PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18496131-10 2008 CONCLUSION: This study indicates that the presently evaluated variant alleles in the CYP2B6, CYP2C9, CYP2C19, CYP3A4, CYP3A5, GSTA1, GSTP1, ALDH1A1 and ALDH3A1 genes do not explain the interindividual variability in cyclophosphamide and 4-hydroxycyclophosphamide pharmacokinetics and are, probably, not the cause of the observed variability in toxicity. Cyclophosphamide 216-232 aldehyde dehydrogenase 1 family member A1 Homo sapiens 140-147 12513786-3 2002 Results showed that a retroviral vector was used to transduce full-length human ALDH1 cDNA into human hematopoietic cell line K562 that was then tested for resistance to 4-hydroxycyclophosphamide (4-HC), an active analogue of cyclophosphamide. Cyclophosphamide 179-195 aldehyde dehydrogenase 1 family member A1 Homo sapiens 80-85 16614850-1 2007 PURPOSE: Aldehyde dehydrogenases class-1A1 (ALDH1A1) and class-3A1 (ALDH3A1) have been associated with resistance to cyclophosphamide (CP) and its derivatives. Cyclophosphamide 117-133 aldehyde dehydrogenase 1 family member A1 Homo sapiens 9-42 16614850-1 2007 PURPOSE: Aldehyde dehydrogenases class-1A1 (ALDH1A1) and class-3A1 (ALDH3A1) have been associated with resistance to cyclophosphamide (CP) and its derivatives. Cyclophosphamide 117-133 aldehyde dehydrogenase 1 family member A1 Homo sapiens 44-51 12513786-4 2002 Overexpression of the ALDH1 gene resulted in a significant increases in cyclophosphamide resistance in transduced K562 cells (50% inhibition concentration, IC50 = 10 micro mol/L). Cyclophosphamide 72-88 aldehyde dehydrogenase 1 family member A1 Homo sapiens 22-27 12513786-5 2002 These findings indicate that ALDH1 overexpression is sufficient to induce cyclophosphamide resistance in vitro and provide a basis for testing the efficacy of ALDH1 gene transduction to protect bone marrow cells from high-dose cyclophosphamide in vivo. Cyclophosphamide 74-90 aldehyde dehydrogenase 1 family member A1 Homo sapiens 29-34 12513786-5 2002 These findings indicate that ALDH1 overexpression is sufficient to induce cyclophosphamide resistance in vitro and provide a basis for testing the efficacy of ALDH1 gene transduction to protect bone marrow cells from high-dose cyclophosphamide in vivo. Cyclophosphamide 227-243 aldehyde dehydrogenase 1 family member A1 Homo sapiens 29-34 10469894-1 1999 As judged by findings in preclinical models, determinants of cellular sensitivity to cyclophosphamide and other oxazaphosphorines include two cytosolic aldehyde dehydrogenases, viz., ALDH1A1 and ALDH3A1. Cyclophosphamide 85-101 aldehyde dehydrogenase 1 family member A1 Homo sapiens 183-190 11914911-0 2002 Cellular levels of aldehyde dehydrogenases (ALDH1A1 and ALDH3A1) as predictors of therapeutic responses to cyclophosphamide-based chemotherapy of breast cancer: a retrospective study. Cyclophosphamide 107-123 aldehyde dehydrogenase 1 family member A1 Homo sapiens 44-51 11914911-2 2002 PURPOSE: In preclinical models, established molecular determinants of cellular sensitivity to cyclophosphamide, long a mainstay of chemotherapeutic regimens used to treat breast cancers, include the aldehyde dehydrogenases that catalyze the detoxification of this agent, namely, ALDH1A1 and ALDH3A1. Cyclophosphamide 94-110 aldehyde dehydrogenase 1 family member A1 Homo sapiens 279-286 11914911-8 2002 The premise that cellular levels of ALDH1A1 and/or ALDH3A1 predict clinical responses to cyclophosphamide-based chemotherapeutic regimens was submitted to statistical analysis. Cyclophosphamide 89-105 aldehyde dehydrogenase 1 family member A1 Homo sapiens 36-43 11914911-11 2002 Retrospective analysis indicated that cellular levels of ALDH1A1, but not those of ALDH3A1, were (1) significantly higher in metastatic tumor cells that had survived exposure to cyclophosphamide than in those that had not been exposed to this drug, and (2) significantly higher in metastatic tumors that did not respond (tumor size did not decrease or even increased) to subsequent treatment with cyclophosphamide-based chemotherapeutic regimens than in those that did respond (tumor size decreased) to such regimens. Cyclophosphamide 178-194 aldehyde dehydrogenase 1 family