Genes that regulate cell growth and division can have mutations or expression errors that cause tissues to grow too rapidly {cancer}|.
cell division
Normal cells can have 70 replications. Cancer cells make, or react to growth-promoting chemicals and make, molecules that trigger cell division. Cancer cells have no cell-division limits. Cancer cells do not respond to molecules from adjacent tissues that normally stop growth and cell division.
cell death
Cell mechanisms for killing cells in response to DNA damage do not affect cancer cells.
steps
Common progression to cancer is inflammation, metaplasia or hyperplasia, dysplasia or neoplasia, and carcinoma or other cancer types. Perhaps, inflammation is from bacteria or toxins. Cancer starts with oncogene activation, followed by transformed-cell proliferation, immune-system-mechanism evasion, and tumor angiogenesis-factor release. Cancer cells have chemokine receptors.
types
Tissue cancers are carcinoma, sarcoma, leukemia, and lymphoma.
Organ cancers are mostly in lung, large intestine, colon, rectum, and breast. Organ cancers have lower frequency in pancreas, prostate, stomach, and brain.
types: immune system
In immune system, genes that regulate transpositions that make antibodies can have mutations or expression errors that express protein {c-myc protein} that can cause leukemia, lymphoma, B-cell tumor, and T-cell tumor.
blood vessels
Tumors can secrete angiogenesis factors that make blood vessels grow.
aneuploidy
Perhaps, cancerous cells first change chromosome number or arrangement {aneuploidy, cancer} and later become cancerous. Chromosome parts duplicate, transfer, switch, join, and become lost, so genes that control cell division {master genes} can mutate or change epigenetically. Perhaps, centrosome RNA genes have master genes. Chromosomes can also add or subtract histone proteins and acidic nuclear proteins. Enediynes break DNA apart.
contagious cancer
Canine venereal tumor disease and devil facial tumor disease are contagious cancers.
Cells can transform from one type to another type {metaplasia}, as when cartilage becomes bone, or cells become cancerous.
Cancer cells can migrate {metastases} {metastasis}|. Migrating cancer cells go through blood-vessel walls and travel in blood and lymph {metastasize} until trapped in small blood vessels or lymph nodes. Cancer cells pass through capillary linings and start secondary tumors.
effects
Tumor cells can invade and destroy cell-cell adhesions, stromal extracellular matrix, basement membrane, and parenchymal cells. Cells deform. Cell motility increases. Cell receptors alter.
factors
Serine proteinase, cysteine proteinase, metalloproteinase can assist cancer invasion.
Gene mutations that alter cell-proliferation repressors start cancer {carcinogenesis}.
If cells have broken DNA or low oxygen, TP53 gene makes p53 protein, which kills cells {apoptosis}. Bcl-x gene regulates apoptosis by making protein in two alternatively spliced forms, Bcl-x(L) and Bcl-x(S).
Tumors, follicle cells, and sperm make antigens {cancer testis antigens}.
Viruses {oncovirus} can cause leukemia, Hodgkin's disease, and other cancers. The first oncovirus discovered was Rous sarcoma virus, which has src oncogene and is in all higher animals. Human papilloma virus {papillomavirus} (HPV) causes cervical cancer and suppresses tumor-suppressor genes. Epstein-Barr virus causes mononucleosis and prevents cell suicide. Retroviruses can cause sarcoma. Perhaps, cytomegalovirus causes glioblastoma.
Tumor angiogenesis factors released by solid tumors start blood-vessel formation {vascularization}, which allows cancers to spread by supplying more oxygen.
Tumors can secrete peptides {angiogenesis factor} that make blood vessels grow.
Cancer-causing chemicals {carcinogen}| mutate DNA. Radioactivity, electromagnetic radiation, air pollutants, chloramine, x-rays, ultraviolet radiation, vinyl chloride, asbestos, arsenic, nickel, coal, benzene, PCB, tris phosphate, perchloroethylene (perc), dimethylbenzanthracene (DMBA), tar in cigarette smoke, high fat diet, saccharin, cyclamate, diethylstilbesterol (DES), nitrites, red food dye, yellow food dye, chloroform, and excess estrogen mutate DNA.
Perhaps, genes {master gene} that control cell division mutate or change epigenetically. Perhaps, centrosome RNA genes have master genes.
Genes {tumor-suppressor gene} {anti-oncogene} {recessive oncogene} can control oncogenes. Tumor-suppressor genes mutate and no longer make enough tumor suppressors, and this allows cancer to begin. For example, p53 gene protein suppresses growth, but p53-gene mutation allows growth. Tumor-suppressor genes {retinoblastoma gene} {Rb gene} {p53 gene} {APC gene} {MYC gene} {BCL-2 gene} {RAS gene} number 15 or more and regulate cell division.
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.
Cancer cells continuously divide to make masses {tumor}| that can be benign or malignant.
Cancerous regions {benign tumor}| can stay in well-defined areas and stop proliferating.
Cancer cells can keep proliferating and spread to other body parts {malignant tumor}|.
Cancers {dysplasia} can have abnormal cell growth.
Cancers {hyperplasia} can be abnormally high numbers of cells in organs or tissues.
Cancers {hypoplasia} can be abnormally low number of cells in organs or tissues.
Cancers {neoplasm} {neoplasia} can be tumors.
Mucosa can have growths {polyp, mucosa}|.
Cancers {adenoma} can be benign gland tumors.
Cancers {prostate cancer}| can make enzymes {prostatic acid phosphatase} (PAP). Gleason scale measures severity. Prostate-cancer cells have SDC1 protein.
Tissue cancers {carcinoma} can be in epithelium. Epithelium has cell-adhesion molecules {epithelial cell adhesion molecule} (EpCAM).
Tissue cancers {leukemia}| can be in bone marrow. Leukemia and organ cancers have low rate.
Tissue cancers {lymphoma}| can be in lymph nodes.
Tissue cancers {sarcoma}| can be in fibrous tissue and blood vessels. Sarcoma is rarest.
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Date Modified: 2022.0225