Cancer Flashcards
(44 cards)
Where can oral and oropharyngeal cancers occurs most often?
Tongue , Tonsils, Oropharynx , Gums, Floor of Mouth
What kind of carcinomas are almost all oral cancers?
Squamous Cell Carcinoma
What is carcinoma in situ? How is it different from invasive squamous cell cancer?
The earliest form of squamous cell cancer that is still at the epithelium. Invasive cancer will have grown deeper into the layer of the oral cavity or oropharynx
What infections cause most of the squamous cell cancers of the oropharynx? Is it the same for the oral cavity?
Certain high-risk types of HPV can cause cancer in the oropharynx but is rarely related to the oral cavity.
What is the prognosis of HPV positive vs negative cancers?
HPV positive related cancers have a better outcome than squamous cell cancers that are HPV-negative
What are the two major classes of genes involved in tumorigensis?
Tumor Suppressor Genes and Oncogenes
What do oncogenes do in relation to cell proliferation? What is cell activity like in these cells?
Oncogenes promote cellular proliferation by up-regulation in tumor cells.
What do tumor suppressor genes do? What is cell activity like in tumor cells?
Tumor Suppressor Genes are supposed to negatively regulate cellular proliferation. In tumor cells, this gene is down regulated.
Cancer requires ______ and _____ to proceed.
Activation of oncogenes and inactivation of tumor suppressor genes
Where do mutations occur for oncogenes? What kind of mutations occur?
Oncogenes are mutated at the SAME amino acid position. Missense mutations are common.
Where do mutations occur for tumor suppressor genes? What kind of mutations occur?
TSG’s can be mutated through the protein length. Nonsense and frameshift mutations are most common.
What are the 3 pathways that can lead to cancer?
Cell Fate , Cell Survival and Genome Maintainence
Describe cell fate. What is favored between proliferation and differentiation?
Genetic alternation results in proliferation being favored over differentiation of cells. The accumulation of undifferentiated cells can make them malignant.
Describe Cell Survival. What allows the cancer cell to flourish?
Cancer cells divide abnormally as is due to autonomous alternations but surrounding healthy cells cannot keep up. As a result, cancer cells will grow too quickly, depleting nutrients. Cancer cells will develop a mutation that will activate growth even without Growth Factor
Describe genome maintenance.
Mutations in DNA repair factors can act by accelerating the acquisition of mutations that function through process of cell fate and survival.
What is commonly found over-expressed in epithelial tissue? How can it cause cancer?
Epidermal Growth Factor Receptor - Tyrosine Kinase.
Normally the EGFR requires GF to activate but mutations can allow for the EGFR to induce proliferation withOUT the ligand (ligand independent firing).
Describe the RAS mutation. Is it a tumor suppressor gene or an oncogene?
RAS is responsible for producing GTPases that are required to turn GTP into GDP to render the protein inactive. The RAS mutation causes is a single-nucleotide change at particular residues that stops it from turning GTP to GDP thus making the cell divide uncontrollably. RAS is an ONCOGENE.
What is the most common RAS mutation?
G12V (missense)
Describe FAT1 mutation. Is it a tumor suppressor gene or an oncogene?
FAT1 normally negatively regulates proliferation and drives differentiation. When active, it shuts off YAP/TAZ via a series of messengers that allows differentiation to occur instead. When mutated, FAT1 has a loss of function which allows YAP/TAZ to move forward with proliferation instead. FAT1 is a TUMOR SUPPRESSOR GENE.
What happens the 3 phases of the cell cycle? What serves as checkpoints for each phase?
G1 - Growth
S- DNA replication
G2-Chromosome Segregation
Eventually leading to mitosis. CDK or cyclin dependent kinases control the cell cycle by phosphorylating factors to allow for progression from one phase to the next.
Describe the CDKN2A mutation. What is another name for this gene. Is it a tumor suppressor or activator?
CDKN2A normally is induced when a cell needs to exit the cycle. The checkpoint also known at p16 is found between G1 and S. When mutated, CDKN2A/p16 is down-regulated thus allowing for cell proliferation. CDKN2A is a TUMOR SUPPRESSOR gene.
What are the 6 characteristics of apoptosis?
- Outer membrane blebbing
- Shrinking
- Condensation of nucleus
- Fragmentation of chromosomes
- Formation of cytoplasmic vacuoles
- Cell fragments generated via apoptosis are often swept up by other cells and phagocytes.
How is apoptosis signaled via the extrinsic pathway?
Death receptors are present on cells that induce the formation of DISC (death-inducing signal complex) when signaled. This recruits pro-caspase 8 and self-cleavage of caspase-8. The cleavage of the caspase-8 can activate caspase 3,6 and 7 causing destruction of cellular proteins.
Where is Cytochrome C released from ?
Mitochondrial Inner Membrane Space
