 --
 
 COPY gene_aliases_genes (gene_alias_id, gene_id) FROM stdin;
-1	1
-2	1
-3	2
-4	2
-5	2
-6	2
-7	2
-8	2
-9	2
-10	3
-11	3
-12	3
-13	3
-14	4
-15	4
-16	4
-17	4
-18	4
-19	4
-20	4
-21	5
-22	5
-23	5
-24	5
-25	6
-26	6
-27	6
-28	6
-29	6
-30	6
-31	6
-32	6
-33	6
-34	7
-35	7
-36	7
-37	7
-38	7
-39	7
-40	7
-41	7
-42	7
-43	7
-44	8
-45	8
-46	8
-47	8
-48	9
-49	9
-50	11
-51	11
-52	12
-53	12
-54	13
-55	13
-56	14
-57	14
-58	14
-59	14
-60	14
-61	14
-62	14
-63	14
-64	14
-65	14
-66	14
-67	14
-68	14
-69	14
-70	14
-71	14
-72	14
-73	14
-74	15
-75	15
-76	16
-77	16
-78	16
-79	16
-80	16
-81	17
-82	17
-83	18
-84	18
-85	18
-86	19
-87	19
-88	19
-89	19
-90	19
-91	19
-92	20
-93	20
-94	20
-95	20
-96	20
-97	20
-98	20
-99	20
-100	21
-101	21
-102	21
-103	21
-104	21
-105	21
-106	22
-107	22
-108	22
-109	22
-110	22
-111	22
-112	22
-113	22
-114	22
-115	22
-116	22
-117	22
-118	23
-119	23
-120	23
-121	23
-122	23
-123	24
-124	24
-125	24
-126	24
-127	25
-128	25
-129	25
-130	25
-131	26
-132	26
-133	26
-134	26
-135	26
-136	26
-137	26
-138	27
-139	27
-134	27
-140	27
-135	27
-141	27
-142	27
-143	28
-144	28
-145	29
-146	29
-147	29
-148	29
-149	30
-150	30
-151	30
-152	30
-153	30
-154	30
-155	30
-156	30
-157	30
-158	30
-159	30
-160	30
-161	31
-162	31
-163	31
-164	31
-165	31
-166	33
-167	33
-168	33
-169	33
-170	33
-171	33
-172	33
-173	33
-174	35
-175	35
-176	36
-177	36
-178	36
-179	36
-180	36
-181	36
-182	37
-183	37
-184	37
-185	37
-186	37
-187	37
-188	37
-189	38
-190	38
-191	38
-192	38
-193	39
-194	39
-195	39
-196	39
-197	40
-198	40
-199	41
-200	41
-201	41
-202	41
-203	41
-204	41
-205	41
-206	41
-207	41
-208	42
-209	42
-210	42
-211	42
-212	42
-213	42
-214	42
-215	42
-216	42
-217	43
-218	43
-219	43
-220	43
-221	43
-222	43
-223	44
-224	44
-225	44
-226	44
-227	44
-228	44
-229	45
-230	45
-231	45
-232	45
-233	46
-234	46
-233	47
-235	47
-236	47
-237	48
-238	48
-239	48
-240	48
-241	48
-242	49
-243	49
-244	49
-245	49
-246	49
-247	49
-248	49
-249	50
-250	50
-251	50
-252	50
-253	51
-254	51
-255	51
-256	51
-257	52
-258	52
-259	52
-260	52
-261	52
-262	53
-263	53
-264	54
-265	54
-266	54
-267	55
-224	55
-268	56
-269	56
-270	56
-271	56
-272	56
-273	57
-274	58
-275	58
-276	58
-277	58
-278	59
-279	59
-280	60
-281	60
-282	60
-283	61
-284	61
-285	61
-286	61
-287	61
-288	61
-289	61
-290	61
-291	61
-292	62
-293	62
-294	63
-295	63
-296	63
-297	63
-298	63
-299	63
-300	63
-301	63
+1844	374
+1845	374
+1846	375
+1847	375
+1848	375
+1849	375
+1850	375
+1851	375
+1852	375
+1853	376
+1854	376
+1855	376
+1856	376
+1857	377
+1858	377
+1859	377
+1860	377
+1861	377
+1862	377
+1863	377
+1864	378
+1865	378
+1866	378
+1867	378
+1868	379
+1869	379
+1870	379
+1871	379
+1872	379
+1873	379
+1874	379
+1875	379
+1876	379
+1877	380
+1878	380
+1879	380
+1880	380
+1881	380
+1882	380
+1883	380
+1884	380
+1885	380
+1886	380
+1887	381
+1888	381
+1889	381
+1890	381
+1891	382
+1892	382
+1893	384
+1894	384
+1895	385
+1896	385
+1897	386
+1898	386
+1899	387
+1900	387
+1901	387
+1902	387
+1903	387
+1904	387
+1905	387
+1906	387
+1907	387
+1908	387
+1909	387
+1910	387
+1911	387
+1912	387
+1913	387
+1914	387
+1915	387
+1916	387
+1917	388
+1918	388
+1919	389
+1920	389
+1921	389
+1922	389
+1923	389
+1924	390
+1925	390
+1926	391
+1927	391
+1928	391
+1929	392
+1930	392
+1931	392
+1932	392
+1933	392
+1934	392
+1935	393
+1936	393
+1937	393
+1938	393
+1939	393
+1940	393
+1941	393
+1942	393
+1943	394
+1944	394
+1945	394
+1946	394
+1947	394
+1948	394
+1949	395
+1950	395
+1951	395
+1952	395
+1953	395
+1954	395
+1955	395
+1956	395
+1957	395
+1958	395
+1959	395
+1960	395
+1961	396
+1962	396
+1963	396
+1964	396
+1965	396
+1966	397
+1967	397
+1968	397
+1969	397
+1970	398
+1971	398
+1972	398
+1973	398
+1974	399
+1975	399
+1976	399
+1977	399
+1978	399
+1979	399
+1980	399
+1981	400
+1982	400
+1977	400
+1983	400
+1978	400
+1984	400
+1985	400
+1986	401
+1987	401
+1988	402
+1989	402
+1990	402
+1991	402
+1992	403
+1993	403
+1994	403
+1995	403
+1996	403
+1997	403
+1998	403
+1999	403
+2000	403
+2001	403
+2002	403
+2003	403
+2004	404
+2005	404
+2006	404
+2007	404
+2008	404
+2009	406
+2010	406
+2011	406
+2012	406
+2013	406
+2014	406
+2015	406
+2016	406
+2017	408
+2018	408
+2019	409
+2020	409
+2021	409
+2022	409
+2023	409
+2024	409
+2025	410
+2026	410
+2027	410
+2028	410
+2029	410
+2030	410
+2031	410
+2032	411
+2033	411
+2034	411
+2035	411
+2036	412
+2037	412
+2038	412
+2039	412
+2040	413
+2041	413
+2042	414
+2043	414
+2044	414
+2045	414
+2046	414
+2047	414
+2048	414
+2049	414
+2050	414
+2051	415
+2052	415
+2053	415
+2054	415
+2055	415
+2056	415
+2057	415
+2058	415
+2059	415
+2060	416
+2061	416
+2062	416
+2063	416
+2064	416