member A1 Homo sapiens 57-64 11914911-11 2002 Retrospective analysis indicated that cellular levels of ALDH1A1, but not those of ALDH3A1, were (1) significantly higher in metastatic tumor cells that had survived exposure to cyclophosphamide than in those that had not been exposed to this drug, and (2) significantly higher in metastatic tumors that did not respond (tumor size did not decrease or even increased) to subsequent treatment with cyclophosphamide-based chemotherapeutic regimens than in those that did respond (tumor size decreased) to such regimens. Cyclophosphamide 397-413 aldehyde dehydrogenase 1 family member A1 Homo sapiens 57-64 11914911-12 2002 The therapeutic outcome of cyclophosphamide-based chemotherapy corresponded to cellular ALDH1A1 levels in 77% of cases. Cyclophosphamide 27-43 aldehyde dehydrogenase 1 family member A1 Homo sapiens 88-95 11914911-14 2002 Thus, partial or complete responses to cyclophosphamide-based chemotherapy occurred 2.3 times more often when the ALDH1A1 level was low than when it was high. Cyclophosphamide 39-55 aldehyde dehydrogenase 1 family member A1 Homo sapiens 114-121 11320670-3 2001 Preclinical models indicate that cellular sensitivity to cyclophosphamide and other oxazaphosphorines, e.g., ifosfamide, is inversely related to the cellular content of two aldehyde dehydrogenases, viz ALDH1A1 and ALDH3A1, and glutathione. Cyclophosphamide 57-73 aldehyde dehydrogenase 1 family member A1 Homo sapiens 202-209 10773007-1 2000 Previous studies in this laboratory showed that the overexpression of human aldehyde dehydrogenase class-1 (ALDH-1) with a retroviral vector resulted in increased resistance to 4-hydroperoxycyclophosphamide (4-HC), an active metabolite of cyclophosphamide. Cyclophosphamide 190-206 aldehyde dehydrogenase 1 family member A1 Homo sapiens 76-106 10773007-1 2000 Previous studies in this laboratory showed that the overexpression of human aldehyde dehydrogenase class-1 (ALDH-1) with a retroviral vector resulted in increased resistance to 4-hydroperoxycyclophosphamide (4-HC), an active metabolite of cyclophosphamide. Cyclophosphamide 190-206 aldehyde dehydrogenase 1 family member A1 Homo sapiens 108-114 8562935-7 1996 These findings indicate that ALDH1 overexpression is sufficient to induce cyclophosphamide resistance in vitro and provide a basis for testing the efficacy of ALDH1 gene transduction to protect bone marrow cells from high-dose cyclophosphamide in vivo. Cyclophosphamide 74-90 aldehyde dehydrogenase 1 family member A1 Homo sapiens 29-34 11741210-8 1999 The calculated %inhibition of ALDH1 activity by acrolein and BCNU in patients receiving BCNU in 4 split doses with CY was 81%, and it increased to 92% in single dose BCNU regimen. Cyclophosphamide 115-117 aldehyde dehydrogenase 1 family member A1 Homo sapiens 30-35 9884322-3 1999 Here, the mechanism for the decrease in ALDH1 activity after CY administration was investigated. Cyclophosphamide 61-63 aldehyde dehydrogenase 1 family member A1 Homo sapiens 40-45 9884322-8 1999 The percentage of inhibition of ALDH1 activity in vivo by acrolein in patients receiving CY was calculated based on the in vitro Ki of acrolein, the in vitro Km of HCY, and the in vivo peak blood concentrations of HCY and acrolein. Cyclophosphamide 89-91 aldehyde dehydrogenase 1 family member A1 Homo sapiens 32-37 9884322-9 1999 The calculations indicated that the activity of ALDH1 was inhibited by 85, 88, and 91% on days 1, 2, and 3 (24 h after the dose on day 2) of CY administration, respectively. Cyclophosphamide 141-143 aldehyde dehydrogenase 1 family member A1 Homo sapiens 48-53 9551609-1 1998 Previously, we have reported the successful expression of human aldehyde dehydrogenase class-1 (ALDH-1) in K562 leukemia cells using a retroviral vector and demonstrated low expression that resulted in up to three-fold increase in resistance to 4-hydroperoxycyclophosphamide (4-HC), an active derivative to cyclophosphamide. Cyclophosphamide 258-274 aldehyde dehydrogenase 1 family member A1 Homo sapiens 64-94 9551609-1 1998 Previously, we have reported the successful expression of human aldehyde dehydrogenase class-1 (ALDH-1) in K562 leukemia cells using a retroviral vector and