update tests

core/src/test/java/org/mskcc/cbio/oncokb/util/IndicatorUtilsTest.java

@@ -35,13 +35,13 @@ public void testProcessQuery() throws Exception {
 
         query = new Query(null, DEFAULT_REFERENCE_GENOME, null, "CD74-CD74", null, "structural_variant", StructuralVariantType.DELETION, "Pancreatic Adenocarcinoma", null, null, null, null);
         indicatorQueryResp = IndicatorUtils.processQuery(query, null, true, null);
-        assertEquals("Gene should not exist, but it does.", false, indicatorQueryResp.getGeneExist());
+        assertEquals("Gene should exist.", true, indicatorQueryResp.getGeneExist());
         assertEquals("The oncogenicity is not unknown, but it should.", Oncogenicity.UNKNOWN.getOncogenic(), indicatorQueryResp.getOncogenic());
         assertTrue("There is treatment(s) in the response, but it should no have any.", indicatorQueryResp.getTreatments().size() == 0);
 
         query = new Query(null, DEFAULT_REFERENCE_GENOME, null, "CD74-CD74", null, "structural_variant", StructuralVariantType.DELETION, "Pancreatic Adenocarcinoma", "fusion", null, null, null);
         indicatorQueryResp = IndicatorUtils.processQuery(query, null, true, null);
-        assertEquals("Gene should not exist, but it does.", false, indicatorQueryResp.getGeneExist());
+        assertEquals("Gene should exist.", true, indicatorQueryResp.getGeneExist());
         assertEquals("The oncogenicity is not unknown, but it should.", Oncogenicity.UNKNOWN.getOncogenic(), indicatorQueryResp.getOncogenic());
         assertTrue("There is treatment(s) in the response, but it should no have any.", indicatorQueryResp.getTreatments().size() == 0);
 

core/src/test/resources/test_cancer_type_treatments.tsv

@@ -78,8 +78,8 @@ BTK	C481Y	Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma	R2: Ibrutinib;
 BTK	T316A	Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma	R2: Ibrutinib;
 
 # Test Heme
-FLT3	Internal Tandem Duplication	AML	1: Gilteritinib; 1: Midostaurin+High Dose Chemotherapy; 3A: Sorafenib; 3A: Crenolanib; 3A: Quizartinib;
-FLT3	Internal Tandem Duplication	APLPMLRARA	1: Gilteritinib; 1: Midostaurin+High Dose Chemotherapy; 3A: Sorafenib; 3A: Crenolanib; 3A: Quizartinib;
+FLT3	Internal Tandem Duplication	AML	1: Gilteritinib; 1: Quizartinib; 1: Midostaurin+High Dose Chemotherapy; 3A: Sorafenib; 3A: Crenolanib;
+FLT3	Internal Tandem Duplication	APLPMLRARA	1: Gilteritinib; 1: Quizartinib; 1: Midostaurin+High Dose Chemotherapy; 3A: Sorafenib; 3A: Crenolanib;
 FLT3	Internal Tandem Duplication	Colorectal Cancer
 SF3B1	K700E	AML	4: H3B-8800;
 SF3B1	K700E	AMLNOS	4: H3B-8800;

