Result
Gene | Variant | Type | Tumor | Drug | Drug level | Reference | More | ||||||||||||||||||||||
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ABL1 | A344V | MUT | Chronic Myeloid Leukemia | Imatinib | RI | 1 | |||||||||||||||||||||||
Evidence region
CGI Patient CriteriaABL1-BCR fusion NoteOptimization of CML treatment is a continuous process. Knowledge is still accumulating, and the therapeutic scenario is still evolving. Here we aimed to provide recommendations to clinicians on how to best integrate BCR-ABL KD mutation analysis in the routine management of CML patients. We acknowledge that the literature is still not comprehensive enough to base all our recommendations on sound evidence. The reader should therefore be warned that these are mostly based on the expert opinion of the members of this panel. Gene name
Full name
ABL proto-oncogene 1, non-receptor tyrosine kinase Gene typeprotein-coding FunctionThis gene is a protooncogene that encodes a protein tyrosine kinase involved in a variety of cellular processes, including cell division, adhesion, differentiation, and response to stress. The activity of the protein is negatively regulated by its SH3 domain, whereby deletion of the region encoding this domain results in an oncogene. The ubiquitously expressed protein has DNA-binding activity that is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function. This gene has been found fused to a variety of translocation partner genes in various leukemias, most notably the t(9;22) translocation that results in a fusion with the 5' end of the breakpoint cluster region gene (BCR; MIM:151410). Alternative splicing of this gene results in two transcript variants, which contain alternative first exons that are spliced to the remaining common exons. [provided by RefSeq, Aug 2014] Drug name
Imatinib DrugBank ID SynonymsImatinib Imatinib Teva Imatinib is a small molecule kinase inhibitor used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It is occasionally referred to as CGP57148B or STI571 (especially in older publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells. Target gene
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ABL1 | A350V | MUT | Chronic Myeloid Leukemia | Imatinib | RI | 1 | |||||||||||||||||||||||
Evidence region
CGI Patient CriteriaABL1-BCR fusion NoteOptimization of CML treatment is a continuous process. Knowledge is still accumulating, and the therapeutic scenario is still evolving. Here we aimed to provide recommendations to clinicians on how to best integrate BCR-ABL KD mutation analysis in the routine management of CML patients. We acknowledge that the literature is still not comprehensive enough to base all our recommendations on sound evidence. The reader should therefore be warned that these are mostly based on the expert opinion of the members of this panel. Gene name
Full name
ABL proto-oncogene 1, non-receptor tyrosine kinase Gene typeprotein-coding FunctionThis gene is a protooncogene that encodes a protein tyrosine kinase involved in a variety of cellular processes, including cell division, adhesion, differentiation, and response to stress. The activity of the protein is negatively regulated by its SH3 domain, whereby deletion of the region encoding this domain results in an oncogene. The ubiquitously expressed protein has DNA-binding activity that is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function. This gene has been found fused to a variety of translocation partner genes in various leukemias, most notably the t(9;22) translocation that results in a fusion with the 5' end of the breakpoint cluster region gene (BCR; MIM:151410). Alternative splicing of this gene results in two transcript variants, which contain alternative first exons that are spliced to the remaining common exons. [provided by RefSeq, Aug 2014] Drug name
Imatinib DrugBank ID SynonymsImatinib Imatinib Teva Imatinib is a small molecule kinase inhibitor used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It is occasionally referred to as CGP57148B or STI571 (especially in older publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells. Target gene
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ABL1 | A365V | MUT | Chronic Myeloid Leukemia | Imatinib | RI | 1 | |||||||||||||||||||||||
Evidence region
CGI Patient CriteriaABL1-BCR fusion NoteOptimization of CML treatment is a continuous process. Knowledge is still accumulating, and the therapeutic scenario is still evolving. Here we aimed to provide recommendations to clinicians on how to best integrate BCR-ABL KD mutation analysis in the routine management of CML patients. We acknowledge that the literature is still not comprehensive enough to base all our recommendations on sound evidence. The reader should therefore be warned that these are mostly based on the expert opinion of the members of this panel. Gene name
Full name