demonstrated low expression that resulted in up to three-fold increase in resistance to 4-hydroperoxycyclophosphamide (4-HC), an active derivative to cyclophosphamide. Cyclophosphamide 258-274 aldehyde dehydrogenase 1 family member A1 Homo sapiens 96-102 9815579-1 1997 Molecular determinants of cellular sensitivity to cyclophosphamide, long the mainstay of chemotherapeutic regimens used to treat metastatic breast cancer, include class 1 and class 3 aldehyde dehydrogenases (ALDH-1 and ALDH-3, respectively), which catalyze the detoxification of this agent. Cyclophosphamide 50-66 aldehyde dehydrogenase 1 family member A1 Homo sapiens 208-214 9322086-1 1997 Class 1 aldehyde dehydrogenases (ALDH-1) function as drug resistance gene products by catalyzing the irreversible conversion of aldophosphamide, an active metabolite of cyclophosphamide, to an inert compound. Cyclophosphamide 169-185 aldehyde dehydrogenase 1 family member A1 Homo sapiens 33-39 9322086-2 1997 Because the dose-limiting toxicity of cyclophosphamide is myelosuppression, retrovirus-mediated transfer of ALDH-1 to bone marrow cells has been proposed as a protective strategy. Cyclophosphamide 38-54 aldehyde dehydrogenase 1 family member A1 Homo sapiens 108-114 8562935-6 1996 ALDH1 transduction into peripheral blood human hematopoietic progenitor cells also led to significant increases (4- to 10-fold; IC50, approximately 3 to 4 mumol/L) in cyclophosphamide resistance in an in vitro colony-forming assay. Cyclophosphamide 167-183 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-5 9394035-1 1997 Detoxification of cyclophosphamide is effected, in part, by hepatic class 1 aldehyde dehydrogenase (ALDH-1)-catalyzed oxidation of aldophosphamide, a pivotal aldehyde intermediate, to the nontoxic metabolite, carboxyphosphamide. Cyclophosphamide 18-34 aldehyde dehydrogenase 1 family member A1 Homo sapiens 100-106 8662658-2 1996 Human class 1 aldehyde dehydrogenase (hALDH-1) can oxidize aldophosphamide, a key aldehyde intermediate in the activation pathway of cyclophosphamide and other oxazaphosphorine (OAP) anti-cancer alkylating agents. Cyclophosphamide 133-149 aldehyde dehydrogenase 1 family member A1 Homo sapiens 38-45 8562935-7 1996 These findings indicate that ALDH1 overexpression is sufficient to induce cyclophosphamide resistance in vitro and provide a basis for testing the efficacy of ALDH1 gene transduction to protect bone marrow cells from high-dose cyclophosphamide in vivo. Cyclophosphamide 227-243 aldehyde dehydrogenase 1 family member A1 Homo sapiens 29-34 34057116-0 2021 Increased aldehyde dehydrogenase 1 (ALDH1) levels are associated with chemo-responsiveness in breast cancer patients treated with taxane-adriamycin-cyclophosphamide regimen. Cyclophosphamide 148-164 aldehyde dehydrogenase 1 family member A1 Homo sapiens 10-34 34089986-7 2021 Total ten selective ALDH1A1 inhibitors with diverse scaffolds and appropriate ADMET were identified that can be further developed as adjuvant therapy in cyclophosphamide and cisplatin resistance cancer. Cyclophosphamide 153-169 aldehyde dehydrogenase 1 family member A1 Homo sapiens 20-27 35618489-1 2022 Aldehyde dehydrogenase 1 (ALDH1A1), an oxidoreductase class of enzymes, is overexpressed in various types of cancer cell lines and is the major cause of resistance to the Food and Drug Administration (FDA)-approved drug, cyclophosphamide (CP). Cyclophosphamide 221-237 aldehyde dehydrogenase 1 family member A1 Homo sapiens 26-33 35606478-9 2022 CONCLUSION: The finding that patients who carry ALDH1A1 rs8187996 may have a lower risk of cyclophosphamide toxicity than wild-type patients contradicts a prior finding for this variant and should be viewed with skepticism. Cyclophosphamide 91-107 aldehyde dehydrogenase 1 family member A1 Homo sapiens 48-55 8785707-2 1996 To investigate the direct role of the human aldehyde dehydrogenase class 1 (ALDH-1) in the resistance to one of these agents, 4-hydroperoxycyclophosphamide (4-HC), an active metabolite of cyclophosphamide, neomycin-selectable plasmid or retroviral constructs harboring the wild-type ALDH-1 complementary DNA in the sense orientation were transfected into K562 leukemic cell lines. Cyclophosphamide 139-155 