cancer Flashcards
intrinsic hallmarks of cancer
identify loss of normal proliferative controls: growth signal autonomy, resistance to inhib growth signals, unlimited replicative capacity, reprogramming of cell metabolim.
resistance to apoptosis. increases in genetic instability - more mutations
extrinisic hall marks of cancer
induction of angiogeneisis (solid tumours dev vasculature for O2 and nutrients), metastatic potential (cells invade surrounding tissue and enter blood/lymphatic system), evasion of immune destruction (cells recruited and activated in tumour microenvironment product cytokines to suppress immune response).
properties of oncogenic cells
Altered morphology || loss of contact inhibition || anchorage independence|| immortalisation (indferinite proliferation) || reduced requirement for growth factors || high saturation density || increased glucose transport || tumourigenicity (express many hallm arks of cancer cells)
what genetic alterations cause cancer
small changes - single base change or indel (frameshift). Structural changes - deletion, inversion, etc.
What are Ras proteins
GTPases that act as signal transducers between signals received by plasma membrane-bound receptors and intracellular effector pathways. activated by recruitment of GEFs to membrane. Ras-GDP inactive.
How is expression of myc gene deregulated
retroviral insertion, mutation of control regions, genomic amplification, chromosomal translocation, persistent stimulation by upstream oncogenic activity. dereg of wt Myc is oncogenic.
new info for essays
There is also some evidence that non-coding RNAs are involved in tumorigenesis.
using p16INK4a genes which is deleted in human cancers and studies have shown reintroduction can inhibit tumour growth. More evidence from immunohistochemistry samples - stain tissue samples w antibodies that bind to protein encoded by tumour suppressor gene - normal tissue staining should be present but in cancer cells - may be absent.
Comparative genomic hybridization has since revealed various genes that can be amplified or deleted in cancer.
To date, ten tumor suppressor genes, all of which are involved in the regulation of genomic integrity, have been associated with hereditary breast cancer
Alterations in upstream components of the PI3K pathway, such as receptor tyrosine kinases, and downstream components such as AKT are frequent in breast cancers. The PTEN tumor suppressor antagonizes the PI3K pathway. Loss of PTEN function, and activating mutations in or amplification of the gene that encodes the PIK3 catalytic subunit (PIK3CA) are both common.
