Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
42 Cards in this Set
- Front
- Back
|
Cancer |
characterized by uncontrolled cell division & metastasis |
|
|
Genetics & Cancer Facts |
- inherited predisposition for 50+ forms - cancer causing chemicals are usually mutagens - some viral genes promote or maintain cancer growth in infected cells - specific chromosomal changes associated with certain forms |
|
|
Leading Risk Factor |
AGE!!!! |
|
|
Cancer Progression |
1. cell becomes cancerous after accumulating specific mutations over a period of time 2. cell escapes control of cell cycle & begins uncontrolled division - cancer cells are clonal descendants of the mutant cell 3. mutations accumulate over time & cancer becomes more aggressive |
|
|
Metastasis |
cancer cells are invasive & can infiltrate surrounding tissues |
|
|
Metastasis Progression |
1. cancer cells break away from original tissue 2. cells attach to walls of blood or lymph vessels & secrete digestive enzymes to create an opening 3. cells cross wall at breach & begin moving along in blood vessel 4. leave bloodstream the way they entered & start new tumors in other tissues |
|
|
Sporadic Cancer |
gradual accumulation of mutations in key genes within a single cell - at least two mutations required - majority of all cancers |
|
|
Inherited Cancer |
a mutant allele is inherited from one parent & the normal allele mutates causing cancer growth = loss of heterozygosity < 5% of all cancers |
|
|
Cell Division Types |
1. non-dividing: muscle & nerve cells 2. divide to replace dead/damaged: liver & kidney cells 3. constantly dividing: epithelial cells |
|
|
Cancer Cells |
carry mutant alleles of genes involved in cell cycle regulation or signal transduction |
|
|
Epithelial Cancer |
80 to 90% of all cancers |
|
|
Types of Epithelial Cancer |
1. basal cell: slow growing & noninvasive 2. squamous cell: fast growing & can be invasive 3. malignant melanoma: dark, fast growing, invasive, deadly |
|
|
Eukaryotic Cell Cycle |
1. Interphase - G1 - S - G2 2. Mitosis - prophase - metaphase - anaphase - telophase 3. Cytokinesis |
|
|
Interphase G1 |
period of cell growth before DNA replication; chromosomes unduplicated |
|
|
Interphase S |
period of cell growth when DNA replication is completed; chromosomes duplicated |
|
|
Interphase G2 |
follows DNA replication & cell prepares to divide |
|
|
G1/S Checkpoint |
proceeds to S or enters inactive G0 state - cells in G0 reenter cycle after receiving external signal to divide = signal transduction |
|
|
G2/M Checkpoint |
monitors completion of DNA synthesis & DNA damage |
|
|
M Checkpoint |
cell monitors attachment of spindle fibers to chromosomes |
|
|
Cell Cycle Regulatory Genes in Cancer |
1. tumor suppressor genes 2. proto-oncogenes |
|
|
Tumor Suppressor Genes |
turn on/off or decrease rate of cell division - normally active at G1/S or G2/M ex: RB1 |
|
|
Proto-oncogenes |
turn on or increase rate of cell division & encode proteins that start/maintain growth & division |
|
|
Oncogenes |
mutant or inactive proto-oncogenes that pass freely through checkpoints & divide uncontrollably |
|
|
Normal Tumor Suppressor |
encoded proteins inhibit cell division |
|
|
RB1 Tumor Suppressor Gene |
controls G/1 S checkpoint - when pRB is active cell does not proceed through G/1 S & binds to E2F - when pRB is inactive E2F is released & cell moves through G1/S *if pRB is mutated or missing E2F is always active & cell grows/divides continuously forming a cancerous tumor |
|
|
ras Proto-oncogene |
encodes a signal transduction protein that processes signals for division & transmits them from cytoplasm to nucleus *mutations at amino acids 12 or 61 cause oncoprotein that permanently remains active & signals division |
|
|
Effects of DNA Repair Gene Defects |
- high mutation rates - chromosomal abnormalities - genomic instability *associated with breast & some forms of colon cancers |
|
|
Breast Cancer |
BRAC1 (17) & BRAC2 (13) mutations can predispose women to breast/ovarian cancers = 15 to 20% of all cases |
|
|
BRCA1 & BRCA2 |
DNA repair genes that encode nuclear proteins - expressed highest at G1/S in rapidly dividing cells |
|
|
BRCA1 |
tumor suppressor gene that normally repairs breaks in DNA during replication ~mutations in DNA accumulate when gene is mutated & cell becomes cancerous |
|
|
Genetic Factors of Colon Cancer |
- several mutations required - predisposition in 5% of all cases 1. FAP 2. HNPCC (both autosomal dominant) - environmental factors = diet & lifestyle |
|
|
FAP |
specific sequence of mutational events - 5 to 7 in single cell = pathway to cancer - fewer mutations result in benign or intermediate malignant growth - normal APC allele leads to some polyps - mutated APC leads to countless polyps *further mutations required to become cancerous |
|
|
HNPCC |
mutations in repair DNA genes MSH2 & MLH1 result in defective repair & increased # of microsatellite repeats = 90% of all HNPCC cases - slow if any accumulation of polyps - mutations in polyps increase rapidly leading to cancer |
|
|
Hybrid Genes & Cancer |
changes in the # & structure of chromosomes are common in cancer cells - most are nonspecific while some are specific to certain cancers |
|
|
Types of Chromosomal Aberrations |
1. translocations - Philadelphia chromosome forms hybrid gene causing CML (9 & 22) 2. deletions 3. chromosome loss 4. aneuploidy 5. duplications 6. amplification of certain genes |
|
|
Karyotype of a Cancer Cell |
changes in # & structure of chromosomes is common |
|
|
Identifying Cancer Causing Mutations |
1. cancer genome sequencing 2. genome-wide association studies goals: catalog all cancer-causing mutations; develop new diagnostic tools & drugs for treatment |
|
|
Epigenetics & Cancer |
abnormal DNA methylation is common in many cancers - demethylation - hypomethylation - hypermethylation *anormal imprinting of NOEY2 gene is associated with breast cancer |
|
|
Targeting Therapies |
focus only on cancer cells |
|
|
Targeting Therapies: CML |
Gleevec = drug that competes for ATP binding site - BCR-ABL protein - keeping signal molecule inactive & prevents cell from completing cycle & dividing |
|
|
Targeting Therapies: Breast Cancer |
cell surfce receptor HER2 receives external signal to initiate signal transduction & start cell growth/division *activated in breast cancer cells causing continuous division - herceptin binds to HER2 & blocks signal which signals immune system to attack cancer cells |
|
|
Cancer & Environmental Factors |
- certain viruses (HPV, herpes, epstein barr) - radiation - chemicals - lifestyle choices (sun exposure & smoking) - internal chemical mutagens (reactive oxygen species) |
