Host cells have genes {proto-oncogene} that regulate cell growth. Chromosome rearrangements can activate proto-oncogenes. In human chronic myelogenous leukemia, chromosome-9 ends, with abl genes, are on chromosome 22 {Philadelphia chromosome}. Retroviruses incorporate proto-oncogenes from normal cells to make oncogenes by transduction.
Tumor-virus genes {oncogene} can make host cells cancerous. Viral oncogenes are SV40 and polyoma T-antigen gene, adenovirus E1A and E1B genes, and papillomavirus E6 and E7 genes. Testicular germ-cell tumor (TGCT) gene, prostate-cancer-susceptibility gene, and familial male breast-cancer gene are on X-chromosomes. Src gene, BRAF gene, c-fos gene, and c-erbb3 are other oncogenes. Oncogenes number more than 100.
transformation
Oncogenes change host genomes by transformation. Oncogene products repress genes that stop cell growth and control oncogenes. Oncogene products start DNA replication, cell growth, and viral gene transcription. Viruses typically affect non-growing cells. Cancer daughter cells are cancerous, too.
mutation
Oncogenes mutate to activate. Perhaps, some cells are more susceptible to mutation.
cell death
Oncogenes send cell-death signals, which survival signals from other genes suppress. Perhaps, oncogenes protect against viruses.
transcription factors
fos gene, myc gene, rel gene, and other oncogenes can be transcription factors. B-cell tumors activate c-myc genes. Neuroblastomas have N-myc-gene over-replication. Avian leukosis virus goes into host genomes and then activates cellular myc proto-oncogene, so it transforms slowly.
signal transduction
Oncogenes can be in signal-transduction pathways. Oncogenic src-gene, abl-gene, and lck-gene protein-tyrosine kinases send signals even if they have not received initiation. Rous-sarcoma-virus src gene transforms quickly.
growth factor
Monkey-retrovirus sis genes encode platelet-derived growth factors that stimulate cells. Viral erbB genes make epidermal growth factor receptors without EGF initiation.
retrovirus
Cancer genes are similar to retrovirus genes. Cancer genes make protein kinases for protein phosphorylation. Phosphorylation cascades phosphorylate tyrosine in ATPase and trigger cell malignancy.
G protein
Harvey-sarcoma-virus ras gene products act like G proteins, but do not remove GTP. Ras-gene proteins associate with proteins {GTPase activating protein} {GAP protein}. IRA-gene products are similar to GAP proteins.
Philadelphia-chromosome BCR and ABL gene fusions {BCR-ABL fused gene} can cause leukemia {chronic myelogenous leukemia}.
Melanoma and moles have human cancer gene {B-RAF gene} mutations. First, cells proliferate. Later, B-RAF-gene products enhance p16 genes, which turn off cell division.
Genes {EGFR gene} can mutate or duplicate in lung and colon tumors.
Genes {HER2 gene} can be in breast and lung cancers.
Genes {HNPCC gene} can be in colon cancers and endometrial-cancer DNA repair.
Mutated genes {P13K gene} can be in solid tumors.
B-RAF-gene products enhance genes {p16 gene} that turn off cell division. p53 genes make proteins that prevent p16 enhancement and so allow cancerous cell division.
Genes {Pop1 gene} can affect breast cancer.
Human genes {PTEN gene} can be in prostate and prevent uncontrolled cell division. When PTEN gene mutates, cancer starts. p53 can activate PTEN gene, so cell division stops.
Genes {ras gene} can repress cell division. Ras-gene product regulates other genes to stop cell division {oncogene-induced cell senescence}. Ras-gene mutation turns on cancerous cell division to make immortalized cells. Human cancer genes {H-RAS gene} can be in bladder cancers [discovered 1982]. Genes {K-ras gene} can code tumor-growth signaling proteins.
Oncogenes {retinoblastoma tumor suppressor gene} {RB1 gene} can be in eye.
Cancer-causing genes {src gene} can be in all higher animals.
Tumor-causing genes {testicular germ-cell tumor gene} {TGCT gene} can be on X-chromosomes.
4-Medicine-Disease-Kinds-Cancer-Genes
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Date Modified: 2022.0225