aldehyde dehydrogenase 1 family member A1 Homo sapiens 44-74 8785707-2 1996 To investigate the direct role of the human aldehyde dehydrogenase class 1 (ALDH-1) in the resistance to one of these agents, 4-hydroperoxycyclophosphamide (4-HC), an active metabolite of cyclophosphamide, neomycin-selectable plasmid or retroviral constructs harboring the wild-type ALDH-1 complementary DNA in the sense orientation were transfected into K562 leukemic cell lines. Cyclophosphamide 139-155 aldehyde dehydrogenase 1 family member A1 Homo sapiens 76-82 34057116-0 2021 Increased aldehyde dehydrogenase 1 (ALDH1) levels are associated with chemo-responsiveness in breast cancer patients treated with taxane-adriamycin-cyclophosphamide regimen. Cyclophosphamide 148-164 aldehyde dehydrogenase 1 family member A1 Homo sapiens 36-41 34057116-3 2021 OBJECTIVE: This study aimed to investigate the correlation between plasma levels of ALDH1 and chemotherapy responses to the taxane-adriamycin-cyclophosphamide (TAC) regimen in breast cancer patients. Cyclophosphamide 142-158 aldehyde dehydrogenase 1 family member A1 Homo sapiens 84-89 32877739-0 2020 Investigating the Role of Missense SNPs on ALDH 1A1 mediated pharmacokinetic resistance to cyclophosphamide. Cyclophosphamide 91-107 aldehyde dehydrogenase 1 family member A1 Homo sapiens 43-51 26398662-9 2015 ALDH1A1(high) expression or beta-catenin(c) expression alone was associated with lymph node metastasis, and worse clinical outcome in breast cancer patients, especially in patients receiving cyclophosphamide treatment. Cyclophosphamide 191-207 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-7 26398662-9 2015 ALDH1A1(high) expression or beta-catenin(c) expression alone was associated with lymph node metastasis, and worse clinical outcome in breast cancer patients, especially in patients receiving cyclophosphamide treatment. Cyclophosphamide 191-207 aldehyde dehydrogenase 1 family member A1 Homo sapiens 8-12 26398662-10 2015 Combined expression of ALDH1A1(high) and beta-catenin(c) was associated with lymph node metastasis, poor outcome, and resistance to cyclophosphamide treatment. Cyclophosphamide 132-148 aldehyde dehydrogenase 1 family member A1 Homo sapiens 23-36 24387105-3 2014 Upon activation, cyclophosphamide forms an intermediate, aldophosphamide, which can be detoxified to carboxyphosphamide by aldehyde dehydrogenases (ALDH), especially ALDH1A1 and ALDH3A1. Cyclophosphamide 17-33 aldehyde dehydrogenase 1 family member A1 Homo sapiens 148-152 24387105-3 2014 Upon activation, cyclophosphamide forms an intermediate, aldophosphamide, which can be detoxified to carboxyphosphamide by aldehyde dehydrogenases (ALDH), especially ALDH1A1 and ALDH3A1. Cyclophosphamide 17-33 aldehyde dehydrogenase 1 family member A1 Homo sapiens 166-173 22080062-2 2012 ALDH1A1 inactivates cyclophosphamide, which is an integral agent in breast cancer chemotherapy regimens. Cyclophosphamide 20-36 aldehyde dehydrogenase 1 family member A1 Homo sapiens 0-7 22080062-3 2012 The purposes of this study were to verify these results, to correlate ALDH1A1 expression with clinical outcome in patients treated with cyclophosphamide as part of the chemotherapy (adjuvant or neoadjuvant), and to evaluate ALDH1A1 as a useful marker to predict the clinical outcome of breast cancer subsets. Cyclophosphamide 136-152 aldehyde dehydrogenase 1 family member A1 Homo sapiens 70-77 18560594-9 2008 Aldehyde dehydrogenase 1 gene expression and enzymatic activity are elevated in CoCSC and using an in vitro culture system that maintains CoCSC as demonstrated by serial transplants and lentiviral marking of single cell-derived clones, we further show that ALDH1 enzymatic activity is a major mediator of resistance to cyclophosphamide: a classical chemotherapeutic agent. Cyclophosphamide 319-335 aldehyde dehydrogenase 1 family member A1 Homo sapiens 257-262 25344211-2 2014 The aim of this study was to investigate the role of aldehyde dehydrogenase (ALDH) 1A1 in the resistance of diffuse large B cell lymphoma to the chemotherapeutic mixture consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP). Cyclophosphamide 184-200 aldehyde dehydrogenase 1 family member A1 Homo sapiens 53-86