+2065	416
+2066	417
+2067	417
+2068	417
+2069	417
+2070	417
+2071	417
+2072	418
+2073	418
+2074	418
+2075	418
+2076	419
+2077	419
+2076	420
+2078	420
+2079	420
+2080	421
+2081	421
+2082	421
+2083	421
+2084	421
+2085	422
+2086	422
+2087	422
+2088	422
+2089	422
+2090	422
+2091	422
+2092	423
+2093	423
+2094	423
+2095	423
+2096	424
+2097	424
+2098	424
+2099	424
+2100	425
+2101	425
+2102	425
+2103	425
+2104	425
+2105	426
+2106	426
+2107	427
+2108	427
+2109	427
 \.
 
 

--

COPY genes (id, entrez_id, name, description, official_name, created_at, updated_at, clinical_description, deleted, deleted_at) FROM stdin;
1	238	ALK	ALK amplifications, fusions and mutations have been shown to be driving events in non-small cell lung cancer. While crizontinib has demonstrated efficacy in treating the amplification, mutations in ALK have been shown to confer resistance to current tyrosine kinase inhibitors. Second-generation TKI's have seen varied success in treating these resistant cases, and the HSP90 inhibitor 17-AAG has been shown to be cytostatic in ALK-altered cell lines.	anaplastic lymphoma receptor tyrosine kinase	2015-07-22 18:46:55.37169	2015-07-22 18:46:55.37169	\N	f	\N
2	207	AKT1	AKT1, also referred to as protein kinase B, is a known oncogene. AKT activation relies on the PI3K pathway, and is recognized as a critical node in the pathway. The E17 hotspot is the most characterized of AKT1 mutations, and has been shown to result in activation of the protein. Mutations in AKT1 have also been shown to confer resistance to allosteric kinase inhibitors in vitro.	v-akt murine thymoma viral oncogene homolog 1	2015-07-22 18:46:55.739924	2015-07-22 18:46:55.739924	\N	f	\N
3	369	ARAF	ARAF has recently become increasingly considered for its oncogenic potential. Its potential as a target for informing clinical action was demonstrated by a single case of advanced lung adenocarcinoma harboring an S214C mutation that, when treated with sorafenib, acheived near-complete clinical remission. This finding has brought new focus on ARAF as a marker that should be assayed for in cancer treatment.	A-Raf proto-oncogene, serine/threonine kinase	2015-07-22 18:46:55.982708	2015-07-22 18:46:55.982708	\N	f	\N
4	25	ABL1	ABL1 is most relevant to cancer in its role in the BCR-ABL fusion protein that has become a signature of chronic myeloid leukemia (CML). Cells harboring this fusion have shown sensitivity to imatinib, greatly improving the prognostic outlook of the disease. However, additional mutations in ABL1 have been shown to confer resistance to imatinib. In these resistance cases, second-generation tyrosine kinase inhibitors such as dasatinib and nilotinib have exhibited some efficacy and are currently undergoing clinical trials for treating acquired resistance in CML.	ABL proto-oncogene 1, non-receptor tyrosine kinase	2015-07-22 18:46:56.262899	2015-07-22 18:46:56.262899	\N	f	\N
5	673	BRAF	BRAF mutations are found to be recurrent in many cancer types. Of these, the mutation of valine 600 to glutamic acid (V600E) is the most prevalent. V600E has been determined to be an activating mutation, and cells that harbor it, along with other V600 mutations are sensitive to the BRAF inhibitor dabrafenib. It is also common to use MEK inhibition as a substitute for BRAF inhibitors, and the MEK inhibitor trametinib has seen some success in BRAF mutant melanomas. BRAF mutations have also been correlated with poor prognosis in many cancer types, although there is at least one study that questions this conclusion in papillary thyroid cancer.	B-Raf proto-oncogene, serine/threonine kinase	2015-07-22 18:46:56.563464	2015-07-22 18:46:56.563464	\N	f	\N
6	672	BRCA1	BRCA1 mutations in the germline have become a hallmark for hereditary breast and ovarian cancers. Variants that have been demonstrated to reduce the function of the protein have been shown to increase risk for these cancers, as well as prostate and pancreatic cancer. These findings have been the impetus for the increased popularity of genetic testing of healthy indivudals to assess risk.	breast cancer 1, early onset	2015-07-22 18:46:56.833662	2015-07-22 18:46:56.833662	\N	f	\N
7	675	BRCA2	BRCA2 mutations in the germline have become a hallmark for hereditary breast and ovarian cancers. Variants that have been demonstrated to reduce the function of the protein have been shown to increase risk for these cancers, as well as prostate and pancreatic cancer. These findings have been the impetus for the increased popularity of genetic testing of healthy indivudals to assess risk.	breast cancer 2, early onset	2015-07-22 18:46:57.104555	2015-07-22 18:46:57.104555	\N	f	\N
