diff --git a/core/src/test/resources/test_cancer_type_treatments.tsv b/core/src/test/resources/test_cancer_type_treatments.tsv index 80146271d..0f6720c61 100644 --- a/core/src/test/resources/test_cancer_type_treatments.tsv +++ b/core/src/test/resources/test_cancer_type_treatments.tsv @@ -149,20 +149,19 @@ KRAS G12C AML KRAS G12D AML KRAS G12C Leukemia KRAS G12D Leukemia -BRAF V600E Anaplastic Thyroid Cancer 1: Dabrafenib+Trametinib; 3B: Dabrafenib; 3B: Encorafenib+Cetuximab; 3B: Selumetinib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Encorafenib+Panitumumab; 3B: Trametinib; 3B: Vemurafenib; 3B: Vemurafenib+Cobimetinib; 3B: Encorafenib+Binimetinib; -BRAF V600K Anaplastic Thyroid Cancer 3B: Dabrafenib+Trametinib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Trametinib; 3B: Vemurafenib+Cobimetinib; 3B: Encorafenib+Binimetinib; -BRAF V600E Melanoma 1: Dabrafenib; 1: Dabrafenib+Trametinib; 1: Vemurafenib+Atezolizumab+Cobimetinib; 1: Trametinib; 1: Vemurafenib; 1: Vemurafenib+Cobimetinib; 1: Encorafenib+Binimetinib; 3B: Encorafenib+Cetuximab; 3B: Selumetinib; 3B: Encorafenib+Panitumumab; -BRAF V600K Melanoma 1: Dabrafenib+Trametinib; 1: Vemurafenib+Atezolizumab+Cobimetinib; 1: Trametinib; 1: Vemurafenib+Cobimetinib; 1: Encorafenib+Binimetinib; -BRAF V600G Melanoma 1: Vemurafenib+Atezolizumab+Cobimetinib; 2: Encorafenib+Binimetinib; 2: Dabrafenib+Trametinib; 2: Vemurafenib+Cobimetinib; -BRAF V600E NSCLC 1: Dabrafenib+Trametinib; 1: Encorafenib+Binimetinib; 3B: Dabrafenib; 3B: Encorafenib+Cetuximab; 3B: Selumetinib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Encorafenib+Panitumumab; 3B: Trametinib; 3B: Vemurafenib; 3B: Vemurafenib+Cobimetinib; -BRAF V600K NSCLC 3B: Dabrafenib+Trametinib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Trametinib; 3B: Vemurafenib+Cobimetinib; 3B: Encorafenib+Binimetinib; -BRAF V600G NSCLC 3B: Encorafenib+Binimetinib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Dabrafenib+Trametinib; 3B: Vemurafenib+Cobimetinib; -BRAF V600K NSCLC 3B: Dabrafenib+Trametinib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Trametinib; 3B: Vemurafenib+Cobimetinib; 3B: Encorafenib+Binimetinib; -BRAF V600E Colorectal Cancer 1: Encorafenib+Cetuximab; 2: Encorafenib+Panitumumab; 3B: Dabrafenib; 3B: Dabrafenib+Trametinib; 3B: Selumetinib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Trametinib; 3B: Vemurafenib; 3B: Vemurafenib+Cobimetinib; 3B: Encorafenib+Binimetinib; -BRAF V600K Colorectal Cancer 3B: Dabrafenib+Trametinib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Trametinib; 3B: Vemurafenib+Cobimetinib; 3B: Encorafenib+Binimetinib; +BRAF V600E Anaplastic Thyroid Cancer 1: Dabrafenib+Trametinib; 3B: Dabrafenib; 3B: Encorafenib+Cetuximab; 3B: Selumetinib; 3B: Tovorafenib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Encorafenib+Panitumumab; 3B: Trametinib; 3B: Vemurafenib; 3B: Vemurafenib+Cobimetinib; 3B: Encorafenib+Binimetinib; +BRAF V600K Anaplastic Thyroid Cancer 3B: Dabrafenib+Trametinib; 3B: Tovorafenib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Trametinib; 3B: Vemurafenib+Cobimetinib; 3B: Encorafenib+Binimetinib; +BRAF V600E Melanoma 1: Dabrafenib; 1: Dabrafenib+Trametinib; 1: Vemurafenib+Atezolizumab+Cobimetinib; 1: Trametinib; 1: Vemurafenib; 1: Vemurafenib+Cobimetinib; 1: Encorafenib+Binimetinib; 3B: Encorafenib+Cetuximab; 3B: Selumetinib; 3B: Tovorafenib; 3B: Encorafenib+Panitumumab; +BRAF V600K Melanoma 1: Dabrafenib+Trametinib; 1: Vemurafenib+Atezolizumab+Cobimetinib; 1: Trametinib; 1: Vemurafenib+Cobimetinib; 1: Encorafenib+Binimetinib; 3B: Tovorafenib; +BRAF V600G Melanoma 1: Vemurafenib+Atezolizumab+Cobimetinib; 2: Encorafenib+Binimetinib; 2: Dabrafenib+Trametinib; 2: Vemurafenib+Cobimetinib; 3B: Tovorafenib; +BRAF V600E NSCLC 1: Dabrafenib+Trametinib; 1: Encorafenib+Binimetinib; 3B: Dabrafenib; 3B: Encorafenib+Cetuximab; 3B: Selumetinib; 3B: Tovorafenib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Encorafenib+Panitumumab; 