Cancer genetics

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1 Cancer genetics General information about tumorogenesis. Cancer induced by viruses. The role of somatic mutations in cancer production. Oncogenes and Tumor Suppressor Genes (TSG). Hereditary cancer. 1 st period up to 1970 cancer was characterized as a complex of different diseases. In an unestablished way benign tumors may turn into malign tumors. 2 nd period there is a single cancer disease determined by changes in genetic apparatus. Under influence of carcinogens the cells start unlimited divisions, and, after a critic point, obtain the property to invade other tissues. Clonal evolution ofcancer starting from a modified cell: Cancer developing underinfluence ofmutagens Existence of inherited cancer (6% - AD) and family cancer (non-mendelian inheritance) High risk of cancer in (up to 5 times higher) in families where there are affected members Chromosomal errors associated with cancer (Ph chromosome) 3 rd period after 1980 identification of genes involved in production and development of some types of cancers 1

2 Factors involved in cancer production There are 3 types of mechanisms of carcinogenesis induced by: Viruses Mutations Inherited genes Steps in transition to tumor Immortalization out of control cell divisions. The cells have normal phenotype and properties. Such cellaggregations may cause benign tumors; Transformation changes in structure, function and fate of cells. The cells become independent of growth factors, and change the shape into spherical; Metastasis formation the cells obtain the property to move through tissues and to produce colonies in new places. These colonies are called metastasis and they produce malign tumors or cancer. Characteristic of cancer genes There are 291 cancer genes, which represent more than 1% of human genome 70% of cancer genes contain somatic mutations, 20% - germinal mutations, 10% - both The most frequent mutations are translocations, which produce chimeric genes Most of genes were described for leukemia, lymphoma and sarcoma, in spite these cancers represent just 10%. The most affected domains in proteins: protein-kinase Interaction with DNA Control of transcription Cancer genes Oncogenes Initially were detected in viruses that cause transformation of target cells (viral oncogenes are named v-onc). Homologous cellular genes are called protooncogenes. Their mutation or abnormal activation lead to tomorogenesis (cellular oncogenesare named c-onc). 2

3 Oncogenes Protooncogenes encode for: Main components of intracellular signaling, Growth factors, Growth factors receptors, Transcription factors, Regulatory cytoplasmatic proteins. Oncogenes Growth Factors or Receptors for Growth Factors PDGF Platelet Derived Growth Factor (brain and breast cancer) erb-b, erb-b2, RET receptor for epidermal growth factor (brain, thyroid, salivary, and breast cancer) Cytoplasmic Relays in Stimulatory Signalling Pathways Ki-ras, N-ras activated by active growth factor receptor proteins (lung, ovarian, colon and pancreatic cancer, leukemias) c-src is a protein kinase that becomes overactive in phosphorylation of target proteins Transcription Factors that Activate Growth Promoting Genes c-myc activates transcription of growth stimulation genes (leukemia, brest, stomach, and lung cancer) N-myc (nerve and brain cancer) c-jun and c-fos function as transcription factors Other types of molecules Bcl-2 normal protein blocks cell suicide (lymphoma) Bcl-1 encodes for cyclin D1, stimulatory protein of the cell cycle (breast, neck, head cancers) MDM2 encodes for antagonist of p53 (sarcomas) Tumor Suppressor Genes (GST) Normally, these genes assure control of cell cycle. There are about 10 GST (p53, RB1). The final products of these genes stop cell division and assure cell differentiation and specialization. Deletion or inactivation of these genes lead to tumorogenesis. TSGs Cytoplasmic Proteins APC (colon and stomach cancers) DPC4 encodes relay molecule in cell division inhibitory pathway (pancreatic cancer) NF-1 encodes protein that inhibits a stimulatory (Ras) protein (brain, nerve, and leukemia), NF-2 (brain and nerve cancers) Nuclear Proteins MTS1 encodes for p16 protein, brake on cell cycle clock (many cancers) RB encodes prb protein, master brake on cell cycle (retinoblastoma, bone, bladder, lung, and breast cancer) p53 encodes p53 protein, halts cell cycle in G1 and induces cell suicide (many cancers) p16 inhibits cyclin D-dependent kinase activity WT1 (Wilms tumor of the kidney) BRCA1 functions in repair of damage to DNA (breast and ovarian cancers) BRCA2 functions in repair of damage to DNA (breast cancer) Location not clear VHL (kidney cancer) z Animatie 3

4 Mutations associated with cancer The role of translocations in human cancers Somatic Generative Both Translocations Non-translocations Both Types of mutations in human cancers Association of mutations and type of cancer Germinal Somatic Germinal Somatic Dominant Recessive Numerous Leukaemia Epithelial Mesenchymal Other 4

5 Familial Familial Dominant APC MMR POLD LKB1 Colorectal cancer High penetrance Recessive MYH Other Low penetrance APC TGF BLM Sporadic Genes involved in colon cancer Genetic factors Environment factors Mutations resulted from mismatch DNA repair in Lynch syndrome Translocation t(9;22)(q34;q11) Philadelphia chromosome 100% 80% 60% 40% 20% 0% MSH2 MLH1 MSH6 Nonsens Frame-shift Missens ins/del Other 5

6 Virus transformation DNA viruses contain genes able to inhibit TSG Retriviruses contain oncogenes After infection permissive cells are destroyed After infection non-permissive cells integrate virus in their genome Only a part of transformed cells are turned into tumoral Most of cells infected with retrovirus are turned into tumoral After integration the virus may inhibit a suppressor gene through: Promoter inactivation Polypeptide inactivation Viral promoter may activate a silent gene After integration will result a hybrid carcinogenic polypeptide Indications for genetic counseling People with 1 or more of the following may be candidates for genetic counseling: Diagnosed with cancer at an atypically young age. Have a rare cancer, e.g., childhood adrenocortical carcinoma. Have an unusual presentation, e.g., right-sided colon cancer. Have multiple primary cancers. Have cancers associated with birth defects. Have, in some cases, extreme cancer anxiety, even in the absence of risk. Family anamnesis Clustering of the same type of cancer in close relatives. Unusually early age of cancer onset. Two or more primary cancers in a single relative. Evidence of autosomal-dominant inheritance. Bilaterality in paired organs. Patterns of cancer in the family that are associated with a known cancer syndrome. 6

7 Familial anamnesis if there are affected members Type of each primary cancer. Age of diagnosis for each primary cancer. Where the relative was diagnosed and/or treated. If the individual is still living, current age; if deceased, age at death and cause of death. Carcinogenic exposures (e.g., tobacco use, radiation exposure). Other significant health problems. Familial anamnesis if there are no affected members Current age or age at death. If deceased, cause of death. Any surgeries that reduce the risk for cancer. Whether routinely screened for cancer. Any nonmalignant features of the syndrome in question. Carcinogenic exposures. Other significant health problems. 7

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