disruption of spindle organization, resulting in a transient mitotic delay.	MLN 8237	26-35	aurora kinase A	Homo sapiens	14-22
24101146-4	2013	The spindle organization defects induced by alisertib have been used to develop a pharmacodynamic (PD) assay for Aurora A inhibition based on the percentage of mitotic cells with proper chromosomal alignment at the metaphase plate (% aligned spindles, abbreviated as AS).	MLN 8237	44-53	aurora kinase A	Homo sapiens	113-121
23686525-4	2013	Blockade of AURKA by the specific inhibitor MLN8237 or a short hairpin RNA (shRNA) against AURKA significantly inhibited proliferation, impaired self-renewal capability and induced apoptosis of CD34(+) /CD38(-) AML cells, in association with modulation of levels of Bcl-2 family member proteins.	MLN 8237	44-51	aurora kinase A	Homo sapiens	12-17
23686525-4	2013	Blockade of AURKA by the specific inhibitor MLN8237 or a short hairpin RNA (shRNA) against AURKA significantly inhibited proliferation, impaired self-renewal capability and induced apoptosis of CD34(+) /CD38(-) AML cells, in association with modulation of levels of Bcl-2 family member proteins.	MLN 8237	44-51	CD34 molecule	Homo sapiens	194-198
23686525-4	2013	Blockade of AURKA by the specific inhibitor MLN8237 or a short hairpin RNA (shRNA) against AURKA significantly inhibited proliferation, impaired self-renewal capability and induced apoptosis of CD34(+) /CD38(-) AML cells, in association with modulation of levels of Bcl-2 family member proteins.	MLN 8237	44-51	CD38 molecule	Homo sapiens	203-207
23403633-0	2013	The investigational Aurora kinase A inhibitor MLN8237 induces defects in cell viability and cell-cycle progression in malignant bladder cancer cells in vitro and in vivo.	MLN 8237	46-53	aurora kinase A	Homo sapiens	20-35
23403633-6	2013	The Aurora kinase A inhibitor MLN8237 induced cell-cycle arrest, aneuploidy, mitotic spindle failure, and apoptosis in the human bladder cancer cell lines T24 and UM-UC-3.	MLN 8237	30-37	aurora kinase A	Homo sapiens	4-19
23403633-10	2013	Given our demonstration of the ability of the Aurora A inhibitor MLN8237 to inhibit growth of bladder cancer in vitro and in vivo, we conclude that Aurora kinase inhibitors warrant further therapeutic investigation in bladder cancer.	MLN 8237	65-72	aurora kinase A	Homo sapiens	46-54
23153524-0	2013	Alisertib (MLN8237) an investigational agent suppresses Aurora A and B activity, inhibits proliferation, promotes endo-reduplication and induces apoptosis in T-NHL cell lines supporting its importance in PTCL treatment.	MLN 8237	0-9	aurora kinase A	Homo sapiens	56-64
23153524-0	2013	Alisertib (MLN8237) an investigational agent suppresses Aurora A and B activity, inhibits proliferation, promotes endo-reduplication and induces apoptosis in T-NHL cell lines supporting its importance in PTCL treatment.	MLN 8237	11-18	aurora kinase A	Homo sapiens	56-64
23153524-2	2013	Alisertib (MLN8237) an investigational agent that inhibits Aurora A Ser/Thr kinase has shown activity in PTCL patients.	MLN 8237	0-9	aurora kinase A	Homo sapiens	59-67
23153524-2	2013	Alisertib (MLN8237) an investigational agent that inhibits Aurora A Ser/Thr kinase has shown activity in PTCL patients.	MLN 8237	11-18	aurora kinase A	Homo sapiens	59-67
22972611-0	2013	The combination of alisertib, an investigational Aurora kinase A inhibitor, and docetaxel promotes cell death and reduces tumor growth in preclinical cell models of upper gastrointestinal adenocarcinomas.	MLN 8237	19-28	aurora kinase A	Homo sapiens	49-64
22972611-5	2013	RESULTS: By using the AGS, FLO-1, and OE33 UGC cell lines, which have constitutive AURKA overexpression and variable tumor protein 53 (p53) status, significantly enhanced inhibition of cancer cell survival was observed with alisertib and docetaxel treatment in combination (P < .001), compared with single-agent treatments.	MLN 8237	224-233	aurora kinase A	Homo sapiens	83-88
22669335-2	2013	Vorinostat and MLN8237, a selective Aurora A kinase inhibitor, disrupt the spindle assembly and the mitotic checkpoint at different points, suggesting that the combination could have increased antitumor activity.	MLN 8237	15-22	aurora kinase A	Homo sapiens	36-44
22488249-0	2012	Targeting Aurora A kinase activity with the investigational agent alisertib increases the efficacy of cytarabine through a FOXO-dependent mechanism.	MLN 8237	66-75	aurora kinase A	Homo sapiens	10-18
22488249-2	2012	The investigational drug alisertib (MLN8237) is a novel Aurora A kinase inhibitor being studied in multiple Phase I and II studies.	MLN 8237	25-34	aurora kinase A	Homo sapiens	56-64
22488249-2	2012	The investigational drug alisertib (MLN8237) is a novel Aurora A kinase inhibitor being studied in multiple Phase I and II studies.	MLN 8237	36-43	aurora kinase A	Homo sapiens	56-64
22488249-4	2012	Here, we report that alisertib disrupted cell viability, diminished clonogenic survival, induced expression of the FOXO3a targets p27 and BIM and triggered apoptosis.	MLN 8237	21-30	forkhead box O3	Homo sapiens	115-121
