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Lecture 22

BIO 2400 Lecture 22: Ch. 22

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Appalachian State University
BIO 2400
Annkatrin Rose

Ch. 22 • Karyotype FISH Analysis o Fluorescent in-situ hybridization ▪ Fluorescent probe used to detect gene deletion • Genetic Testing Prior to Birth o Amniocentesis o Chorionic Villi Sampling • Issues with Genetic Testing o No treatment for genetic disorder o About 2/3 of diagnosed Down syndrome pregnancies are terminated o Lifetime risk for breast cancer with BRCA1 and BRCA2 mutations is in the range of 26-85% o Chance of developing Huntington’s disease for a carrier is 100% o PRIVACY ISSUES • Genetic Basis of Cancer o Cancer= uncontrolled cell division o Caused by somatic mutations in a single body cell ▪ Single mutation is not enough • Cancer Characteristics o Most cancers originate in a single cell ▪ Clonal o Multistep process: ▪ Precancerous genetic change (ex. Benign growth) ▪ Additional genetic changes ▪ Progression to cancerous cell growth • Malignant growth • Clonal Evolution of a Tumor • • Age and Carcinogens o At least 80% of cancers are related to exposure to mutagens • Certain Viruses Can Cause Cancer o Oncoviruses o Virus research led to the discovery of oncogenes (genes that promote cancer) o Viral oncogenes have cellular origins (proto-oncogenes)- the virus acquires them from their host cells o • Oncogenes and their effects on cell division o Oncogenes keep the cell growth signaling pathway permanently ON ▪ Oncogene may be overexpressed- promoter mutations ▪ Oncogene may produce an abnormal protein- mutations in coding sequence  Oncogenes are typically the result of “gain-of-function” mutations. What kind of mutation would NOT work to convert a proto-oncogene to an oncogene? Knock out mutation • Tumor- Suppressor Genes and their effects on cell division o Tumor suppressor genes prevent the proliferation of cancer cells ▪ Cancer may occur if their function is lost due to mutation o First human tumor-suppressor was identified was retinoblastoma o “two hit” model for retinoblastoma • Two-hit hypothesis o Retinoblastoma requires two mutations ▪ Loss of function mutations are typically recessive o Spontaneous mutation scenarios:
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