8	595	CCND1	Cyclin D has been shown in many cancer types to be misregulated. Well established for their oncogenic properties, the cyclins and the cyclin-dependent kinases (CDK's) they activate have been the focus of major research and development efforts over the past decade. The methods by which the cyclins are misregulated are widely variable, ranging from genomic amplification to changes in promoter methylation. While Cyclin D2 has only been found to be significantly deregulated in glioma, Cyclin D1 in particular seems to be a pan-cancer actor. Cyclin D misregulation has been shown to lead to poorer outcomes in a number of studies, and currently there are no FDA-approved targeted therapies.	cyclin D1	2015-07-22 18:46:57.334277	2015-07-22 18:46:57.334277	\N	f	\N
9	894	CCND2	Cyclin D has been shown in many cancer types to be misregulated. Well established for their oncogenic properties, the cyclins and the cyclin-dependent kinases (CDK's) they activate have been the focus of major research and development efforts over the past decade. The methods by which the cyclins are misregulated are widely variable, ranging from genomic amplification to changes in promoter methylation. While Cyclin D2 has only been found to be significantly deregulated in glioma, Cyclin D1 in particular seems to be a pan-cancer actor. Cyclin D misregulation has been shown to lead to poorer outcomes in a number of studies, and currently there are no FDA-approved targeted therapies.	cyclin D2	2015-07-22 18:46:57.561765	2015-07-22 18:46:57.561765	\N	f	\N
10	896	CCND3	Cyclin D has been shown in many cancer types to be misregulated. Well established for their oncogenic properties, the cyclins and the cyclin-dependent kinases (CDK's) they activate have been the focus of major research and development efforts over the past decade. The methods by which the cyclins are misregulated are widely variable, ranging from genomic amplification to changes in promoter methylation. Cyclin D3 loss has been reported in T-ALL, a seemingly unique trend when compared to the amplifcations and overexpressions of the other cyclin D's. In a mouse study, the targeted therapeutic palbociclib significantly increased the median survival of the cyclin D3 knockouts.	cyclin D3	2015-07-22 18:46:57.744404	2015-07-22 18:46:57.744404	\N	f	\N
11	898	CCNE1	Cyclin E, while currenly not as widely implicated as its cyclin D counterparts, has been implicated in various carcinomas, including breast, gastric, stomach and colorectal. High levels of cyclin E, either by gene amplification or overexpression, have been shown to lead to poorer prognosis in gastic carcinoma, and these measurements are correlated with later stage disease. In lung cancer, neoplastic cells with higher levels of the cyclin E/CDK2 complex are more radiosensitive than their more lowly expressed counterparts.	cyclin E1	2015-07-22 18:46:57.94328	2015-07-22 18:46:57.94328	\N	f	\N
12	1021	CDK6	CDK6, along with its partner CDK4, are key players in cell cycle progression. The complex has been implicated in a number of cancer types, and is the focus of therapeutic research and development. One targeted therapy for CDK inhibition is palbociclib, which may slow the growth of advanced stage breast cancers. It has also been shown, in mouse, that CDK inhibition may sensitize mutant PIK3CA tumors to PI3K inhibitors.	cyclin-dependent kinase 6	2015-07-22 18:46:58.157179	2015-07-22 18:46:58.157179	\N	f	\N
13	1019	CDK4	CDK4, along with its partner CDK6, are key players in cell cycle progression. The complex has been implicated in a number of cancer types, and is the focus of therapeutic research and development. One targeted therapy for CDK inhibition is palbociclib, which may slow the growth of advanced stage breast cancers. It has also been shown, in mouse, that CDK inhibition may sensitize mutant PIK3CA tumors to PI3K inhibitors.	cyclin-dependent kinase 4	2015-07-22 18:46:58.372476	2015-07-22 18:46:58.372476	\N	f	\N
14	1029	CDKN2A	CDKN2A loss has been shown to be a significant event in a number of cancer types. While no targeted therapeutic has been engaged in clinical trials, the prognostic impact has been studied by a number of meta-analyses. One mechanism by which loss of CDKN2A can occur is by hypermethylation of the promoter region for the gene. However, the prognostic impact of promoter hypermethylation has been relatively ambiguous. Many studies have suggesting poorer prognostic outcome for patients with hypermethylation in colorectal, liver, and younger lung cancer patients. This being said, there is still research to be done before this becomes a widely-accepted prognostic indicator.	cyclin-dependent kinase inhibitor 2A	2015-07-22 18:46:58.650565	2015-07-22 18:46:58.650565	\N	f	\N