22488249-4	2012	Here, we report that alisertib disrupted cell viability, diminished clonogenic survival, induced expression of the FOXO3a targets p27 and BIM and triggered apoptosis.	MLN 8237	21-30	interferon alpha inducible protein 27	Homo sapiens	130-133
22488249-7	2012	Targeted FOXO3a knockdown significantly blunted the pro-apoptotic effects of the alisertib/ara-C combination, indicating that it is an important regulator of sensitivity to these agents.	MLN 8237	81-90	forkhead box O3	Homo sapiens	9-15
22488249-8	2012	In vivo studies demonstrated that alisertib significantly augmented the efficacy of ara-C without affecting its pharmacokinetic profile and led to the induction of p27 and BIM.	MLN 8237	34-43	interferon alpha inducible protein 27	Homo sapiens	164-167
22488249-9	2012	Our collective data indicate that targeting Aurora A with alisertib represents a novel approach to increase the efficacy of ara-C that warrants further investigation.	MLN 8237	58-67	aurora kinase A	Homo sapiens	44-52
22988055-1	2012	PURPOSE: MLN8237, a selective small-molecule inhibitor of Aurora kinase A, has activity in a broad range of preclinical pediatric cancer models.	MLN 8237	9-16	aurora kinase A	Homo sapiens	58-73
22811580-9	2012	Furthermore, an AURKA selective inhibitor, MLN8237, stabilized tumor volume and significantly increased survival of mice with MPNST xenografts.	MLN 8237	43-50	aurora kinase A	Mus musculus	16-21
22825030-5	2012	Similar apoptotic effects were observed with treatment with the Aurora A-specific inhibitor, MLN8237.	MLN 8237	93-100	aurora kinase A	Homo sapiens	64-72
22863010-6	2012	We further find that MLN8237 (Alisertib), a selective inhibitor of AURKA, induced polyploidization and expression of mature megakaryocyte markers in acute megakaryocytic leukemia (AMKL) blasts and displayed potent anti-AMKL activity in vivo.	MLN 8237	21-28	aurora kinase A	Homo sapiens	67-72
22863010-6	2012	We further find that MLN8237 (Alisertib), a selective inhibitor of AURKA, induced polyploidization and expression of mature megakaryocyte markers in acute megakaryocytic leukemia (AMKL) blasts and displayed potent anti-AMKL activity in vivo.	MLN 8237	30-39	aurora kinase A	Homo sapiens	67-72
22588779-13	2012	MLN8237 (alisertib) is a small molecule inhibitor of aurora kinase A that is currently in early-phase clinical testing.	MLN 8237	0-7	aurora kinase A	Homo sapiens	53-68
22588779-13	2012	MLN8237 (alisertib) is a small molecule inhibitor of aurora kinase A that is currently in early-phase clinical testing.	MLN 8237	9-18	aurora kinase A	Homo sapiens	53-68
22374334-0	2012	Aurora A inhibitor (MLN8237) plus vincristine plus rituximab is synthetic lethal and a potential curative therapy in aggressive B-cell non-Hodgkin lymphoma.	MLN 8237	20-27	aurora kinase A	Mus musculus	0-8
22302096-0	2012	The aurora kinase A inhibitor MLN8237 enhances cisplatin-induced cell death in esophageal adenocarcinoma cells.	MLN 8237	30-37	aurora kinase A	Homo sapiens	4-19
22274399-11	2012	Furthermore, we report that the selective Aurora A inhibitor MLN8237 is potently cytotoxic to glioblastoma cells, and that MLN8237 cytotoxicty is potentiated by ionizing radiation.	MLN 8237	61-68	aurora kinase A	Homo sapiens	42-50
22016509-0	2011	Characterization of Alisertib (MLN8237), an investigational small-molecule inhibitor of aurora A kinase using novel in vivo pharmacodynamic assays.	MLN 8237	20-29	aurora kinase A	Homo sapiens	88-96
22016509-0	2011	Characterization of Alisertib (MLN8237), an investigational small-molecule inhibitor of aurora A kinase using novel in vivo pharmacodynamic assays.	MLN 8237	31-38	aurora kinase A	Homo sapiens	88-96
21448591-0	2011	Efficacy and pharmacokinetic/pharmacodynamic evaluation of the Aurora kinase A inhibitor MLN8237 against preclinical models of pediatric cancer.	MLN 8237	89-96	aurora kinase A	Homo sapiens	63-78
21448591-1	2011	PURPOSE: To gain a greater understanding of the potential of the Aurora kinase A inhibitor MLN8237 in the treatment of pediatric malignancies.	MLN 8237	91-98	aurora kinase A	Homo sapiens	65-80
22011530-4	2011	RESULTS: We inactivated Aurora-A in human U2OS osteosarcoma cells either by RNA-interference-mediated silencing or treating cultures with the specific inhibitor MLN8237.	MLN 8237	161-168	aurora kinase A	Homo sapiens	24-32
21291867-5	2011	MLN8237, an Aurora inhibitor induced G2/M arrest with polyploidy and abrogated Aurora A and histone-H3 phosphorylation.	MLN 8237	0-7	aurora kinase A	Homo sapiens	79-87
20724522-12	2010	A more potent, selective, second-generation Aurora A kinase inhibitor, MLN8237, is in clinical development.	MLN 8237	71-78	aurora kinase A	Homo sapiens	44-52
20108338-0	2010	Initial testing of the aurora kinase A inhibitor MLN8237 by the Pediatric Preclinical Testing Program (PPTP).	MLN 8237	49-56	aurora kinase A	Homo sapiens	23-38
20382844-0	2010	A novel Aurora-A kinase inhibitor MLN8237 induces cytotoxicity and cell-cycle arrest in multiple myeloma.	MLN 8237	34-41	aurora kinase A	Homo sapiens	8-16