core/src/test/resources/test_tumor_type_summaries.tsv

@@ -183,11 +183,11 @@ FGFR3	ST7L-FGFR3 fusion	Glioma	FGFR3, a receptor tyrosine kinase, is altered by
 FGFR3	FGFR3-WHSC1 fusion	Breast Cancer	FGFR3, a receptor tyrosine kinase, is altered by mutation, chromosomal rearrangement or amplification in various cancers, most frequently in bladder cancer.	The FGFR3-WHSC1 fusion is likely oncogenic.	While the pan-FGFR-targeted inhibitor erdafitinib is FDA-approved for the treatment of patients with FGFR3 fusion-positive metastatic urothelial cancer, its clinical utility in patients with FGFR3 fusion-positive breast cancer is unknown.
 FLT3	N676S	Endometrial Cancer	FLT3, a receptor tyrosine kinase, is recurrently altered in acute myeloid leukemia and other hematologic malignancies.	The FLT3 N676S is a known resistance mutation.	While the multikinase inhibitor midostaurin in combination with intensive chemotherapy is FDA-approved for the treatment of patients with FLT3 mutant acute myeloid leukemia, its clinical utility in patients with FLT3 N676S mutant endometrial cancer is unknown.
 FLT3	D324N	Glioma	FLT3, a receptor tyrosine kinase, is recurrently altered in acute myeloid leukemia and other hematologic malignancies.	The FLT3 D324N mutation is likely neutral.	There are no FDA-approved or NCCN-compendium listed treatments specifically for patients with FLT3 D324N mutant glioma.
-FLT3	Y572_Y630ins	Acute Myeloid Leukemia	FLT3, a receptor tyrosine kinase, is recurrently altered in acute myeloid leukemia and other hematologic malignancies.	The FLT3 Y572_Y630ins alteration has been identified as a statistically significant hotspot and is likely to be oncogenic.	The multikinase inhibitor gilteritinib and the multikinase inhibitor midostaurin in combination with intensive chemotherapy are FDA-approved for the treatment of patients with FLT3-internal tandem duplication (ITD) positive acute myeloid leukemia (AML). Additionally, there is promising clinical data in patients with FLT3-ITD positive AML treated with the multikinase inhbitors crenolanib, quizartinib and sorafenib.
-FLT3	Y572_Y630ins	Gastrointestinal Stromal Tumor	FLT3, a receptor tyrosine kinase, is recurrently altered in acute myeloid leukemia and other hematologic malignancies.	The FLT3 Y572_Y630ins alteration has been identified as a statistically significant hotspot and is likely to be oncogenic.	While the multikinase inhibitor gilteritinib and the multikinase inhibitor midostaurin in combination with intensive chemotherapy are FDA-approved for the treatment of patients with FLT3-internal tandem duplication (ITD) positive acute myeloid leukemia, their clinical utility in patients with FLT3 Y572_Y630ins altered gastrointestinal stromal tumors is unknown.
+FLT3	Y572_Y630ins	Acute Myeloid Leukemia	FLT3, a receptor tyrosine kinase, is recurrently altered in acute myeloid leukemia and other hematologic malignancies.	The FLT3 Y572_Y630ins alteration has been identified as a statistically significant hotspot and is likely to be oncogenic.	The multikinase inhibitors gilteritinib, midostaurin, and quizartinib are FDA-approved for the treatment of patients with FLT3-internal tandem duplication (ITD)-positive acute myeloid leukemia (AML).
+FLT3	Y572_Y630ins	Gastrointestinal Stromal Tumor	FLT3, a receptor tyrosine kinase, is recurrently altered in acute myeloid leukemia and other hematologic malignancies.	The FLT3 Y572_Y630ins alteration has been identified as a statistically significant hotspot and is likely to be oncogenic.	While the multikinase inhibitors gilteritinib and quizartinib and the multikinase inhibitor midostaurin in combination with intensive chemotherapy are FDA-approved for the treatment of patients with FLT3-internal tandem duplication (ITD)-positive acute myeloid leukemia, their clinical utility in patients with FLT3 Y572_Y630ins altered gastrointestinal stromal tumors is unknown.
 IDH1	Y139D	Acute Myeloid Leukemia	IDH1, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia and gliomas.	The IDH1 Y139D mutation is likely oncogenic.	While the IDH1-targeted inhibitors ivosidenib and olutasidenib are FDA-approved for the treatment of patients with IDH1-mutant acute myeloid leukemia, and ivosidenib is FDA-approved for the treatment of patients with IDH1-mutant cholangiocarcinoma, the clinical utility of these agents in patients with IDH1 Y139D mutant acute myeloid leukemia is unknown.