15	1050	CEBPA	AML with mutated CEBPA' is a provisional entity in the WHO classification of acute myeloid leukemia (AML) and is recommended to be tested for in patients with AML. CEBPA mutations are particularly associated with cytogenetically normal AML (CN-AML). CEBPA is an intronless gene that is required for granulocyte formation in mice. N-terminal nonsense mutations result in a dominant negative C/EBP-alpha protein while C-terminal mutations reduce the DNA-binding potential of this transcription factor. CEBPA mutations are associated with a favorable prognosis, however, NPM1 and FLT3 mutations should also be assessed in CN-AML patients as concurrent mutations may have prognostic implications.	CCAAT/enhancer binding protein (C/EBP), alpha	2015-07-22 18:46:58.906066	2015-07-22 18:46:58.906066	\N	f	\N
16	3337	DNAJB1	DNAJB1 works upstream of MDM2, stabilizing the complex and facilitating p53 turnover. In hepatocellular fibrolamellar carcinoma (FL-HCC), the fusion DNAJB1 to PRKACA is suggested to be a diagnostic marker for this rare subtype of HCC. In one study, this fusion was observed in 15/15 FL-HCC cases examined and functional studies found that the fusion retained kinase activity.	DnaJ (Hsp40) homolog, subfamily B, member 1	2015-07-22 18:46:59.15031	2015-07-22 18:46:59.15031	\N	f	\N
17	5566	PRKACA	PRKACA has been studied in breast cancer and has been found to mediate resistance to HER2 targeted therapies. It has also been found to contain a mutation hotspot that contributes to neoplastic behavior in neuroendocrine cancers. In hepatocellular fibrolamellar carcinoma (FL-HCC), the fusion DNAJB1 to PRKACA is suggested to be a diagnostic marker for this rare subtype of HCC. In one study, this fusion was observed in 15/15 FL-HCC cases examined and functional studies found that the fusion retained kinase activity.	protein kinase, cAMP-dependent, catalytic, alpha	2015-07-22 18:46:59.375427	2015-07-22 18:46:59.375427	\N	f	\N
18	1788	DNMT3A	DNMT3A is one of several epigenetic modifiers identified as recurrently mutated in acute myeloid leukemia (AML). DNMT3A mutations are associated with cytogenetically normal AML. In vitro experiments indicate that the R882H mutation acts in a dominant negative manner to disrupt the de novo methyltransferase activity of wildtype homotetramers. AML patient bone marrow harboring R882 mutations were similarly demonstrated to be hypomethylated compared to patients with wildtype DNMT3A. These studies also indicated that non-R882 DNMT3A mutations may act in a functionally distinct manner from R882 mutations. Alternative mechanisms indicate independent prognostic outcomes and treatment protocols may need to be considered for these two classes of DNMT3A mutations.	DNA (cytosine-5-)-methyltransferase 3 alpha	2015-07-22 18:46:59.58746	2015-07-22 18:46:59.58746	\N	f	\N
19	1956	EGFR	EGFR is widely recognized for its importance in cancer. Amplification and mutations have been shown to be driving events in many cancer types. Its role in non-small cell lung cancer has spurred many research and drug development efforts. Tyrosine kinase inhibitors have shown efficacy in EGFR amplfied tumors, most notably gefitinib and erlotinib. Mutations in EGFR have been shown to confer resistance to these drugs, particularly the variant T790M, which has been functionally characterized as a resistance marker for both of these drugs. The later generation TKI's have seen some success in treating these resistant cases, and targeted sequencing of the EGFR locus has become a common practice in non-small cell lung cancer.	epidermal growth factor receptor	2015-07-22 18:46:59.847388	2015-07-22 18:46:59.847388	\N	f	\N
20	2064	ERBB2	ERBB2, commonly referred to as HER2, is amplified in HER2-positive breast cancer, and is treated in a separate manner than the other subtypes of breast cancer. Apart from being amplified, ERBB2 activating mutations have been shown to have clinical importance in HER2-negative breast cancer. These mutations have shown sensitivity to the tyrosine kinase inhibitor neratinib, and highlight the importance of clinical sequencing efforts in treating breast cancer.	erb-b2 receptor tyrosine kinase 2	2015-07-22 18:47:00.136365	2015-07-22 18:47:00.136365	\N	f	\N