3B: Trametinib; 3B: Vemurafenib; 3B: Vemurafenib+Cobimetinib; +BRAF V600K NSCLC 3B: Dabrafenib+Trametinib; 3B: Tovorafenib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Trametinib; 3B: Vemurafenib+Cobimetinib; 3B: Encorafenib+Binimetinib; +BRAF V600G NSCLC 3B: Encorafenib+Binimetinib; 3B: Tovorafenib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Dabrafenib+Trametinib; 3B: Vemurafenib+Cobimetinib; +BRAF V600E Colorectal Cancer 1: Encorafenib+Cetuximab; 2: Encorafenib+Panitumumab; 3B: Dabrafenib; 3B: Dabrafenib+Trametinib; 3B: Selumetinib; 3B: Tovorafenib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Trametinib; 3B: Vemurafenib; 3B: Vemurafenib+Cobimetinib; 3B: Encorafenib+Binimetinib; +BRAF V600K Colorectal Cancer 3B: Dabrafenib+Trametinib; 3B: Tovorafenib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Trametinib; 3B: Vemurafenib+Cobimetinib; 3B: Encorafenib+Binimetinib; BRAF V600E HCL 2: Vemurafenib; BRAF V600K Pilocytic Astrocytoma 3B: Dabrafenib+Trametinib; 3B: Trametinib; 3B: Vemurafenib+Cobimetinib; 3B: Encorafenib+Binimetinib; -BRAF V600E Pilocytic Astrocytoma 1: Dabrafenib+Trametinib; 2: Selumetinib; 2: Vemurafenib+Cobimetinib; 3B: Dabrafenib; 3B: Encorafenib+Cetuximab; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Encorafenib+Panitumumab; 3B: Trametinib; 3B: Vemurafenib; 3B: Encorafenib+Binimetinib; +BRAF V600E Pilocytic Astrocytoma 1: Dabrafenib+Trametinib; 2: Selumetinib; 2: Vemurafenib+Cobimetinib; 3B: Dabrafenib; 3B: Encorafenib+Cetuximab; 3B: Tovorafenib; 3B: Vemurafenib+Atezolizumab+Cobimetinib; 3B: Encorafenib+Panitumumab; 3B: Trametinib; 3B: Vemurafenib; 3B: Encorafenib+Binimetinib; BRAF V600K HCL AKT1 E17K Breast Cancer 1: Capivasertib+Fulvestrant; 3B: Capivasertib; AKT1 E17K NSCLC 3B: Capivasertib; 3B: Capivasertib+Fulvestrant; @@ -193,8 +192,8 @@ KRAS G12A Histiocytosis 3A: Cobimetinib; 3A: Trametinib; IDH1 R132H AML 1: Ivosidenib; 1: Olutasidenib; IDH1 R132G AML 1: Ivosidenib; 1: Olutasidenib; FGFR2 FGFR2-BICC1 Fusion Cholangiocarcinoma 1: Pemigatinib; 1: Futibatinib; 3A: RLY-4008; 4: Erdafitinib; 4: AZD4547; -ERBB2 Amplification Breast Cancer 1: Trastuzumab; 1: Trastuzumab+Chemotherapy; 1: Ado-Trastuzumab Emtansine; 1: Lapatinib+Capecitabine; 1: Lapatinib+Letrozole; 1: Trastuzumab+Pertuzumab+Chemotherapy; 1: Neratinib; 1: Neratinib+Capecitabine; 1: Trastuzumab+Tucatinib+Capecitabine; 1: Trastuzumab Deruxtecan; 1: Margetuximab+Chemotherapy; 3B: Trastuzumab+Carboplatin-Taxol Regimen; 3B: Trastuzumab+Pertuzumab; 3B: Lapatinib+Trastuzumab; 3B: Pembrolizumab+Trastuzumab+Chemotherapy; 3B: Tucatinib+Trastuzumab; -ERBB2 Amplification Colorectal Cancer 1: Tucatinib+Trastuzumab; 2: Trastuzumab+Pertuzumab; 2: Lapatinib+Trastuzumab; 2: Trastuzumab Deruxtecan; 3B: Trastuzumab; 3B: Trastuzumab+Carboplatin-Taxol Regimen; 3B: Trastuzumab+Chemotherapy; 3B: Ado-Trastuzumab Emtansine; 3B: Pembrolizumab+Trastuzumab+Chemotherapy; 3B: Lapatinib+Capecitabine; 3B: Lapatinib+Letrozole; 3B: Trastuzumab+Tucatinib+Capecitabine; 3B: Margetuximab+Chemotherapy; +ERBB2 Amplification Breast Cancer 1: Trastuzumab; 1: Trastuzumab+Chemotherapy; 1: Ado-Trastuzumab Emtansine; 1: Lapatinib+Capecitabine; 1: Lapatinib+Letrozole; 1: Trastuzumab+Pertuzumab+Chemotherapy; 1: Neratinib; 1: Neratinib+Capecitabine; 1: Trastuzumab+Tucatinib+Capecitabine; 1: Trastuzumab Deruxtecan; 1: Margetuximab+Chemotherapy; 3B: Trastuzumab+Carboplatin-Taxol Regimen; 3B: Trastuzumab+Pertuzumab; 3B: Lapatinib+Trastuzumab; 3B: Trastuzumab+Docetaxel; 3B: Pembrolizumab+Trastuzumab+Chemotherapy; 3B: Tucatinib+Trastuzumab; +ERBB2 Amplification Colorectal Cancer 1: Tucatinib+Trastuzumab; 2: Trastuzumab+Pertuzumab; 2: Lapatinib+Trastuzumab; 2: Trastuzumab Deruxtecan; 3B: Trastuzumab; 3B: Trastuzumab+Carboplatin-Taxol Regimen; 3B: Trastuzumab+Chemotherapy; 3B: Trastuzumab+Docetaxel; 3B: Ado-Trastuzumab Emtansine; 3B: Pembrolizumab+Trastuzumab+Chemotherapy; 3B: Lapatinib+Capecitabine; 3B: Lapatinib+Letrozole; 3B: Trastuzumab+Pertuzumab+Chemotherapy; 3B: Neratinib; 3B: Neratinib+Capecitabine; 3B: Trastuzumab+Tucatinib+Capecitabine; 3B: Margetuximab+Chemotherapy; RET KIF5B-RET Fusion NSCLC 1: Selpercatinib; 1: Pralsetinib; 2: Cabozantinib; 3A: Vandetanib; RET KIF5B-RET Fusion Bladder Cancer 1: Selpercatinib; 3B: Cabozantinib; 3B: Vandetanib; 3B: Pralsetinib; MET Amplification Non-Small Cell Lung Cancer 2: Crizotinib; 2: Capmatinib; 2: Tepotinib; 3A: Telisotuzumab Vedotin; R2: Erlotinib; R2: Gefitinib; R2: Osimertinib; diff --git a/core/src/test/resources/test_tumor_type_summaries.tsv b/core/src/test/resources/test_tumor_type_summaries.tsv index a191e4c04..c9c0e43c3 100644 --- a/core/src/test/resources/test_tumor_type_summaries.tsv +++ b/core/src/test/resources/test_tumor_type_summaries.tsv @@ -41,7 +41,8 @@ ARAF S214Y Colorectal Cancer ARAF, an intracellular kinase, is infrequently alte BRAF N486_P490del Histiocytosis BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF N486_P490del alteration is likely oncogenic. There is promising clinical data in patients with histiocytic neoplasms harboring MAPK pathway alterations treated with the MEK-targeted inhibitors cobimetinib or trametinib as monotherapy. BRAF T599delinsIP Melanoma BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. There is no available functional data about the BRAF T599delinsIP alteration (last reviewed on 03/29/2023). However, it has been identified as a statistically significant hotspot and is likely to be oncogenic. While the RAF-inhibitors dabrafenib and vemurafenib, alone and in combination with the MEK-inhibitors trametinib and cobimetinib respectively, are FDA-approved for the treatment of patients with BRAF V600E and V600K mutant melanoma, their clinical utility in patients with BRAF T599delinsIP altered melanoma is unknown. BRAF L505H Melanoma BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF L505H mutation is known to be oncogenic. While the RAF-inhibitors dabrafenib and vemurafenib, alone and in combination with the MEK-inhibitors trametinib and cobimetinib respectively, are FDA-approved for the treatment of patients with BRAF V600E and V600K mutant melanoma, their clinical utility in patients with BRAF L505H mutant melanoma is unknown. -BRAF BRAF-MKRN1 fusion Non-Small Cell Lung Cancer BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF-MKRN1 fusion is likely oncogenic. While the MEK1/2-targeted inhibitor selumetinib is NCCN-compendium listed as a treatment option for patients with BRAF fusion-positive pilocytic astrocytoma and there is promising clinical data demonstrating the clinical utility of MEK1/2-targeted inhibitors such as the FDA-approved trametinib in patients with BRAF fusion-positive melanoma and ovarian cancer, their clinical utility in patients with BRAF-MKRN1 fusion-positive non-small cell lung cancer is unknown. +BRAF BRAF-MKRN1 fusion Non-Small Cell Lung Cancer BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF-MKRN1 fusion is likely oncogenic. While the pan-RAF kinase inhibitor tovorafenib is FDA-approved for the treatment of patients 6 months of age and older with pediatric low-grade glioma harboring a BRAF fusion or rearrangement, and there is promising clinical data demonstrating the clinical utility of MEK1/2-targeted inhibitors such as the FDA-approved trametinib in patients with BRAF fusion-positive melanoma and ovarian cancer, their clinical utility in patients with BRAF-MKRN1 fusion-positive non-small cell lung cancer is unknown. +older with pediatric low-grade glioma harboring a BRAF fusion or rearrangement, and there is promising clinical data demonstrating the clinical utility of MEK1/2-targeted inhibitors such as the FDA-approved trametinib in patients with BRAF fusion-positive melanoma and ovarian cancer, their clinical utility in patients with BRAF-MKRN1 fusion-positive non-small cell lung cancer is unknown. BRAF N581I Non-Small Cell Lung Cancer BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF N581I mutation is known to be oncogenic. While the RAF-inhibitor dabrafenib in combination with the MEK-inhibitor trametinib is FDA-approved for the treatment of patients with BRAF V600E mutant non-small cell lung cancer, their clinical utility in patients with BRAF N581I mutant non-small cell lung cancer is unknown. BRAF G469R Cancer of Unknown Primary BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF G469R mutation is known to be oncogenic. BRAF class II mutations including BRAF G469R are insensitive to the RAF-targeted inhibitors vemurafenib and dabrafenib. Laboratory data suggest that cancer cells with oncogenic, non-V600 BRAF mutations may be sensitive to novel BRAF inhibitors such as PLX8394. BRAF L485W Melanoma BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. There is conflicting and/or weak data describing the biological significance of the BRAF L485W mutation. There are no FDA-approved or NCCN-compendium listed treatments specifically for patients with BRAF L485W mutant melanoma. @@ -61,8 +62,8 @@ BRAF L597V Colorectal Cancer BRAF, an intracellular kinase, is frequently mutate BRAF L597P Melanoma BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF L597P has been found in the context of resistance to a targeted therapy(s). There is promising clinical data in patients with BRAF L597-mutant melanoma treated with the FDA-approved MEK-targeted inhibitor trametinib. BRAF L597P Colorectal Cancer BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF L597P has been found in the context of resistance to a targeted therapy(s). While there is promising clinical data supporting the use of the FDA-approved MEK-inhibitor trametinib in patients with BRAF L597-mutant melanoma, its clinical utility in patients with BRAF L597P mutant colorectal cancer is unknown. BRAF class II mutations including BRAF L597P are insensitive to the RAF inhibitors vemurafenib and dabrafenib. Laboratory data suggest that cancer cells with oncogenic, BRAF class II mutations may be sensitive to novel BRAF inhibitors such as PLX8394. BRAF L597P Gastrointestinal Stromal Tumor BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF L597P has been found in the context of resistance to a targeted therapy(s). While there is promising clinical data supporting the use of the FDA-approved MEK-inhibitor trametinib in patients with BRAF L597-mutant melanoma, its clinical utility in patients with BRAF L597P mutant gastrointestinal stromal tumors is unknown. BRAF class II mutations including BRAF L597P are insensitive to the RAF inhibitors vemurafenib and dabrafenib. Laboratory data suggest that cancer cells with oncogenic, BRAF class II mutations may be sensitive to novel BRAF inhibitors such as PLX8394. -BRAF MKRN1-BRAF Fusion Breast Cancer BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The MKRN1-BRAF fusion is likely oncogenic. While the MEK1/2-targeted inhibitor selumetinib is NCCN-compendium listed as a treatment option for patients with BRAF fusion-positive pilocytic astrocytoma and there is promising clinical data demonstrating the clinical utility of MEK1/2-targeted inhibitors such as the FDA-approved trametinib in patients with BRAF fusion-positive melanoma and ovarian cancer, their clinical utility in patients with MKRN1-BRAF fusion-positive breast cancer is unknown. -BRAF CUL1-BRAF Fusion Breast Cancer BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The CUL1-BRAF fusion is likely oncogenic. While the MEK1/2-targeted inhibitor selumetinib is NCCN-compendium listed as a treatment option for patients with BRAF fusion-positive pilocytic astrocytoma and there is promising clinical data demonstrating the clinical utility of MEK1/2-targeted inhibitors such as the FDA-approved trametinib in patients with BRAF fusion-positive melanoma and ovarian cancer, their clinical utility in patients with CUL1-BRAF fusion-positive breast cancer is unknown. +BRAF MKRN1-BRAF Fusion Breast Cancer BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The MKRN1-BRAF fusion is likely oncogenic. While the pan-RAF kinase inhibitor tovorafenib is FDA-approved for the treatment of patients 6 months of age and older with pediatric low-grade glioma harboring a BRAF fusion or rearrangement, and there is promising clinical data demonstrating the clinical utility of MEK1/2-targeted inhibitors such as the FDA-approved trametinib in patients with BRAF fusion-positive melanoma and ovarian cancer, their clinical utility in patients with MKRN1-BRAF fusion-positive breast cancer is unknown. +BRAF CUL1-BRAF Fusion Breast Cancer BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The CUL1-BRAF fusion is likely oncogenic. While the pan-RAF kinase inhibitor tovorafenib is FDA-approved for the treatment of patients 6 months of age and older with pediatric low-grade glioma harboring a BRAF fusion or rearrangement, and there is promising clinical data demonstrating the clinical utility of MEK1/2-targeted inhibitors such as the FDA-approved trametinib in patients with BRAF fusion-positive melanoma and ovarian cancer, their clinical utility in patients with CUL1-BRAF fusion-positive breast cancer is unknown. BRAF CUL1-BRAF Fusion Pilocytic Astrocytoma BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The CUL1-BRAF fusion is likely oncogenic. The MEK inhibitor selumetinib is NCCN-compendium listed as a treatment option for patients with BRAF fusion-positive pilocytic astrocytoma. BRAF MKRN1-BRAF Fusion Ovarian Cancer BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The MKRN1-BRAF fusion is likely oncogenic. There is promising clinical data from a case study in a patient with BRAF fusion-positive ovarian cancer treated with the FDA-approved MEK1/2-targeted inhibitor selumetinib in combination with paclitaxel, and in patients with BRAF fusion-positive melanoma treated with the FDA-approved MEK1/2-targeted inhibitor trametinib. BRAF CUL1-BRAF Fusion Ovarian Cancer BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The CUL1-BRAF fusion is likely oncogenic. There is promising clinical data from a case study in a patient with BRAF fusion-positive ovarian cancer treated with the FDA-approved MEK1/2-targeted inhibitor selumetinib in combination with paclitaxel, and in patients with BRAF fusion-positive melanoma treated with the FDA-approved MEK1/2-targeted inhibitor trametinib. @@ -93,9 +94,9 @@ BRAF V600G Non-Small Cell Lung Cancer BRAF, an intracellular kinase, is frequent BRAF V600E Gastrointestinal Stromal Tumor BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF V600E mutation is known to be oncogenic. The RAF inhibitor dabrafenib in combination with the MEK1/2 inhibitor trametinib is FDA-approved for the treatment of patients with BRAF V600E-mutant solid tumors. BRAF V600K Gastrointestinal Stromal Tumor BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF V600K mutation is known to be oncogenic. While the MEK1/2-targeted inhibitor trametinib, alone or in combination with the RAF-targeted inhibitor dabrafenib, and the MEK-targeted inhibitor cobimetinib in combination with the RAF-targeted inhibitor vemurafenib are FDA-approved for the treatment of patients with BRAF V600K mutant melanoma, their clinical utility in patients with BRAF V600K mutant gastrointestinal stromal tumors has yet to be defined. BRAF V600M Gastrointestinal Stromal Tumor BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. There is conflicting and/or weak data describing the biological significance of the BRAF V600M mutation. There are no FDA-approved or NCCN-compendium listed treatments specifically for patients with BRAF V600M mutant gastrointestinal stromal tumors. -BRAF V600R Gastrointestinal Stromal Tumor BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF V600R mutation is known to be oncogenic. While the RAF-targeted inhibitor dabrafenib in combination with the MEK1/2-targeted inhibitor trametinib is FDA-approved for the