ABL proto-oncogene 1, non-receptor tyrosine kinase Gene typeprotein-coding FunctionThis gene is a protooncogene that encodes a protein tyrosine kinase involved in a variety of cellular processes, including cell division, adhesion, differentiation, and response to stress. The activity of the protein is negatively regulated by its SH3 domain, whereby deletion of the region encoding this domain results in an oncogene. The ubiquitously expressed protein has DNA-binding activity that is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function. This gene has been found fused to a variety of translocation partner genes in various leukemias, most notably the t(9;22) translocation that results in a fusion with the 5' end of the breakpoint cluster region gene (BCR; MIM:151410). Alternative splicing of this gene results in two transcript variants, which contain alternative first exons that are spliced to the remaining common exons. [provided by RefSeq, Aug 2014] Drug name
Imatinib DrugBank ID SynonymsImatinib Imatinib Teva Imatinib is a small molecule kinase inhibitor used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It is occasionally referred to as CGP57148B or STI571 (especially in older publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells. Target gene
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ABL1 | A366G | MUT | Chronic Myeloid Leukemia | Imatinib | RI | 1 | |||||||||||||||||||||||
Evidence region
CGI Patient CriteriaABL1-BCR fusion NoteOptimization of CML treatment is a continuous process. Knowledge is still accumulating, and the therapeutic scenario is still evolving. Here we aimed to provide recommendations to clinicians on how to best integrate BCR-ABL KD mutation analysis in the routine management of CML patients. We acknowledge that the literature is still not comprehensive enough to base all our recommendations on sound evidence. The reader should therefore be warned that these are mostly based on the expert opinion of the members of this panel. Gene name
Full name
ABL proto-oncogene 1, non-receptor tyrosine kinase Gene typeprotein-coding FunctionThis gene is a protooncogene that encodes a protein tyrosine kinase involved in a variety of cellular processes, including cell division, adhesion, differentiation, and response to stress. The activity of the protein is negatively regulated by its SH3 domain, whereby deletion of the region encoding this domain results in an oncogene. The ubiquitously expressed protein has DNA-binding activity that is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function. This gene has been found fused to a variety of translocation partner genes in various leukemias, most notably the t(9;22) translocation that results in a fusion with the 5' end of the breakpoint cluster region gene (BCR; MIM:151410). Alternative splicing of this gene results in two transcript variants, which contain alternative first exons that are spliced to the remaining common exons. [provided by RefSeq, Aug 2014] Drug name
Imatinib DrugBank ID SynonymsImatinib Imatinib Teva Imatinib is a small molecule kinase inhibitor used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It is occasionally referred to as CGP57148B or STI571 (especially in older publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells. Target gene
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ABL1 | A380T | MUT | Chronic Myeloid Leukemia | Imatinib | RI | 1 | |||||||||||||||||||||||
Evidence region
CGI Patient CriteriaABL1-BCR fusion NoteOptimization of CML treatment is a continuous process. Knowledge is still accumulating, and the therapeutic scenario is still evolving. Here we aimed to provide recommendations to clinicians on how to best integrate BCR-ABL KD mutation analysis in the routine management of CML patients. We acknowledge that the literature is still not comprehensive enough to base all our recommendations on sound evidence. The reader should therefore be warned that these are mostly based on the expert opinion of the members of this panel. Gene name
Full name
ABL proto-oncogene 1, non-receptor tyrosine kinase Gene typeprotein-coding FunctionThis gene is a protooncogene that encodes a protein tyrosine kinase involved in a variety of cellular processes, including cell division, adhesion, differentiation, and response to stress. The activity of the protein is negatively regulated by its SH3 domain, whereby deletion of the region encoding this domain results in an oncogene. The ubiquitously expressed protein has DNA-binding activity that is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function. This gene has been found fused to a variety of translocation partner genes in various leukemias, most notably the t(9;22) translocation that results in a fusion with the 5' end of the breakpoint cluster region gene (BCR; MIM:151410). Alternative splicing of this gene results in two transcript variants, which contain alternative first exons that are spliced to the remaining common exons. [provided by RefSeq, Aug 2014] Drug name
