Biology And Biomedical Sciences BIOL 2960 Lecture Notes - Lecture 41: Tumor Suppressor Gene, Cpg Oligodeoxynucleotide, Gene Duplication
13 Dec 2016
School
Department
29 April 2016
Lecture 41: Cancer Biology
I. Cancer Biology
A. Cancer Genetics (from L40)
1. Oncogenes
a. An oncogene needs to be activated to promote unregulated progression through
the cell cycle, an accelerator
b. Overactive mutation (“gain of function”)
c. Only one mutation needed (on gene, on one homolog) to take effect
d. Conversion of a proto-oncogene to an oncogene can result from multiple forms of
activating mutations
• Deletion or point mutation in coding sequence (hyperactive or inactive protein
• Regulatory sequence mutations (overproduction)
• Gene amplification (overproduction)
• Chromosome rearrangement via gene placement near an active promoter or
fusion of a gene to an actively transcribed gene (overproduction)
e. Ex: growth factor receptor signaling pathway promotes cell proliferation, uses
Ras GTPase protein, Ras is an oncogene
• The Ras oncogene is induced by a point mutation
• The mutation in Ras decreases GTPase activity, which keeps Ras active
longer
2. Tumor Suppressor Genes
a. Needs to be inactivated to promote progression through the cell cycle (a brake)
b. Underactivity mutation (“loss of function”)
c. The mutation must be in both copies of a gene (from each homolog) or by
complete DNA methylation of promoter CpG sequences for the gene
d. Inactivation of a tumor suppressor gene can result from changes in gene function
that are genetic or epigenetic
e. How can investigators identify tumor suppressor genes?
• Hereditary predisposition to cancer
• Genes that are hyper-methylated at CpG sites in tumo cell DNA
• Sequencing of cancer genomes reveals inactivating mutations in both alleles
f. Ex: the retinoblastoma (Rb) gene
find more resources at oneclass.com
find more resources at oneclass.com