treatment of patients with BRAF V600E mutant melanoma, non-small cell lung cancer and anaplastic thyroid cancer, the clinical utility of dabrafenib in combination with trametinib in patients with BRAF V600R mutant gastrointestinal stromal tumors has yet to be defined. -BRAF V600D Gastrointestinal Stromal Tumor BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF V600D mutation is known to be oncogenic. While the RAF-targeted inhibitor dabrafenib in combination with the MEK1/2-targeted inhibitor trametinib is FDA-approved for the treatment of patients with BRAF V600E mutant melanoma, non-small cell lung cancer and anaplastic thyroid cancer, the clinical utility of dabrafenib in combination with trametinib in patients with BRAF V600D mutant gastrointestinal stromal tumors has yet to be defined. -BRAF V600G Gastrointestinal Stromal Tumor BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF V600G mutation is likely oncogenic. While the RAF-targeted inhibitor dabrafenib in combination with the MEK1/2-targeted inhibitor trametinib is FDA-approved for the treatment of patients with BRAF V600E mutant melanoma, non-small cell lung cancer and anaplastic thyroid cancer, the clinical utility of dabrafenib in combination with trametinib in patients with BRAF V600G mutant gastrointestinal stromal tumors has yet to be defined. +BRAF V600R Gastrointestinal Stromal Tumor BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF V600R mutation is known to be oncogenic. While the anti-PD-L1 antibody atezolizumab is FDA-approved in combination with the MEK1/2-targeted inhibitor cobimetinib and the RAF-targeted inhibitor vemurafenib for the treatment of patients with BRAF V600-mutant melanoma, and the pan-RAF kinase inhibitor tovorafenib is FDA-approved for the treatment of patients with BRAF V600-mutant pediatric low-grade glioma, the clinical utility of RAF and MEK inhibitors (alone or in combination) in patients with BRAF V600R mutant gastrointestinal stromal tumors is unknown. +BRAF V600D Gastrointestinal Stromal Tumor BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF V600D mutation is known to be oncogenic. While the anti-PD-L1 antibody atezolizumab is FDA-approved in combination with the MEK1/2-targeted inhibitor cobimetinib and the RAF-targeted inhibitor vemurafenib for the treatment of patients with BRAF V600-mutant melanoma, and the pan-RAF kinase inhibitor tovorafenib is FDA-approved for the treatment of patients with BRAF V600-mutant pediatric low-grade glioma, the clinical utility of RAF and MEK inhibitors (alone or in combination) in patients with BRAF V600D mutant gastrointestinal stromal tumors is unknown. +BRAF V600G Gastrointestinal Stromal Tumor BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF V600G mutation is likely oncogenic. While the anti-PD-L1 antibody atezolizumab is FDA-approved in combination with the MEK1/2-targeted inhibitor cobimetinib and the RAF-targeted inhibitor vemurafenib for the treatment of patients with BRAF V600-mutant melanoma, and the pan-RAF kinase inhibitor tovorafenib is FDA-approved for the treatment of patients with BRAF V600-mutant pediatric low-grade glioma, the clinical utility of RAF and MEK inhibitors (alone or in combination) in patients with BRAF V600G mutant gastrointestinal stromal tumors is unknown. BRAF R558Q Colorectal Cancer BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. The BRAF R558Q mutation is likely oncogenic. While the RAF-inhibitor dabrafenib in combination with the MEK-inhibitor trametinib is FDA-approved for the treatment of patients with BRAF V600E mutant melanoma, non-small cell lung cancer, and anaplastic thyroid cancer, and the RAF-inhibitor vemurafenib is FDA-approved as monotherapy in BRAF V600-mutant Erdheim-Chester disease, their clinical utility in patients with BRAF R558Q mutant colorectal cancer is unknown. BRAF P277Hfs*2 Colorectal Cancer BRAF, an intracellular kinase, is frequently mutated in melanoma, thyroid and