3.2 - Biology of Cancer Flashcards
What is Cancer
- cells divide uncontrollably and invade other tissues
Benign VS. Malignant Tumour
Benign
- grows slowly
- well-defined boundary (encapsulated; so don’t invade other tissues)
- not invasive
- well-differentiated
- low mitotic index (not many cells are dividing)
- does not metastasize
Malignant
- grows rapidly
- not ecapsulated (invades)
- poorly differentiated
- high mitotic index
- metastasizes
Types of Benign Tumours
1) Lipoma - fatty tissues
2) Leiomyoma - arises in smooth muscle tissue
3) Meningioma - arises from meninges
Types of Malignant Tumours
1) Carcinoma - epithelial tissue
2) Adenocarcinoma - glandular/ductal tissues
3) Sarcoma - mesenchymal tissues (supports bone, muscle, and fat)
4) Lymphoma - lymphatic tissues
5) Leukemia - blood forming cells
Carcinoma In Situ
- originates in epithelial or glandular tissue
- pre invasive (bc it has not yet invaded)
- cancer cells that have not yet invaded surrounding tissue (has NOT broken through basement membrane)
Characteristics of Cancer Cells
1) Decreased need for growth factors
- normal cells require signals for when to grow and divide
- cancer cells just keep growing
2) Lack contact inhibition
- normal cells stop growing when they touch neighbouring cell
- cancer cells ignore this
3) Anchor dependence
- normal cells are attached to a surface
- cancer cells are not attached to anything
4) Immortality
- cancer cells can divide infinitely bc they have telomerase to maintain their chromosomes
Proto-Oncogenes VS. Oncogenes and Tumour-Suppressor Genes
Proto-Oncogenes
- normal genes
- regulate cell growth and protein production
- become oncogenes, when mutated
Oncogenes
- mutant gene that causes uncontrolled proliferation
Tumour-Suppressor Genes
- aka anti-oncogene
- help control cell growth
How are oncogenes activated
- RAS regulates cell growth (acts a switch that turns growth signals on/off)
- point mutation in RAS causes switch to get stuck on = uncontrolled proliferation
Types of Translocation that Sustain Proliferative Signalling
1) Burkitt Lymphoma
2) Chronic Myeloid Leukemia
3) Gene Amplification
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What is Genomic Instability
- increased tendency for cells to accumulate mutations
- genetic errors can lead to activation of oncogenes or de-activation of tumour-suppressor genes
Caretaker Proteins: encodes for proteins involved in DNA repair
Chromosomal Instability - changes in chromosome # and structure
- results in chromosome loss, loss of heterozygosity (2nd copy provides protection)n
- chromosomal amplification (extra copies can lead to overexpression of oncogenes)
Telomeres
telomeres: caps at the end of chromosomes
- everytime a cell divides, telomeres shrink
- when it becomes too short cell is signalled to stop dividing
- cancer cells have an enzyme - telomerase - which extends telomeres and allows cells to continue dividing
What is Angiogenesis
angiogenesis: formation of new blood vessels
- they need more blood vessels to be supplied with nutrients and oxygen to continue growing
- cancers secrete angiogenic factors that support blood vessels and help endothelial cells migrate to tumour
How cancer cells support their own growth
1) Warburg Effect
- cancer cells prefer to use glycolysis instead of oxygen
- cancer cells us by products of glycolysis to help them build new cell structures and continue growing
- warburg effect is driven by inactivation of tumour-suppressor genes
Reverse Warburg
- cancer cells influence surrounding cells to witch to glycolysis so they can increase their energy supply from the byproducts
Resisting Apoptosis
- defects in intrinsic and extrinsic pathways provide resistance to apoptosis
Intrinsic Path
- triggered by internal signals (DNA damage)
- normally activates apoptosis
- mutations (p53) disable this pathway
Extrinsic Path
- activated by external signals from other cells or receptors
- cancer cells can block receptors from receiving apoptotic signals