Cell Cycle pt. 2 Flashcards
(45 cards)
tumors
lesions that may or may not be neoplasms
neoplasms
abnormal growth with abnormal regulation, benign or malignant
cancer
malignant neoplasm
metastasis
secondary growth of cancer at a different location
initiation of carcinogenesis
simple mutation in one or more genes that control key regulatory pathways of cells
genotitic even (change in DNA sequence)
Promotion of carcionigenesis
selective functional enhancement of signal transduction pathways that were induced by initiator by continous exposure
epigenetic event, change in gene regulation
Progression of carcinogenesis
continuiing change of the basically unstable karyotype
clastogenic event
Things to know about initiation
irreversible
no threshold
caused by chemicals, radiation, ROS, viruses
change in cellular DNA
single mutation, chromosomal translocation, gene amplification
can lead to activation of onocogenes and inactivation of tumor supressor genes
Things to know about promotion
occurs over long span of time
reversibly in early stages, lifestyle changes may prevent
involves gene activation or repression such that latent phenotyp of intiated cell becomes expressed through cellular selection and clonal expansion
there is a threshold
can inhibit cell death of initiated cells
monoclonal tumors
come from one type of cell
polyclonal tumors come from
many typs of cells
Things to know about progression
complex genetic changes
irreversible gene expression changes
evolution of karyotypic instability
selection for optimal growth in repsonse to cellualr environment
results in the conversion of benign tumors to malignat ones and maybe metastasis
Cancer cells evade death by
being self sufficient, using growth signals, becoming insensitive to inhibitory signals, acquire limitiless replcaition potential, avoid immunology, promote inflamation, reprogram metabolism, sustain angiogenesis, so cool
oncogenes
cellular genes that stimulate cell division and/or growth
loss of regulation can lead to enhanced expression of these proteins and tell the cell “Divide! Divide!” (unregulated cell division and growth)
tumor supressors
cellular genes that serve to check or inhibit cell division
loss of expression of these proteins leads to cell growth or cell division
oncogenes are always
dominant mutations/overexpressions
they result from a gain of function mitation
only one of the two alleles needs to be activated for it to affect cell
rarely in germline inheritance
Three forms of oncogenes
cellular proto-oncogenes that have been captured by retrovirus
virus specific genes that behave like cellular proto-oncogenes that have been mutated
cellular proto-oncogenes that have been mutated
Raus Sarcoma
chicken
src oncogene
non-receptor TK
colon carcinoma
oncogeneic element in type 1 transducing viruses
cellular oncogene carred in retrovirus
basically, when retroviruses go into cellular DNA, they leave and take oncogenes with them
oncogenic element in type 2 non-transducing viruses
cellular oncogene activated by proviral insertion/integration
basically, virus goes into genome and changes promoter (oncogenese can be promoted)
oncogenic element in type 3 non-transducing long latency viruses
retroviral transactivating protein disrupting normal regulation of cellular transcription
retrovirus activates disrupting DNA (?)
oncogenic element in type 4 retroviruses that contain an envelope that signal
inappropriate cellular signaling resulting from viral enveleop/cell receptor interactions
acts like a mitogen
conversion of protooncogenes to oncogenes: truncatoin
loss of regulatory domain
product is over active
conversion of protonocogenes to oncogenes: point mutation
in coding region-unregulated product
in promoter or enhancer-overproduced