lung cancers among others. There is no available functional data about the BRAF P277Hfs*2 mutation (last reviewed on 04/03/2023), and therefore its biological significance is unknown. There are no FDA-approved or NCCN-compendium listed treatments specifically for patients with BRAF P277Hfs*2 mutant colorectal cancer. BRCA1 W1782* Gastrointestinal Stromal Tumor BRCA1, a tumor suppressor involved in the DNA damage response, is mutated in various cancer types. The BRCA1 W1782* is a truncating mutation in a tumor suppressor gene, and therefore is likely oncogenic. While the PARP inhibitors olaparib, rucaparib, niraparib and talazoparib are FDA-approved for the treatment of patients with various BRCA1-mutant cancer types, their clinical utility in patients with gastrointestinal stromal tumors harboring the somatic BRCA1 W1782* mutation is unknown. @@ -144,9 +145,9 @@ ERBB2 V777L Breast Cancer ERBB2, a receptor tyrosine kinase, is altered by mutat ERBB2 V777M Breast Cancer ERBB2, a receptor tyrosine kinase, is altered by mutation, amplification and/or overexpression in various cancer types, most frequently in breast, esophagogastric and endometrial cancers. The ERBB2 V777M mutation is likely oncogenic. There is promising clinical data in patients with breast cancer with known oncogenic ERBB2 alterations treated with the ERBB-targeted inhibitor neratinib. ERBB2 G778_P780dup Melanoma ERBB2, a receptor tyrosine kinase, is altered by mutation, amplification and/or overexpression in various cancer types, most frequently in breast, esophagogastric and endometrial cancers. The ERBB2 G778_P780dup alteration is known to be oncogenic. While the anti-HER2 antibody ado-trastuzumab emtansine (T-DM1) is NCCN-compendium listed for the treatment of patients with ERBB2 mutant non-small cell lung cancer (NSCLC) and there is promising clinical data in patients with breast and NSCLC with known oncogenic ERBB2 alterations treated with the ERBB-targeted inhibitor neratinib, their clinical utility in patients with ERBB2 G778_P780dup altered melanoma is unknown. ERBB2 IKZF3-ERBB2 fusion Breast Cancer ERBB2, a receptor tyrosine kinase, is altered by mutation, amplification and/or overexpression in various cancer types, most frequently in breast, esophagogastric and endometrial cancers. There is conflicting and/or weak data describing the biological significance of the IKZF3-ERBB2 fusion. There are no FDA-approved or NCCN-compendium listed treatments specifically for patients with IKZF3-ERBB2 fusion-positive breast cancer. -ERBB2 Amplification Breast Cancer ERBB2, a receptor tyrosine kinase, is altered by mutation, amplification and/or overexpression in various cancer types, most frequently in breast, esophagogastric and endometrial cancers. ERBB2 amplification is known to be oncogenic. Several HER2 targeted therapies are FDA-approved for the treatment of patients with HER2-positive breast cancer including the HER2 targeted antibodies trastuzumab, pertuzumab and margetuximab-cmkb, the antibody-drug conjugates ado-trastuzumab emtansine (TDM1) and trastuzumab deruxtecan, and the HER kinase inhibitors lapatinib, neratinib, and tucatinib. -ERBB2 Amplification Esophagogastric Cancer ERBB2, a receptor tyrosine kinase, is altered by mutation, amplification and/or overexpression in various cancer types, most frequently in breast, esophagogastric and endometrial cancers. ERBB2 amplification is known to be oncogenic. The anti-HER2 targeted antibody trastuzumab (in combination with chemotherapy with or without the anti-PD-1 antibody pembrolizumab) and the related antibody-drug conjugate fam-trastuzumab deruxtecan-nxki are FDA-approved for the treatment of patients with ERBB2-amplified, HER2-positive gastric cancer. -ERBB2 Amplification Melanoma ERBB2, a receptor tyrosine kinase, is altered by mutation, amplification and/or overexpression in various cancer types, most frequently in breast, esophagogastric and endometrial cancers. ERBB2 