PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 35565194-8 2022 When treated with first-line platinum doublet (n = 195), KRASMUT was a negative factor for survival (p = 0.018), with median OS of 9 months vs. KRASWT at 11 months. Platinum 29-37 KRAS proto-oncogene, GTPase Homo sapiens 57-64 34824550-13 2021 GSEA predicted that ATP1A2, CASQ2 and RYR2 may act on the KRAS and mTORC1 pathways and participate in metabolic reprogramming and regulation of calcium homeostasis in platinum-resistant cells. Platinum 167-175 KRAS proto-oncogene, GTPase Homo sapiens 58-62 34419376-0 2022 Near-Complete Response to Combined Pembrolizumab and Platinum-Doublet in a Patient With STK11/KRAS Mutated Advanced Lung Adenocarcinoma. Platinum 53-61 KRAS proto-oncogene, GTPase Homo sapiens 94-98 35443055-7 2022 KRAS mutations were significantly associated with age at diagnosis >50 years (p=0.02) and platinum-sensitive disease (p=0.03). Platinum 90-98 KRAS proto-oncogene, GTPase Homo sapiens 0-4 35443055-12 2022 CONCLUSIONS: This study showed MAPK pathway alterations in LGSC, including KRAS mutations, are independently associated with platinum sensitivity and prolonged survival. Platinum 125-133 KRAS proto-oncogene, GTPase Homo sapiens 75-79 35565194-13 2022 kRAS mutations are associated with better response to treatment with immune checkpoint blockade and worse response to platinum doublet chemotherapy as well as shorter general OS in Stage IV NSCLC. Platinum 118-126 KRAS proto-oncogene, GTPase Homo sapiens 0-4 33099543-13 2021 In this pilot study including few patients by subgroups, patients with KRAS (HR=3.60, 95%CI [1.06-12.04]) and BRAF (HR=4.25, 95%CI [1.11-16.40]) mutations had shorter progression-free survival (PFS) under platinum-etoposide, while the two patients with RB1 mutations had shorter PFS under FOLFIRI-based chemotherapy. Platinum 205-213 KRAS proto-oncogene, GTPase Homo sapiens 71-75 32753889-6 2020 Nonsynonymous variants in EGFR, TTN, TP53 and KRAS, and copy number variations (SCNVs) in chromosome 8q24.3 and 22q11.21 were identified to be associated with platinum response. Platinum 159-167 KRAS proto-oncogene, GTPase Homo sapiens 46-50 32891532-4 2020 METHODS: We performed a subgroup analysis of the Japanese PanNEN-G3 study (multicenter, retrospective study), which revealed that Rb loss and KRAS mutation were predictors of the response to platinum-based regimen in PanNEN-G3. Platinum 191-199 KRAS proto-oncogene, GTPase Homo sapiens 142-146 32891532-7 2020 Patients with Rb loss and/or KRAS mutation showed a higher response rate to first-line platinum-based regimen than those without Rb loss or KRAS mutation (object response rate 70.0% vs 33.3%, odds ratio 9.22; 95% CI 1.26-67.3, P = 0.029), but tended to have shorter overall survival rates than those without Rb loss or KRAS mutation (median 239 vs 473 days, hazard ratio 2.11; 95% CI 0.92-4.86, P = 0.077). Platinum 87-95 KRAS proto-oncogene, GTPase Homo sapiens 29-33 32891532-9 2020 When grouped based on Rb loss and KRAS mutation, there seemed to be two groups with distinct prognoses and responses to the platinum-based regimen. Platinum 124-132 KRAS proto-oncogene, GTPase Homo sapiens 34-38 32751518-2 2020 We prospectively investigate whether KRAS status and DNA polymerase beta expression could help identify patients responding to platinum compounds. Platinum 127-135 KRAS proto-oncogene, GTPase Homo sapiens 37-41 32751518-9 2020 KRAS may have a negative role in platinum-based therapy responses in NSCLC, but its impact is limited. Platinum 33-41 KRAS proto-oncogene, GTPase Homo sapiens 0-4 31332704-7 2020 After adjusting for performance status, age and the presence of brain metastasis at baseline, treatment with pemetrexed-based platinum doublet was associated with an increased risk of death [HR 2.27 (95% CI 1.12-4.63), P = 0.02] among KRAS-mutant patients in multivariate analysis. Platinum 126-134 KRAS proto-oncogene, GTPase Homo sapiens 235-239 30149143-11 2018 This study lays the foundations for combining metformin with standard platinum-based chemotherapy in the treatment of KRAS/LKB1 co-mutated NSCLC. Platinum 70-78 KRAS proto-oncogene, GTPase Homo sapiens 118-122 30217639-3 2018 PATIENTS AND METHODS: We retrospectively reviewed data from 1190 patients with KRAS mutations who underwent first-line platinum-based chemotherapy for stage IV NSCLC. Platinum 