Fix log4j configuration in docker

There are some failing tests, because we recently updated oncokb isoform override files. Isoform overrides files are stored at: https://github.com/genome-nexus/genome-nexus-importer/tree/master/data/common_input Oncokb files are originally from: https://www.oncokb.org/api/v1/utils/allCuratedGenes?includeEvidence=true E.g.:

{
    "grch37Isoform": "ENST00000349310",
    "grch37RefSeq": "NM_001014431.1",
    "grch38Isoform": "ENST00000349310",
    "grch38RefSeq": "NM_001014431.1",
    "entrezGeneId": 207,
    "hugoSymbol": "AKT1",
    "oncogene": true,
    "highestSensitiveLevel": "3A",
    "highestResistanceLevel": "",
    "summary": "AKT1, an intracellular kinase, is altered predominantly by mutation in various cancer types including breast and endometrial cancers.",
    "background": "AKT1 is a serine/threonine protein kinase that is a critical downstream effector in the PI3K (phosphoinositide 3-kinase) signaling pathway. Following activation of PI3K, cytosolic inactive AKT1 is recruited to the membrane and engages PIP3 (PtdIns3,4,5-P3), leading to phosphorylation and activation of AKT1 (PMID: 28431241). AKT1 can activate a number of downstream substrates, including GSK3, FOXO and mTORC1, which are critical for cellular survival, proliferation, and metabolism (PMID: 9843996, 7611497). Negative regulation of AKT1 occurs when PI3K signaling is terminated by PTEN phosphatase activity (PMID: 28431241). AKT1 is frequently activated in cancers, typically through activation of the PI3K pathway or by inactivation of PTEN (PMID: 28431241). Activating mutations in AKT1 (PMID: 17611497, 23134728, 20440266) and infrequent AKT1 gene amplification (PMID: 18767981) have been identified in human cancers, which allow for phosphoinositide-independent AKT1 activation. The ATP-competitive AKT1 inhibitor AZD5363 has demonstrated activity in patients with AKT1-mutant cancers (PMID: 28489509). Negative feedback mechanisms can mediate AKT-inhibitor resistance in human cancers with dysregulated AKT signaling (PMID: 29535262, 29339542).",
    "tsg": false,
    "highestResistancLevel": ""
  },

  {
    "grch37Isoform": "ENST00000407977",
    "grch37RefSeq": "NM_017763.4",
    "grch38Isoform": "ENST00000407977",
    "grch38RefSeq": "NM_017763.4",
    "entrezGeneId": 54894,
    "hugoSymbol": "RNF43",
    "oncogene": false,
    "highestSensitiveLevel": "",
    "highestResistanceLevel": "",
    "summary": "RNF43, a ubiquitin ligase, is mutated in various cancers including gastrointestinal and gynecological cancers.",
    "background": "RNF43 encodes for ring finger protein 43 is a transmembrane protein that has ubiquitin ligase activity (PMID: 24532711). It inhibits the Wnt pathway signaling by controlling Frizzled receptor expression through ubiquitination and protein degradation (PMID:26863187, 25891077). It binds to the ligand R-spondin which inhibits its activity (PMID:22575959). RNF43 is expressed in LGR5 positive colonic stem cells and regulates their growth and differentiation through Wnt signaling (PMID:22895187). Mutations are found in colorectal, endometrial, ovarian, gastric, cholangiocarcinoma, and pancreatic neoplasms (PMID:26257827, 25344691, 24816253, 22561520, 26505881, 23847203, 24293293, 26924569). Mutations have been characterized as loss of function and may lead to susceptibility to treatment with Wnt pathway inhibitors (PMID:25901018).",
    "tsg": true,
    "highestResistancLevel": ""
  },

genome-nexus / genome-nexus-annotation-pipeline

Fix log4j configuration in docker #245