10 - Cancer (Unfinished) Flashcards
Anaplasia
Loss of cellular differentiation
Pleomorphic
Variable in size and shape
Stroma
General word for “supporting structure”
Metastasis
Ability to spread beyond tissue of origin, most deadly characteristic of malignant tumors
Carcinoma
cancer arising from epithelial tissue
Adenocarcinoma
cancer arising from ductal or glandular structures
Carcinoma in situ (CIS)
Preinvasive epithelial tumours of glandular or squamous cells origin. Have not yet invaded surrounding stroma, not considered malignant.
Contact Inhibition
Three stages of Cancer
- Tumor initiaion (inital cancer cell)
- Tumor promotion (population of cancer cells increase, w/ addition mutations
3.Tumor progression (metastasis)
Point Mutations
alteration of one or a few
nucleotide base pairs / can have profound effects on activity of resultant proteins
Driver mutations
Mutations that “drive” the progression of cancer
Passenger mutations
Mutations that don’t contribute to malignancy, just random events (incidental)
Chromosome translocations
Section of one chromosome is translocated to another chromosome, large change in chromosome structure
Gene amplification
Instead of normal two copies of gene, tens or even hundreds of copies are present.
Example: gene expression of HER2 proteins
Clonal Proliferation Model
Selective advantage cancer cell has over neighboring cells = it can replicate faster than nonmutant neighbors
Proto-oncogenes
Normal genes that direct protein synthesis and cellular growth
Oncogenes
Mutated proto-oncogenes cells, operate independent of body regulatory mechanisms, allows uncontrolled growth
Burkitt Lymphoma
Cancer where translocation changes normal chromosomes to produce oncogenes and abnormal B lymphocytes.
Anti-oncogenes
Tumour supressing genes, must be inactivated for caner proliferation to occur.
P53
Referred to as “Guardian of the Genome” Monitors cellular stress and activates caretaker genes to repair genetic damage, inactivation requires at least two mutations
Hayflick Limit
Limit to cellular division
Telomeres
Cap on end of chromosome, “ticket” that must be used in order to divide, limits cell division
Telomerase
Enzyme that maintains telomeres, usually only active in gonads, but is also activated by cancer for unlimited proliferation
Angiogenesis
Production of new blood vessels.
Cancers secrete angiogenic factors to form vessels that support them.
Warburg effect
aerobic glycolosis, allows cancer cells to continually produce lactate which is a source of molecular building blocks
Intrinsic controlled apoptosis
Monitors cellular stress, if cell can recover, activation of BAX. If cell must be destroyed, activation of BAK. (regulate release of pro-apotoptic molecules)
Extrinsic controlled apoptosis
Dormant until death receptor is activated by BAK
Anoikis
Induction of apoptosis when a cell has seperated from its ECM attatchment
Epithelial-mesenchymal transition (EMT)
Model for transition of cancer cells to metastatic cancer cells
-occurs normally in embryonic development and wound healing
1.Transition from epithelial like cells to more undifferentiated cells
2.Undiferentiated cells avoid anoikis, enter circulation and spread,
Intravasation
Extravasation
Tumour-Initiaitng Cells (TICs)
Dormancy
a stable non-proliferating state that is reversible
oncolytic viruses
Viruses that specifically attack cancer cells
Stage I Cancer
Stage II Cancer
Paraneoplastic Syndromes
Cachexia Syndrome
leukopenia
Thrombocytopenia
Asthenia