119-127 KRAS proto-oncogene, GTPase Homo sapiens 79-83 30217639-10 2018 CONCLUSION: KRAS-specific AAS appears to induce different responses to chemotherapy regimens after first-line platinum-based chemotherapy in advanced NSCLC. Platinum 110-118 KRAS proto-oncogene, GTPase Homo sapiens 12-16 31597567-5 2019 Moreover, neoplastic cells carrying a specific set of somatic mutations, such as EGFR(L858R), KRAS (p.G12C) were obviously correlated with platinum treatment. Platinum 139-147 KRAS proto-oncogene, GTPase Homo sapiens 94-98 31600989-0 2019 KRAS Mutations Predict Response and Outcome in Advanced Lung Adenocarcinoma Patients Receiving First-Line Bevacizumab and Platinum-Based Chemotherapy. Platinum 122-130 KRAS proto-oncogene, GTPase Homo sapiens 0-4 29089357-8 2018 Co-mutation of KRAS and KEAP1/ NFE2L2 is an independent prognostic factor, predicting shorter survival, duration of response to initial platinum-based chemotherapy, and survival from the start of immune therapy. Platinum 136-144 KRAS proto-oncogene, GTPase Homo sapiens 15-19 26415993-0 2015 Comparison of clinical outcome after first-line platinum-based chemotherapy in different types of KRAS mutated advanced non-small-cell lung cancer. Platinum 48-56 KRAS proto-oncogene, GTPase Homo sapiens 98-102 29163686-0 2017 Characterization of distinct types of KRAS mutation and its impact on first-line platinum-based chemotherapy in Chinese patients with advanced non-small cell lung cancer. Platinum 81-89 KRAS proto-oncogene, GTPase Homo sapiens 38-42 29163686-1 2017 We performed this retrospective study to investigate whether the KRAS mutation status and its subtypes could predict the effect of first-line platinum-based chemotherapy in Chinese patients with non-small cell lung cancer (NSCLC). Platinum 142-150 KRAS proto-oncogene, GTPase Homo sapiens 65-69 29163686-11 2017 In conclusion, KRAS mutation was a negative predictive factor of PFS in Chinese patients with advanced NSCLC who received first platinum-based chemotherapy. Platinum 128-136 KRAS proto-oncogene, GTPase Homo sapiens 15-19 28455360-0 2017 Rb Loss and KRAS Mutation Are Predictors of the Response to Platinum-Based Chemotherapy in Pancreatic Neuroendocrine Neoplasm with Grade 3: A Japanese Multicenter Pancreatic NEN-G3 Study. Platinum 60-68 KRAS proto-oncogene, GTPase Homo sapiens 12-16 28455360-8 2017 When we stratified PanNEN-G3 with Rb and KRAS, PanNENs-G3 with Rb loss and those with mutated KRAS showed significantly higher RRs to platinum-based chemotherapy than those without (Rb loss, 80% vs. normal Rb, 24%, P = 0.006; mutated KRAS, 77% versus wild type, 23%, P = 0.023). Platinum 134-142 KRAS proto-oncogene, GTPase Homo sapiens 41-45 28455360-8 2017 When we stratified PanNEN-G3 with Rb and KRAS, PanNENs-G3 with Rb loss and those with mutated KRAS showed significantly higher RRs to platinum-based chemotherapy than those without (Rb loss, 80% vs. normal Rb, 24%, P = 0.006; mutated KRAS, 77% versus wild type, 23%, P = 0.023). Platinum 134-142 KRAS proto-oncogene, GTPase Homo sapiens 94-98 28455360-8 2017 When we stratified PanNEN-G3 with Rb and KRAS, PanNENs-G3 with Rb loss and those with mutated KRAS showed significantly higher RRs to platinum-based chemotherapy than those without (Rb loss, 80% vs. normal Rb, 24%, P = 0.006; mutated KRAS, 77% versus wild type, 23%, P = 0.023). Platinum 134-142 KRAS proto-oncogene, GTPase Homo sapiens 94-98 28455360-11 2017 Rb and KRAS are promising predictors of response to platinum-based chemotherapy for PanNEN-G3, and Rb for NEC-G3. Platinum 52-60 KRAS proto-oncogene, GTPase Homo sapiens 7-11 26740498-0 2016 Poor response to platinum-based chemotherapy is associated with KRAS mutation and concomitant low expression of BRAC1 and TYMS in NSCLC. Platinum 17-25 KRAS proto-oncogene, GTPase Homo sapiens 64-68 26416458-0 2015 KRAS mutations affect prognosis of non-small-cell lung cancer patients treated with first-line platinum containing chemotherapy. Platinum 95-103 KRAS proto-oncogene, GTPase Homo sapiens 0-4 26416458-2 2015 The aim of this planned ancillary study within the TAILOR trial was to assess the prognostic value of KRAS mutations in advanced NSCLC patients treated with platinum-based first-line chemotherapy. Platinum 157-165 KRAS proto-oncogene, GTPase Homo sapiens 102-106 26416458-6 2015 This study, with all consecutive patients