21	2099	ESR1	ESR1 has been a focus in breast cancer for quite some time, but has also shown significance in endometrial, ovarian and other cancer types. ER-positive breast cancer that is resistant to hormone therapy has instigated clinical sequencing efforts to shed light on the mechanisms of this resistance. A number of mutations in the ligand binding domain of the protein have been implicated in hormone resistance and anti-estrogen therapies. This has spurred efforts to develop therapeutics that act to degrade the protein, rather than act as an antagonist. These agents are currently in clinical trials and have seen some success, highlighting the importance of sequencing efforts in treating breast cancer.	estrogen receptor 1	2015-07-22 18:47:00.407739	2015-07-22 18:47:00.407739	\N	f	\N
22	2263	FGFR2	The FGFR proteins are involved in a wide array of pathways known to play a signficant role in cancer. Activation of these receptors can lead to activation of the RAS-MAPK pathway and the PI3K-AKT pathway, among others. The mechanisms by which FGFR can be misregulated vary between cancers. Amplification of the receptors has been observed in lung and breast cancers, coding mutations and deletions have been seen in many cancers, and more recently, FGFR fusions that lead to pathway actiation have been demonstrated to have oncogenic potential across multiple cancer types. The targeted therapeutics ponatinib, dovitinib and pazopanib have seen success in treating over-active FGFR signalling, prompting use of diagnostic sequencing targeting the FGFR genes, especially in lung cancer patients.	fibroblast growth factor receptor 2	2015-07-22 18:47:00.695514	2015-07-22 18:47:00.695514	\N	f	\N
23	2261	FGFR3	The FGFR proteins are involved in a wide array of pathways known to play a signficant role in cancer. Activation of these receptors can lead to activation of the RAS-MAPK pathway and the PI3K-AKT pathway, among others. The mechanisms by which FGFR can be misregulated vary between cancers. Amplification of the receptors has been observed in lung and breast cancers, coding mutations and deletions have been seen in many cancers, and more recently, FGFR fusions that lead to pathway actiation have been demonstrated to have oncogenic potential across multiple cancer types. The targeted therapeutics ponatinib, dovitinib and pazopanib have seen success in treating over-active FGFR signalling, prompting use of diagnostic sequencing targeting the FGFR genes, especially in lung cancer patients.	fibroblast growth factor receptor 3	2015-07-22 18:47:00.95088	2015-07-22 18:47:00.95088	\N	f	\N
24	2322	FLT3	FLT3 is an important cytokine receptor involved in normal hematopoiesis. Mutations in this gene are common in acute myeloid leukemia (AML) and screening for mutations in this gene has been recommended by the World Health Organization in patients with AML, particularly in cases of cytogenetically normal AML (CN-AML). FLT3 mutations commonly co-occur with mutations such as NPM1 that are associated with CN-AML and likely modulate prognostic impact. While FLT3-ITD mutations have been associated with poorer prognosis in AML, the prognostic impact of FLT3-TKD mutations are still up for debate.	fms-related tyrosine kinase 3	2015-07-22 18:47:01.171436	2015-07-22 18:47:01.171436	\N	f	\N
25	2624	GATA2	GATA2 is a transcription factor involved in stem cell maintenance with key roles in hematopoietic development. GATA2 mutations are associated with a variety of inherited and acquired immune disorders including myelodysplastic syndrome and acute myeloid leukemia. In addition to a role in hematopoiesis, the maintenance GATA2 expression has been implicated as a requirement in KRAS-driven non-small cell lung cancer. Preclinical models have indicated therapeutic benefit from targeting GATA2-mediated pathways in the context of KRAS-driven NSCLC.	GATA binding protein 2	2015-07-22 18:47:01.399293	2015-07-22 18:47:01.399293	\N	f	\N
26	3417	IDH1	IDH1 mutations have been observed in a number of cancer types, including sarcomas, hematologic malignancies, colon cancer and brain cancer. Mutations in the two isocitrate dehydrogenase enzymes involved in cytoplasmic (IDH1) and mitochondrial (IDH2) conversion of alpha-ketoglutarate to D-2-hydroxyglutarate have been described as mutually exclusive in many of these cancer types. The most frequent mutations involve R132 (IDH1) and R172 (IDH2) involve the active site and result in neomorphic enzyme activity. The implications of mutations in this gene vary greatly by cancer type. In myelodysplastic syndromes and acute myeloid leukemia (AML), IDH1 mutations have been associated with worse outcome, shorter overall survival, and normal karyotype. However, in glioblastoma and astrocytoma, patients with IDH1 mutations have shown better overall survival than patients with wild-type IDH1. Unlike the association with cytogenetically normal AML, in glioblastoma, IDH1 mutations have been associated with specific cytogenetic abnormalities, 1p and 19q deletions.	isocitrate dehydrogenase 1 (NADP+), soluble	2015-07-22 18:47:01.651951	2015-07-22 18:47:01.651951	\N	f	\N