Imatinib DrugBank ID SynonymsImatinib Imatinib Teva Imatinib is a small molecule kinase inhibitor used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It is occasionally referred to as CGP57148B or STI571 (especially in older publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells. Target gene
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ABL1 | A397P | MUT | Chronic Myeloid Leukemia | Imatinib | RI | 1 | |||||||||||||||||||||||
Evidence region
CGI Patient CriteriaABL1-BCR fusion NoteOptimization of CML treatment is a continuous process. Knowledge is still accumulating, and the therapeutic scenario is still evolving. Here we aimed to provide recommendations to clinicians on how to best integrate BCR-ABL KD mutation analysis in the routine management of CML patients. We acknowledge that the literature is still not comprehensive enough to base all our recommendations on sound evidence. The reader should therefore be warned that these are mostly based on the expert opinion of the members of this panel. Gene name
Full name
ABL proto-oncogene 1, non-receptor tyrosine kinase Gene typeprotein-coding FunctionThis gene is a protooncogene that encodes a protein tyrosine kinase involved in a variety of cellular processes, including cell division, adhesion, differentiation, and response to stress. The activity of the protein is negatively regulated by its SH3 domain, whereby deletion of the region encoding this domain results in an oncogene. The ubiquitously expressed protein has DNA-binding activity that is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function. This gene has been found fused to a variety of translocation partner genes in various leukemias, most notably the t(9;22) translocation that results in a fusion with the 5' end of the breakpoint cluster region gene (BCR; MIM:151410). Alternative splicing of this gene results in two transcript variants, which contain alternative first exons that are spliced to the remaining common exons. [provided by RefSeq, Aug 2014] Drug name
Imatinib DrugBank ID SynonymsImatinib Imatinib Teva Imatinib is a small molecule kinase inhibitor used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It is occasionally referred to as CGP57148B or STI571 (especially in older publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells. Target gene
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ABL1 | A433T | MUT | Chronic Myeloid Leukemia | Imatinib | RI | 1 | |||||||||||||||||||||||
Evidence region
CGI Patient CriteriaABL1-BCR fusion NoteOptimization of CML treatment is a continuous process. Knowledge is still accumulating, and the therapeutic scenario is still evolving. Here we aimed to provide recommendations to clinicians on how to best integrate BCR-ABL KD mutation analysis in the routine management of CML patients. We acknowledge that the literature is still not comprehensive enough to base all our recommendations on sound evidence. The reader should therefore be warned that these are mostly based on the expert opinion of the members of this panel. Gene name
Full name
ABL proto-oncogene 1, non-receptor tyrosine kinase Gene typeprotein-coding FunctionThis gene is a protooncogene that encodes a protein tyrosine kinase involved in a variety of cellular processes, including cell division, adhesion, differentiation, and response to stress. The activity of the protein is negatively regulated by its SH3 domain, whereby deletion of the region encoding this domain results in an oncogene. The ubiquitously expressed protein has DNA-binding activity that is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function. This gene has been found fused to a variety of translocation partner genes in various leukemias, most notably the t(9;22) translocation that results in a fusion with the 5' end of the breakpoint cluster region gene (BCR; MIM:151410). Alternative splicing of this gene results in two transcript variants, which contain alternative first exons that are spliced to the remaining common exons. [provided by RefSeq, Aug 2014] Drug name
Imatinib DrugBank ID SynonymsImatinib Imatinib Teva Imatinib is a small molecule kinase inhibitor used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It is occasionally referred to as CGP57148B or STI571 (especially in older publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells. Target gene
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ABL1 | ABL1-. | FUS | Acute Lymphoblastic Leukemia | TK Inhibitors | IV | 1 | |||||||||||||||||||||||
Evidence region
