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Basis of Human Cancer

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University of Windsor
Biological Sciences

The Genetic Basis of Human Cancer – B. Vogelstein 9/21/2006 Tumor – swelling of excess tissue • Non-neoplastic – cysts • Neoplastic – excess of cells o Benign: non-invasive, not defined by size (polyps, adenomas, nevi) o Malignant = cancer: can be invasive (carcinomas, sarcomas, leukemias)  Final stage of malignancy is metastasis  Each metastatic tumor is about a million cells that came from one invasive cell that migrated  Many different types of cancer; several different kinds of tumors can form in each organ  Metastasis results in the overtaking and destruction of organs and vessels, leading to death Essence of neoplasia • Cell cycle control (cell birth) • Apoptosis control (cell death) • Ratio of cell birth to cell death in a normal adult is 1. If cell death is greater than cell birth, leads to atrophy. Even a tiny increase of cell birth relative to cell death results in net cell growth  tumor (can take 20-30 years) What causes cancer? • Components that can contribute include viruses, other infectious agents, breakdown in immunity, changes in gene expression • The basis of cancer is mutations in specific genes • Some people are predisposed to getting cancer via a hereditary mutation, but this is not enough to cause cancer on its own • More mutations (non-hereditary) must be acquired during a person’s lifetime for cancer to develop • A cancer cell has some growth advantage so it can predominate over normal cells, leading to a wave of clonal expansion. Its progeny also predominate over other cells, leading to more waves of clonal expansion and so on Cancer Causing Genes • Oncogenes – normally stimulate growth • Suppressor genes – normally inhibit growth • Repair genes – normally limit mutations, but if the repair gene is defective it will accelerate the onset of mutations Tumor Suppressor Genes • Wilms’ Tumor (a solid tumor)– effects children; observations of this type of tumor stimulated the Two-Hit Hypothesis • Clinical Basis for Two-Hit Hypothesis o Familial and non-familial forms of the cancer exist o Familial form  10,000x incidence relative to non-familial  often multiple tumors (vs only 1 for non-familial)  often occurs earlier than non-familial  only small portion of cells become cancers • Classic fusion experiment o Normal cell + tumor cell  no tumor in most cases because normal cell supplies good copies of tumor suppressor genes o An exception is in the case of myeloma cells. These will form tumors when fused with normal cells (like when making monoclonal antibodies) o Wilms’ tumor cell + chromosome 11  no tumor – this suggests that there is a tumor suppressor gene on chromosome 11 • Non-familial form: o First hit = somatic mutation o Second hit = another somatic mutation (or LOH) in a cell that already has one mutated allele • Familial form: o First hit = mutation in germ-line on one allele (present in every cell) o Second hit = somatic mutation on other allele (or LOH) – the point here is that only one somatic hit is necessary for tumor initiation Retinoblastoma – also 2-Hit; on ch
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