27	3418	IDH2	IDH2 mutations have been observed in a number of cancer types, including sarcomas, hematologic malignancies, colon cancer and brain cancer. Mutations in the two isocitrate dehydrogenase enzymes involved in cytoplasmic (IDH1) and mitochondrial (IDH2) conversion of alpha-ketoglutarate to D-2-hydroxyglutarate have been described as mutually exclusive in many of these cancer types. The most frequent mutations involve R132 (IDH1) and R172 (IDH2) involve the active site and result in neomorphic enzyme activity. Although IDH2 (R172) mutations are associated with poorer overall prognosis in AML patients, its utility as a prognostic marker in MDS is still under debate. Additionally, IDH2 (R140) has been associated with improved overall survival in AML. IDH2 mutations have been associated with improved prognosis in gliomas.	isocitrate dehydrogenase 2 (NADP+), mitochondrial	2015-07-22 18:47:01.905458	2015-07-22 18:47:01.905458	\N	f	\N
28	3717	JAK2	JAK2 is a kinase that is misregulated or mutated in a number of myeloproliferative diseases and cancers. The mutation V617F is the most clinically relevant variant, and is seen in around half of myeloproliferative disorders. The variant is a known activating mutation, and activated JAK2 is sufficient to drive myeloproliferative disorders in mouse models. V617F, while most recurrent, is not the only mechanism by which JAK2 can be activated in patients. JAK2 is now one of the first diagnostic markers tested upon diagnosis with a myeloproliferative disorder.	Janus kinase 2	2015-07-22 18:47:02.127411	2015-07-22 18:47:02.127411	\N	f	\N
29	3815	KIT	c-KIT activation has been shown to have oncogenic activity in gastrointestinal stromal tumors (GISTs), melanomas, lung cancer, and other tumor types. The targeted therapeutics nilotinib and sunitinib have shown efficacy in treating KIT overactive patients, and are in late-stage trials in melanoma and GIST. KIT overactivity can be the result of many genomic events from genomic amplification to overexpression to missense mutations. Missense mutations have been shown to be key players in mediating clinical response and acquired resistance in patients being treated with these targeted therapeutics.	v-kit Hardy-Zuckerman 4 feline sarcoma viral oncogene homolog	2015-07-22 18:47:02.340371	2015-07-22 18:47:02.340371	\N	f	\N
30	3845	KRAS	Mutations in the RAS family of proteins have frequently observed across cancer types. The amino acid positions account for the overwhelming majority of these mutations, G12, G13 and Q61. The isoforms, despite their raw similarity, also behave very differently when expressed in non-native tissue types, likely due to differences in the C-terminal hyper-variable regions. Mis-regulation of isoform expression has been shown to be a driving event in cancer, as well as missense mutations at the three hotspots previously mentioned. While highly recurrent in cancer, targeted these RAS mutants has also been very elusive, and has not yet become common practice in the clinic.	Kirsten rat sarcoma viral oncogene homolog	2015-07-22 18:47:02.60495	2015-07-22 18:47:02.60495	\N	f	\N
31	5604	MAP2K1		mitogen-activated protein kinase kinase 1	2015-07-22 18:47:02.839543	2015-07-22 18:47:02.839543	\N	f	\N
32	4209	MEF2D		myocyte enhancer factor 2D	2015-07-22 18:47:03.031105	2015-07-22 18:47:03.031105	\N	f	\N
33	1436	CSF1R		colony stimulating factor 1 receptor	2015-07-22 18:47:03.249777	2015-07-22 18:47:03.249777	\N	f	\N
34	4255	MGMT		O-6-methylguanine-DNA methyltransferase	2015-07-22 18:47:03.434063	2015-07-22 18:47:03.434063	\N	f	\N
35	4869	NPM1	AML with mutated NPM1 is provisional entity in the WHO classification of AML and is recommended to be tested for in patients with cytogenetically normal AML (CN-AML). Evaluation of FLT3 mutations should be evaluated concurrently as they have prognostic consequences. NPM1 mutations are concentrated in exon 12, most frequently W288fs which results in cytoplasmic sequestration of the protein. Exon 12 NPM1 mutations in the absence of FLT3-ITD are associated with good prognostic outcomes. Mice expressing the Npm1-W288fs mutation develop myeloproliferative neoplasms but not overt leukemia, indicating it may require additional mutations to promote leukemic development.	nucleophosmin (nucleolar phosphoprotein B23, numatrin)	2015-07-22 18:47:03.700326	2015-07-22 18:47:03.700326	\N	f	\N