 IDH1	Y139D	Glioma	IDH1, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia and gliomas.	The IDH1 Y139D mutation is likely oncogenic.	While the IDH1-targeted inhibitors ivosidenib and olutasidenib are FDA-approved for the treatment of patients with IDH1-mutant acute myeloid leukemia, and ivosidenib is FDA-approved for the treatment of patients with IDH1-mutant cholangiocarcinoma, the clinical utility of these agents in patients with IDH1 Y139D mutant glioma is unknown.
-IDH1	R132I	Acute Myeloid Leukemia	IDH1, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia and gliomas.	The biologic significance of the IDH1 R132I mutation is unknown (last reviewed 02/02/2023). However, it has been identified as a statistically significant hotspot and is likely to be oncogenic.	While the IDH1-targeted inhibitors ivosidenib and olutasidenib are FDA-approved for the treatment of patients with IDH1-mutant acute myeloid leukemia, and ivosidenib is FDA-approved for the treatment of patients with IDH1-mutant cholangiocarcinoma, the clinical utility of these agents in patients with IDH1 R132I mutant acute myeloid leukemia is unknown.
+IDH1	R132I	Acute Myeloid Leukemia	IDH1, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia and gliomas.	The biologic significance of the IDH1 R132I mutation is unknown (last reviewed 07/12/2023). However, it has been identified as a statistically significant hotspot and is likely to be oncogenic.	While the IDH1-targeted inhibitors ivosidenib and olutasidenib are FDA-approved for the treatment of patients with IDH1-mutant acute myeloid leukemia, and ivosidenib is FDA-approved for the treatment of patients with IDH1-mutant cholangiocarcinoma, the clinical utility of these agents in patients with IDH1 R132I mutant acute myeloid leukemia is unknown.
 IDH1	R132C	Acute Myeloid Leukemia	IDH1, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia and gliomas.	The IDH1 R132C mutation is known to be oncogenic.	The IDH1-targeted inhibitors ivosidenib and olutasidenib are FDA-approved for the treatment of patients with IDH1 R132-mutant acute myeloid leukemia.
 IDH1	R132G	Acute Myeloid Leukemia	IDH1, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia and gliomas.	The IDH1 R132G mutation is known to be oncogenic.	The IDH1-targeted inhibitors ivosidenib and olutasidenib are FDA-approved for the treatment of patients with IDH1 R132-mutant acute myeloid leukemia.
 IDH1	R132H	Acute Myeloid Leukemia	IDH1, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia and gliomas.	The IDH1 R132H mutation is known to be oncogenic.	The IDH1-targeted inhibitors ivosidenib and olutasidenib are FDA-approved for the treatment of patients with IDH1 R132-mutant acute myeloid leukemia.
@@ -196,7 +196,7 @@ IDH1	R132C	Glioma	IDH1, a cell metabolism enzyme, is recurrently mutated in vari
 IDH1	R132G	Glioma	IDH1, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia and gliomas.	The IDH1 R132G mutation is known to be oncogenic.	There are promising clinical data in patients with contrast non-enhancing IDH1 R132-mutant glioma treated with the IDH1-targeted inhibitor ivosidenib.
 IDH1	R132H	Glioma	IDH1, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia and gliomas.	The IDH1 R132H mutation is known to be oncogenic.	There are promising clinical data in patients with contrast non-enhancing IDH1 R132-mutant glioma treated with the IDH1-targeted inhibitor ivosidenib.
 IDH1	R132Q	Glioma	IDH1, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia and gliomas.	The IDH1 R132Q mutation is likely oncogenic.	There are promising clinical data in patients with contrast non-enhancing IDH1 R132-mutant glioma treated with the IDH1-targeted inhibitor ivosidenib.
-IDH1	R132I	Glioma	IDH1, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia and gliomas.	The biologic significance of the IDH1 R132I mutation is unknown (last reviewed 02/02/2023). However, it has been identified as a statistically significant hotspot and is likely to be oncogenic.	There are promising clinical data in patients with contrast non-enhancing IDH1 R132-mutant glioma treated with the IDH1-targeted inhibitor ivosidenib.
+IDH1	R132I	Glioma	IDH1, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia and gliomas.	The biologic significance of the IDH1 R132I mutation is unknown (last reviewed 07/12/2023). However, it has been identified as a statistically significant hotspot and is likely to be oncogenic.	There are promising clinical data in patients with contrast non-enhancing IDH1 R132-mutant glioma treated with the IDH1-targeted inhibitor ivosidenib.