amplification is known to be oncogenic. While the HER2-targeted antibody trastuzumab is FDA-approved for the treatment of patients with HER2-positive breast and gastric cancers, and the HER2-targeted kinase inhibitor tucatinib in combination with trastuzumab is FDA-approved for patients with HER2-positive colorectal cancer, their clinical utility in patients with HER2-positive melanoma is unknown. +ERBB2 Amplification Breast Cancer ERBB2, a receptor tyrosine kinase, is altered by mutation, amplification and/or overexpression in various cancer types, most frequently in breast, esophagogastric and endometrial cancers. ERBB2 amplification is known to be oncogenic. This sample has amplification of the ERBB2 gene. ERBB2 amplification correlates with HER2-overexpression in breast cancer. Several HER2-targeted therapies are FDA-approved for the treatment of patients with HER2-positive breast cancer including the HER2-targeted antibodies trastuzumab, pertuzumab and margetuximab, the antibody-drug conjugates ado-trastuzumab emtansine (TDM1) and trastuzumab deruxtecan, and the HER kinase inhibitors lapatinib, neratinib, and tucatinib. +ERBB2 Amplification Esophagogastric Cancer ERBB2, a receptor tyrosine kinase, is altered by mutation, amplification and/or overexpression in various cancer types, most frequently in breast, esophagogastric and endometrial cancers. ERBB2 amplification is known to be oncogenic. This sample has amplification of the ERBB2 gene. ERBB2 amplification correlates with HER2-overexpression in gastric cancer. The HER2-targeted antibody trastuzumab (in combination with chemotherapy with or without the anti-PD-1 antibody pembrolizumab) and the antibody-drug conjugate trastuzumab deruxtecan are FDA-approved for the treatment of patients with HER2-positive gastric cancer. +ERBB2 Amplification Melanoma ERBB2, a receptor tyrosine kinase, is altered by mutation, amplification and/or overexpression in various cancer types, most frequently in breast, esophagogastric and endometrial cancers. ERBB2 amplification is known to be oncogenic. This sample has amplification of the ERBB2 gene. ERBB2 amplification may be associated with HER2-overexpression in this cancer type. The HER2-directed antibody-drug conjugate trastuzumab deruxtecan is FDA-approved for the treatment of adult patients with HER2-positive (defined as immunohistochemistry (IHC) 3+) solid tumors. ERBB2 V659E Breast Cancer ERBB2, a receptor tyrosine kinase, is altered by mutation, amplification and/or overexpression in various cancer types, most frequently in breast, esophagogastric and endometrial cancers. The ERBB2 V659E mutation is known to be oncogenic. There is promising clinical data in patients with breast cancer with known oncogenic ERBB2 alterations treated with the ERBB-targeted inhibitor neratinib. ERBB2 V659E Non-Small Cell Lung Cancer ERBB2, a receptor tyrosine kinase, is altered by mutation, amplification and/or overexpression in various cancer types, most frequently in breast, esophagogastric and endometrial cancers. The ERBB2 V659E mutation is known to be oncogenic. The antibody-drug conjugate fam-trastuzumab deruxtecan-nxki (T-DXd) is FDA-approved for the treatment of patients with ERBB2-mutant non-small cell lung cancer. ERBB2 V659E Gastrointestinal Stromal Tumor ERBB2, a receptor tyrosine kinase, is altered by mutation, amplification and/or overexpression in various cancer types, most frequently in breast, esophagogastric and endometrial cancers. The ERBB2 V659E mutation is known to be oncogenic. While the anti-HER2 antibody ado-trastuzumab emtansine (T-DM1) is NCCN-compendium listed for the treatment of patients with ERBB2 mutant non-small cell lung cancer (NSCLC) and there is promising clinical data in patients with breast and NSCLC with known oncogenic ERBB2 alterations treated with the ERBB-targeted inhibitor neratinib, their clinical utility in patients with ERBB2 V659E mutant gastrointestinal stromal tumors is unknown.