36	4893	NRAS	Mutations in the RAS family of proteins have frequently observed across cancer types. The amino acid positions account for the overwhelming majority of these mutations, G12, G13 and Q61. The isoforms, despite their raw similarity, also behave very differently when expressed in non-native tissue types, likely due to differences in the C-terminal hyper-variable regions. Mis-regulation of isoform expression has been shown to be a driving event in cancer, as well as missense mutations at the three hotspots previously mentioned. While highly recurrent in cancer, targeted these RAS mutants has also been very elusive, and has not yet become common practice in the clinic.	neuroblastoma RAS viral (v-ras) oncogene homolog	2015-07-22 18:47:03.927344	2015-07-22 18:47:03.927344	\N	f	\N
37	5290	PIK3CA	PIK3CA is the most recurrently mutated gene in breast cancer, and has been found to important in a number of cancer types. An integral part of the PI3K pathway, PIK3CA has long been described as an oncogene, with two main hotspots for activating mutations, the 542/545 region of the helical domain, and the 1047 region of the kinase domain. PIK3CA, and its interaction with the AKT and mTOR pathways, is the subject of an immense amount of research and development, and PI3K inhibition has seen some limited success in recent clinical trials. While monotherapies seem to be limited in their potential, there is a recent interest in pursuing PI3K inhibition as part of a combination therapy regiment with inhibition partners including TKI's, MEK inhibitors, PARP inhibitors, and in breast cancer, aromatase inhibitors.	phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha	2015-07-22 18:47:04.157659	2015-07-22 18:47:04.157659	\N	f	\N
38	5156	PDGFRA		platelet-derived growth factor receptor, alpha polypeptide	2015-07-22 18:47:04.371226	2015-07-22 18:47:04.371226	\N	f	\N
39	5371	PML	The PML-RARA fusion is the result of a recurrent, balanced translocation between chromosomes 15 and 17, denoted as t(15;17)(q22;q12), and a diagnostic event in acute promyelocytic leukemia (APL). Both in vitro and in vivo studies have shown sensitivity to ATRA (all-trans retinoic acid) in APL patients harboring the PML-RARA fusion. Recent interest has been shown in combining ATRA and arsenic trioxide for treating these patients, and early results seem promising.	promyelocytic leukemia	2015-07-22 18:47:04.581562	2015-07-22 18:47:04.581562	\N	f	\N
40	5914	RARA	The PML-RARA fusion is the result of a recurrent, balanced translocation between chromosomes 15 and 17, denoted as t(15;17)(q22;q12), and a diagnostic event in acute promyelocytic leukemia (APL). Both in vitro and in vivo studies have shown sensitivity to ATRA (all-trans retinoic acid) in APL patients harboring the PML-RARA fusion. Recent interest has been shown in combining ATRA and arsenic trioxide for treating these patients, and early results seem promising.	retinoic acid receptor, alpha	2015-07-22 18:47:04.793094	2015-07-22 18:47:04.793094	\N	f	\N
41	5728	PTEN		phosphatase and tensin homolog	2015-07-22 18:47:05.089338	2015-07-22 18:47:05.089338	\N	f	\N
42	5979	RET	RET mutations and the RET fusion RET-PTC lead to activation of this tyrosine kinase receptor and are associated with thyroid cancers. RET point mutations are the most common mutations identified in medullary thyroid cancer (MTC) with germline and somatic mutations in RET associated with hereditary and sporadic forms, respectively. The most common somatic form mutation is M918T (exon 16) and a variety of other mutations effecting exons 10, 11 and 15 have been described. The prognostic significance of these mutations have been hotly debated in the field, however, data suggests that some RET mutation may confer drug resistence. No RET-specific agents are currently clinically available but several promiscuous kinase inhibitors that target RET, among others, have been approved for MTC treatment.	ret proto-oncogene	2015-07-22 18:47:05.363732	2015-07-22 18:47:05.363732	\N	f	\N
43	861	RUNX1		runt-related transcription factor 1	2015-07-22 18:47:05.629792	2015-07-22 18:47:05.629792	\N	f	\N