Literature Patient Criteria- NoteIn conclusion, we report the largest cohort of patients with ABL-class kinase rearrangement exposed to TKI frontline or at relapse, and show promising MRD response and outcome, reminiscent of those observed in early trials of imatinib combined with chemotherapy in Ph+ ALL.18 Prospective screening strategies are feasible and should be generalized to identify these high-risk patients and to propose early TKI-based intervention. In future studies, several questions remain to be addressed, including the choice of TKI according to the fusion transcript, whether these patients should receive recently approved blinatumomab,19 and finally the benefit of HSCT in patients who achieve good MRD response upon targeted therapy. Gene name
Full name
ABL proto-oncogene 1, non-receptor tyrosine kinase Gene typeprotein-coding FunctionThis gene is a protooncogene that encodes a protein tyrosine kinase involved in a variety of cellular processes, including cell division, adhesion, differentiation, and response to stress. The activity of the protein is negatively regulated by its SH3 domain, whereby deletion of the region encoding this domain results in an oncogene. The ubiquitously expressed protein has DNA-binding activity that is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function. This gene has been found fused to a variety of translocation partner genes in various leukemias, most notably the t(9;22) translocation that results in a fusion with the 5' end of the breakpoint cluster region gene (BCR; MIM:151410). Alternative splicing of this gene results in two transcript variants, which contain alternative first exons that are spliced to the remaining common exons. [provided by RefSeq, Aug 2014] Sorry, there is no related drug information. |
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ABL1 | ABL1-. | FUS | Acute Lymphoblastic Leukemia | TK Inhibitors | II | 1 | |||||||||||||||||||||||
Evidence region
Literature Patient Criteria NoteIn conclusion, ABL-class fusions are frequent among BCP and T-ALL patients who respond slowly to induction therapy. We have demonstrated a reduced risk of relapse for ABL-class fusion patients with EOI MRD _1% treated with adjuvant TKI without a significant increased risk of severe toxicity. The ALLTogether 01 trial (EUDRACT number: 2018-001795-38) will screen patients at diagnosis for ABL-class fusions and add imatinib from day 15 (day 28 if aged _16 years) to a standard chemotherapy backbone to investigate whether early TKI reduces EOI MRD and improves outcome for all patients with an ABL-class fusion. Gene name
Full name
ABL proto-oncogene 1, non-receptor tyrosine kinase Gene typeprotein-coding FunctionThis gene is a protooncogene that encodes a protein tyrosine kinase involved in a variety of cellular processes, including cell division, adhesion, differentiation, and response to stress. The activity of the protein is negatively regulated by its SH3 domain, whereby deletion of the region encoding this domain results in an oncogene. The ubiquitously expressed protein has DNA-binding activity that is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function. This gene has been found fused to a variety of translocation partner genes in various leukemias, most notably the t(9;22) translocation that results in a fusion with the 5' end of the breakpoint cluster region gene (BCR; MIM:151410). Alternative splicing of this gene results in two transcript variants, which contain alternative first exons that are spliced to the remaining common exons. [provided by RefSeq, Aug 2014] Sorry, there is no related drug information. |
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ABL1 | ABL1-BCR | FUS | Chronic Myeloid Leukemia | Bosutinib | I | 1 | |||||||||||||||||||||||
Evidence region
CGI Patient Criteria- Note- Gene name
Full name
ABL proto-oncogene 1, non-receptor tyrosine kinase Gene typeprotein-coding FunctionThis gene is a protooncogene that encodes a protein tyrosine kinase involved in a variety of cellular processes, including cell division, adhesion, differentiation, and response to stress. The activity of the protein is negatively regulated by its SH3 domain, whereby deletion of the region encoding this domain results in an oncogene. The ubiquitously expressed protein has DNA-binding activity that is regulated by CDC2-mediated phosphorylation, suggesting a cell cycle function. This gene has been found fused to a variety of translocation partner genes in various leukemias, most notably the t(9;22) translocation that results in a fusion with the 5' end of the breakpoint cluster region gene (BCR; MIM:151410). Alternative splicing of this gene results in two transcript variants, which contain alternative first exons that are spliced to the remaining common exons. [provided by RefSeq, Aug 2014] Drug name
Bosutinib DrugBank ID Synonyms4-((2,4-dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methyl-1-piperazinyl)propoxy)-3-quinolinecarbonitrile Bosulif DescriptionBosutinib is a Bcr-Abl kinase inhibitor for the treatment of Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML). Compared to other tyrosine kinase inhibitors, it has a more favourable hematologic toxicity profile. FDA approved on September 4, 2012. Target gene
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