NRS 313 Study Guide - Final Guide: Chromone, Cervical Cancer, Cell Growth
Cancer and Genetics: Essential Concepts
• Tumors
o Benign
▪ Grow slowly
▪ Well-differentiated
▪ Encapsulated
▪ Non-invasive
▪ Do not metastasize
▪ Ex: moles or uterine fibroids
• Endothelial cells are under the control of estrogen. When
progesterone is higher these cells thicken. Sometimes we get a
benign tumor here. Cell growth signals are dysfunctional. If they
want to conceive, these can be a cause for infertility.
o Carcinoma in situ:
▪ early stages of growth
▪ Localized
▪ No penetration of BM=basement membrane
• Layer of cells between specialized tissue
▪ Well defined
▪ No metastasis and encapsulated
o Malignant= cancer is progressing
▪ Fast growing
▪ Poorly differentiated : (anaplasia)
• Not a specialized cell anymore
▪ Not encapsulated
▪ Invasive
▪ Spreads (metastasizes) to other tissues via blood stream or lymphatics
• Malignant vs. Benign tumors
o Benign (Not cancer) tumor cells grow only locally an cannot spread by invasive
or metastasis
o Malignant( Cancer) cells invade neighboring tissues, enter blood vessels, and
metastasize to different sites
o Contact Inhibition: When cells come in contact, their growth stops
o Angiogenesis: blood vessel formation
o Protease: made by cancer cells to cut through proteins
o Autocrine signaling: communicates to itself to replicate
o Telomerase: telomere caps protect ends of chromosomes. Cancer cells make their
own. Allows for the cancer cells to become invincible.
o Shrouded in own platelets: surrounded by fibrin mesh that allows for the cells
to go undetected, Natural killer cells cant find the cancer cells.
• Genetic Basis for Cancer
o Cancer incidence increases with age and exposure to carcinogens
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o Genetic instability
▪ genetic instability is often considered a hallmark of cancer.
▪ Mutations in DNA of gametes (male or female germ cell) is passed on to
offspring
o Genetic inheritance
▪ 50% inheritance rate with dominant gene
▪ 25% inheritance rate with recessive gene
o A culmination of genetic mutations over time
▪ Combined effect of genetics plus environment
▪ One or two mutations is not enough to cause cancer
▪ Tumor suppressor genes should “eliminate” cells that have DNA
mutations
• Mutations
o Mutations are relatively rare:
▪ DNA polymerase: Proofreads the code and corrects errors
• If it notices a significant mismatch it will stop the replication
• Important for inhibiting cancer
▪ Tumor suppressor genes: detect errors and schedule the cell for
apoptosis
o BRACA 1 and 2: in females we see an increase in breast and ovarian cancer if
these TSGs are mutated. In males we see prostate and colon cancer.
▪ These are dominant mutations
o P53: guardian of the genome. Strong tumor suppressor gene. Targets cells for cell
death
o Base pair substitution : still results in a good protein sequence
▪ (mis-sense mutation): Silent mutation. We don’t get the same replication
▪ One pair of bases are substituted for another within one codon
• The dog saw the car and ran.
• The dog saw the cat and ran.
o Frameshift substitution: results in a faulty and/or dysfunctional protein
sequence
▪ One or more pairs of bases are either deleted (missing pair) or inserted
changing the sequence of codons
• hed ogs awt hec ata ndr ant. (Non-sense mutation)
▪ changes entire amino acid combination
• Chromosomes
o DNA is coiled tightly around protein molecules forming chromatin
o When cell divides, chromatin condense into structures called chromosomes
o Somatic Cells have 23 pairs of chromosomes (Thus, 46 chromosomes), one of
each pair from mother and one from father. These are diploid cells.
o Gametes cells have half of each pair (thus, 23 chromosomes). These are haploid
cells
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Cancer and genetics: essential concepts: tumors, benign, grow slowly, well-differentiated, encapsulated, non-invasive, do not metastasize, ex: moles or uterine fibroids, endothelial cells are under the control of estrogen. If it notices a significant mismatch it will stop the replication. Important for inhibiting cancer: tumor suppressor genes: detect errors and schedule the cell for apoptosis, braca 1 and 2: in females we see an increase in breast and ovarian cancer if these tsgs are mutated. In males we see prostate and colon cancer: these are dominant mutations, p53: guardian of the genome. Targets cells for cell death: base pair substitution : still results in a good protein sequence (mis-sense mutation): silent mutation. These are diploid cells: gametes cells have half of each pair (thus, 23 chromosomes). These are haploid cells: chromosomes normally split. Chronic diabetes can be related to infertility: trisomy at chromosome 21=> down syndrome, non dysjunction error during neosis.