 IDH2	R172S	Non-Hodgkin Lymphoma	IDH2, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia, glioblastoma, and cholangiocarcinoma.	The IDH2 R172S mutation is known to be oncogenic.	The IDH2-targeted inhibitor enasidenib is FDA-approved for the treatment of patients with IDH2-mutant acute myeloid leukemia.
 IDH2	R172T	Non-Hodgkin Lymphoma	IDH2, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia, glioblastoma, and cholangiocarcinoma.	The IDH2 R172T mutation is likely oncogenic.	The IDH2-targeted inhibitor enasidenib is FDA-approved for the treatment of patients with IDH2-mutant acute myeloid leukemia.
 IDH2	R140W	Pancreatic Cancer	IDH2, a cell metabolism enzyme, is recurrently mutated in various cancer types including acute myeloid leukemia, glioblastoma, and cholangiocarcinoma.	The IDH2 R140W mutation is likely oncogenic.	While the IDH2-targeted inhibitor enasidenib is FDA-approved for the treatment of patients with acute myeloid leukemia, its clinical utility in patients with IDH2 R140W mutant pancreatic cancer is unknown.
@@ -340,7 +340,7 @@ KIT	D816F	Breast Cancer	KIT, a receptor tyrosine kinase, is recurrently mutated
 KIT	V559A	Breast Cancer	KIT, a receptor tyrosine kinase, is recurrently mutated in gastrointestinal stromal tumors.	The KIT V559A mutation is likely oncogenic.	While the multikinase inhibitors imatinib, sunitinib, regorafenib and ripretinib are FDA-approved for the treatment of patients with KIT-mutant gastrointestinal stromal tumors, their clinical utility in patients with KIT V559A mutant breast cancer is unknown.
 KIT	R634W	Breast Cancer	KIT, a receptor tyrosine kinase, is recurrently mutated in gastrointestinal stromal tumors.	The KIT R634W mutation is likely oncogenic.	There are no FDA-approved or NCCN-compendium listed treatments specifically for patients with KIT R634W mutant breast cancer.
 KIT	E839K	Gastrointestinal Stromal Tumor	KIT, a receptor tyrosine kinase, is recurrently mutated in gastrointestinal stromal tumors.	The KIT E839K mutation is likely neutral.	There are no FDA-approved or NCCN-compendium listed treatments specifically for patients with KIT E839K mutant gastrointestinal stromal tumors.
-KIT	R888W	Gastrointestinal Stromal Tumor	KIT, a receptor tyrosine kinase, is recurrently mutated in gastrointestinal stromal tumors.	The biologic significance of the KIT R888W mutation is unknown (last reviewed 02/03/2023). However, it has been identified as a statistically significant hotspot and is likely to be oncogenic.	The multikinase KIT and PDGFRA inhibitors imatinib, sunitinib, regorafenib and ripretinib are FDA-approved for the treatment of patients with KIT mutation-positive gastrointestinal stromal tumors (GISTs).
+KIT	R888W	Gastrointestinal Stromal Tumor	KIT, a receptor tyrosine kinase, is recurrently mutated in gastrointestinal stromal tumors.	The biologic significance of the KIT R888W mutation is unknown (last reviewed 07/14/2023). However, it has been identified as a statistically significant hotspot and is likely to be oncogenic.	The multikinase KIT and PDGFRA inhibitors imatinib, sunitinib, regorafenib and ripretinib are FDA-approved for the treatment of patients with KIT mutation-positive gastrointestinal stromal tumors (GISTs).
 KIT	K642Q	Gastrointestinal Stromal Tumor	KIT, a receptor tyrosine kinase, is recurrently mutated in gastrointestinal stromal tumors.	The biologic significance of the KIT K642Q mutation is unknown (last reviewed 02/01/2023). However, it has been identified as a statistically significant hotspot and is likely to be oncogenic.	The multikinase KIT and PDGFRA inhibitors imatinib, sunitinib, regorafenib and ripretinib are FDA-approved for the treatment of patients with KIT mutation-positive gastrointestinal stromal tumors (GISTs).
 FOXL2	Amplification	Colorectal Cancer	FOXL2, a transcription factor, is recurrently mutated in adult granulosa cell tumors.	The biologic significance of the FOXL2 amplification is unknown.	There are no FDA-approved or NCCN-compendium listed treatments specifically for patients with FOXL2-amplified colorectal cancer.
 AR	Q58L	Colorectal Cancer	AR (androgen receptor), a transcription factor, is most frequently altered in advanced or castration-resistant prostate cancer.	The biologic significance of the AR Q58L mutation is unknown (last reviewed 09/27/2019).	There are no FDA-approved or NCCN-compendium listed treatments specifically for patients with AR Q58L mutant colorectal cancer.