genotyped, indicates that the presence of KRAS mutations has a mild negative impact on OS in advanced NSCLC patient treated with a first-line platinum-containing regimen. Platinum 184-192 KRAS proto-oncogene, GTPase Homo sapiens 84-88 24768329-0 2014 Subtype-specific KRAS mutations in advanced lung adenocarcinoma: a retrospective study of patients treated with platinum-based chemotherapy. Platinum 112-120 KRAS proto-oncogene, GTPase Homo sapiens 17-21 26353932-7 2015 Systematic analysis of drug uptake, DNA adduct formation and DNA damage responses implicated in cisplatin adducts removal revealed that the KRAS(G12C) mutation might be particular because it stimulates Base Excision Repair to rapidly remove platinum from DNA even before the formation of cross-links. Platinum 241-249 KRAS proto-oncogene, GTPase Homo sapiens 140-144 25081901-12 2014 Conversely, KRAS-variant patients appeared to experience some improvement in disease control when cetuximab was added to their platinum-based regimen (log-rank P = 0.04). Platinum 127-135 KRAS proto-oncogene, GTPase Homo sapiens 12-16 25081901-13 2014 CONCLUSIONS: The TG/GG rs61764370 KRAS-variant is a potential predictive biomarker for poor platinum response in R/M HNSCC patients. Platinum 92-100 KRAS proto-oncogene, GTPase Homo sapiens 34-38 26471290-0 2015 Survival outcome according to KRAS mutation status in newly diagnosed patients with stage IV non-small cell lung cancer treated with platinum doublet chemotherapy. Platinum 133-141 KRAS proto-oncogene, GTPase Homo sapiens 30-34 24139827-9 2014 CONCLUSION: KRAS mutation appears to negatively affect sensitivity to first-line platinum-based chemotherapy in patients with advanced nonsquamous EGFR WT NSCLC. Platinum 81-89 KRAS proto-oncogene, GTPase Homo sapiens 12-16 24439569-13 2014 CONCLUSIONS: KRAS mutant tumors had a lower DCR after the first-line platinum-based CT, but this difference did not translate in PFS or OS. Platinum 69-77 KRAS proto-oncogene, GTPase Homo sapiens 13-17 24139827-0 2014 Clinical outcome with platinum-based chemotherapy in patients with advanced nonsquamous EGFR wild-type non-small-cell lung cancer segregated according to KRAS mutation status. Platinum 22-30 KRAS proto-oncogene, GTPase Homo sapiens 154-158 24139827-1 2014 BACKGROUND: We hypothesized that KRAS mutations function as a marker of poor sensitivity to first-line platinum-based chemotherapy in patients with advanced nonsquamous EGFR wild-type (WT) non-small-cell lung cancer (NSCLC). Platinum 103-111 KRAS proto-oncogene, GTPase Homo sapiens 33-37 23211422-2 2013 The aim of this study was to investigate the response rate in platinum-resistant, KRAS wild-type ovarian cancer patients treated with pegylated liposomal doxorubicin (PLD) supplemented with panitumumab. Platinum 62-70 KRAS proto-oncogene, GTPase Homo sapiens 82-86 23787801-0 2013 KRAS mutations in advanced nonsquamous non-small-cell lung cancer patients treated with first-line platinum-based chemotherapy have no predictive value. Platinum 99-107 KRAS proto-oncogene, GTPase Homo sapiens 0-4 22139083-11 2012 Perhaps explaining this finding, EOC patients with the KRAS variant were significantly more likely to be platinum resistant (odds ratio=3.18, confidence interval: 1.31-7.72, P=0.0106, n=291). Platinum 105-113 KRAS proto-oncogene, GTPase Homo sapiens 55-59 22139083-13 2012 These findings confirm the importance of the KRAS variant in EOC, and indicate that the KRAS variant is a biomarker of poor outcome in EOC likely due to platinum resistance. Platinum 153-161 KRAS proto-oncogene, GTPase Homo sapiens 88-92 21575522-1 2011 OBJECTIVE: To investigate the relationship between the expression of ERCC1, BRCA1, beta-tubulin and K-ras and the clinical efficacy, prognosis in advanced non-small cell lung cancer treated by platinum-based chemotherapy. Platinum 193-201 KRAS proto-oncogene, GTPase Homo sapiens 100-105 19281127-0 2009 [K-ras mutation predictive significance in platinum based chemotherapeutic protocols in patients with advanced non-small cell lung cancer]. Platinum 43-51 KRAS proto-oncogene, GTPase Homo sapiens 1-6 22588152-0 2012 A pooled exploratory analysis of the effect of tumor size and KRAS mutations on survival benefit from adjuvant platinum-based chemotherapy in node-negative non-small cell lung cancer. Platinum 111-119 KRAS proto-oncogene, GTPase Homo sapiens 62-66