44	23451	SF3B1	SF3B1 mutations have been described in several myeloid malignancies, predominantly myelodysplastic syndromes (MDS), as well as other hematologic malignancies and breast cancer. SF3B1 is one of several genes involved in RNA splicing that has been identified as recurrently mutated in MDS and other malignanices. The mutations affecting SF3B1 are typically heterozygous, point mutations suspected to be functionally deleterious with K700E described as a major hotspot mutation. MDS patients with SF3B1 mutations have been reported to have better overall and event-free survival than their wildtype counterparts. Additionally, these mutations are highly associated with subtypes of MDS characterized by ringed sideroblasts (refractory anemia with ringed sideroblasts and refractory cytopenia with multilineage dysplasia and ring sideroblasts).	splicing factor 3b, subunit 1, 155kDa	2015-07-22 18:47:05.876207	2015-07-22 18:47:05.876207	\N	f	\N
45	7157	TP53	TP53 mutations are universal across cancer types. Loss of tumor suppressors is most recognized by large deleterious events, such as frameshift mutations, or premature stop codons. In TP53 however, many of the observed mutations in cancer are found to be single nucleotide variants, or missense mutations. These variants are also very broadly distributed throughout the gene, not localizing in any particular hotspot. While a large proportion of cancer genomics research is focused on somatic variants, TP53 is also of note in the germline. Germline TP53 mutations are the hallmark of Li-Fraumeni syndrome, and many (both germline and somatic) have been found to have prognostic impact on patient outcomes.	tumor protein p53	2015-07-22 18:47:06.15295	2015-07-22 18:47:06.15295	\N	f	\N
46	7248	TSC1		tuberous sclerosis 1	2015-07-22 18:47:06.410703	2015-07-22 18:47:06.410703	\N	f	\N
47	7249	TSC2		tuberous sclerosis 2	2015-07-22 18:47:06.61665	2015-07-22 18:47:06.61665	\N	f	\N
48	7307	U2AF1	U2AF1 is one of several spliceosome complex genes frequently mutated in a variety of hematologic malignancies, particularly de novo myelodysplastic syndromes (MDS), as well as solid tumors such as lung and pancreatic cancers. Two hotspot mutations (S34 and Q157) occur within the two zinc-finger domains of the U2AF1 protein. These mutations have been associated with altered splicing patterns in vitro and in vivo. U2AF1 mutations in MDS have been associated with an increased risk of transformation to secondary acute myeloid leukemia, however, the impact of these mutations on overall survival has been an area of debate.	U2 small nuclear RNA auxiliary factor 1	2015-07-22 18:47:06.83709	2015-07-22 18:47:06.83709	\N	f	\N
49	7490	WT1	WT1 is a tumor suppressor gene associated with the development of Wilms' Tumor, from which it was named. Mutations in exon 7 and 9 of WT1 have been recurrently identified in acute myeloid leukemia and associated with poorer prognosis and chemotherapy resistance.	Wilms tumor 1	2015-07-22 18:47:07.081917	2015-07-22 18:47:07.081917	\N	f	\N
50	4851	NOTCH1		notch 1	2015-07-22 18:47:07.297986	2015-07-22 18:47:07.297986	\N	f	\N
51	4921	DDR2		discoidin domain receptor tyrosine kinase 2	2015-07-22 18:47:07.505277	2015-07-22 18:47:07.505277	\N	f	\N
52	4233	MET		MET proto-oncogene, receptor tyrosine kinase	2015-07-22 18:47:07.722814	2015-07-22 18:47:07.722814	\N	f	\N
53	2313	FLI1		Fli-1 proto-oncogene, ETS transcription factor	2015-07-22 18:47:07.937092	2015-07-22 18:47:07.937092	\N	f	\N
54	2130	EWSR1		EWS RNA-binding protein 1	2015-07-22 18:47:08.138373	2015-07-22 18:47:08.138373	\N	f	\N
55	54790	TET2		tet methylcytosine dioxygenase 2	2015-07-22 18:47:08.331018	2015-07-22 18:47:08.331018	\N	f	\N
56	27086	FOXP1		forkhead box P1	2015-07-22 18:47:08.539779	2015-07-22 18:47:08.539779	\N	f	\N
57	5966	REL		v-rel avian reticuloendotheliosis viral oncogene homolog	2015-07-22 18:47:08.732314	2015-07-22 18:47:08.732314	\N	f	\N
58	7428	VHL		von Hippel-Lindau tumor suppressor, E3 ubiquitin protein ligase	2015-07-22 18:47:08.9467	2015-07-22 18:47:08.9467	\N	f	\N
59	596	BCL2		B-cell CLL/lymphoma 2	2015-07-22 18:47:09.141665	2015-07-22 18:47:09.141665	\N	f	\N
60	3481	IGF2		insulin-like growth factor 2	2015-07-22 18:47:09.333353	2015-07-22 18:47:09.333353	\N	f	\N
61	6790	AURKA		aurora kinase A	2015-07-22 18:47:09.573199	2015-07-22 18:47:09.573199	\N	f	\N
62	55193	PBRM1		polybromo 1	2015-07-22 18:47:09.770023	2015-07-22 18:47:09.770023	\N	f	\N
63	2146	EZH2		enhancer of zeste 2 polycomb repressive complex 2 subunit	2015-07-22 18:47:10.021172	2015-07-22 18:47:10.021172	\N	f	\N
\.



-- Name: sources_id_seq; Type: SEQUENCE SET; Schema: public; Owner: acoffman
--

SELECT pg_catalog.setval('sources_id_seq', 401, true);


--
