Neoplasia 3 Molecular Basis: Other Factors Leading to Cancer Flashcards
type of metabolism that cancer cells tend to use despite what conditions? this is called what?
used to visualize tumors?
is it cancer specific?
why undergo this type of metabolism and not normal way?
is there still oxidative phosphorylation?
how is warburg effect triggered in growing cells?
important points of crosstalk between what two things? examples 3
- p- effect?
- RTK- this causes what to happen? important enzymes? 2
- M- this does what?
tumor suppressors often inhibit what?
Autophagy- in what conditions would this occur?
friend? foe?
Evasion of apoptosis
how is thsi a problem?
anoikis?
bio pathways that lead to programmed cell death
death receptor? apoptosis pathway most frequently disabled in cancer?
intrinsic pathway- stimuli? leads to release of? pro-apoptotic proteins? anti? third set of proteins? BAD and BAX will do what? this will bind to? caspase? caspases held in check via?
Extrinsic pathway- stim by? this leads to? protein? recruits? caspase? cross talk?
best established ways cancer disrupts apoptosis? specific cancer? chromosome? leads to cancer how?
this type and treatment?
other protein/gene involved with avoiding apoptosis? normal proteins that it uses?
extrinsic pathway and cancer- 2 ways?
evasion of apoptosis
Key Concepts- apop thorugh what pathways?
more common pathway disruption in cancer?
what gene fucked up in B-cell lymphomas?
in drug resistance?
cancer cells and immortality?
3 factors critical to immortality?
immortal
evasion of senescence- what would normally cause it?
Immortal
Evasion of mitotic crisis
what is mitotic crisis? normally what kills?
if mutated what happens? end result?
if in crisis what will help? 2 ways?
immortal
self renewal- comes from being what type of cell?
what allows self-renewal? name of the two types?
immortal
since cancers are immortal must contain what cells?
cancer stem cells from transformation of stem cells or conversion of somatic? ex?
treatments concerning cancer stem cells?
Angiogenesis:
without cant enlarge past?
neovascularization dual effect on tumor growth?
normal vessels made?
important for what process?
normal angiogenesis controlled by? so in cancer?
inhibitors?
local balance of angiogenic and anti factors influenced by what factors? 3
- lack of oxygen leads to? activates transcription of? these do what?
- mutations involving tumor suppressors?
- transcription of via what signaling?
Angiogenesis and treatment?
Key concepts
hypoxia leads to?
other factors regulate angio?
treatment outcome?
invasion and metastasis
result of what? major cause of? metastasis inefficient how?
2 phases of metastatic cascade?
invasion of ECM
structure of ECM? pathway to circulation?
invasion of ECM steps? 4
1st step- what is it? important for this?
cancer ex?
2nd step of invasion- accomplished how? cleavage products can cause? ex?
3rd step- normal epithelial cells have what that do what? in cancer?
4th step of invasion- what is it? go through what structure? movement stim by? ex?
second step in metastasis- vascular dissemination and homing of tumor cells
tumor cells vulnerable in circulation?
may enhance tumor cell survival? also enhances? emboli?
of interest for adhesion in tumor cells?
Vascular Dissemination and Homing of Tumor Cells
site circulating tumor leave cap to form secondary deposits related to? but observations say?
3 mechanisms for where tumor cells may go?
circ cells good at colonizing?
molecular genetics of metastasis development
why only some tumors metastasize? 4
Molecular Genetics of Metastasis Development
metastasis suppressor gene defined as?
metastasis oncogenes? 2 promote what?
evasion of host defense
if host cant take out tumor what does that mean?
tumor cells different type of tumor antigens?
4
Tumor antigens
products of mutated genes
get recognized by?
ex?
Tumor antigens
overexpressed or aberrantly expressed cellular proteins
ex? how is this make a response?
others?
Tumor antigens
Tumor antigens produced by oncogenic viruses
most potent of these are?
Tumor antigens
oncofetal antigens
what are they? when do you see them normally?
ex?
Tumor antigens
altered cell surface _____ and ______
tumors express these abnormally how? ex?
focused for diagnostic/ therapeutic?
for treatments?
Tumor antigens
cell type-specific differentiation antigens
what are these? importance of them?
ex?
antibodies for these?
stategy effective for?
anti tumor effector mechanisms
dominant branch of immune system?
CD8- especially what kind? correlates with better prognosis?
NK- important for? activated by? therapy?
M- do what? kill how?
immune surveillance and escape
what is it?
most are what type?
ways tumor cells evade/escape immune system?
5
activaiton of immunreg pathways ex?
evasion of immune surveillance
key concepts
Genomic instability. what is it? caused by? you get more of what?
usually happens when? defects in what DNA repair systems contribute to cancer?
cancer that arises from DNA mismatch repair?
what is it? hereditary? trouble arises from what type of mutation?
Hallmark of mismatch-repair defects? what are they? in tumor cells?
what genes? in HNPCC
what do you get with loss of nucleotide excision repair system? what is this? risk for?
Diseases with defects in DNA repair by homologous recombination. share what hereditary?
characterized by?
Ataxia-telangiectasia? gene mutated? its fucnction?
fanconi anemia complex? of interest?
familial breast cancer? involves? lack of these genes? will work with what proteins?
Cancers resulting from mutations induced by regulated genomic instability?
tumors of what? what important proteins? they do what?
genomic instability as enabler of malignancy
key concepts look over
cancer enabling inflammation
advanced cancer inflammation can do what? inflammation also does what for cancer?
cancer-enablign effefcts of inflammatory cells and resident stromal cells include? 6
important for evading immune destruction?
inflammation and treatment of cancer?
