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10 Cards in this Set

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talk about steroidal signaling and what cancers are typically involved:

talk about androgen inhibition:
estrogen production/reception involved in breast and uterine cancer.

androgen production/reception involved in prostate cancer

glucocorticoids are good at downregulating the immune system and so stop proliferation of lympocytes

in prostate cancer, you can downregulate the production of androgens by killing off the LHRH, so you have LHRH agonists that bind pituitary and turn off LHRH (pretend too much LHRH), stop LH, stop testosterone making. Also synthetic anti-androgens that competatively anatagonize the action of androgens.

also five alpha reductase inhibitors, stop androgen production from the adrenals?
what if we want to eliminate estrogens?
same deal - still use LHRH agonists to fool the pituitary into thinking there's too much LHRH and downregulate it - stop making LHRH, stop making LH, stop releasing estrogen.

also, AROMATASE INHIBITORS - remember that testoerone is the precursof for estrogen, need aromatase to make estrogen.

also, SERMS - anti-estrogens or estrogen receptor antagonists (tamoxifen is one of these). selective estrogen regulators.
what's the "druggable target" in CML? what does this drug also work on?

this kind of target - what breast cancer variant has something smiliar?
the ABL kinase. imatiniib binds the ATP biding pocket of ABL kinase.

GIST tumors - gastrointestinal stromal tumors have "ckit" which can be hit also by imatinib.

breast cancer has HER-2/Neu, which is a receptor-like tyrosine kinase - if overexpressing (oncogene), you have worse prognosis. can use Trastuzimab (herceptin). don't forget that it causes serious heart problems.
what are our anti-angiogenesis drugs?
This is genentech's baby - Bevacizumab - this binds VEG-F (beVa = VegF). Breast, lung, colon.

also Sunitinib! it's the VEG-F receptor's tyrosine kinase inhibitor. Renal cancer.
how do cancers outsmart drugs? examples? there's a mutation we need to know for the test here.
cancers are mutation factories - you can mutate the androgen receptors, the bcr-abl kinase's ATP pocket, the EGF receptor, etc.

know that sometimes the anti-drug you're giving can suddenly DRIVE the cancer (receptors mutate to be up-regulated by your anti-cancer drug). so removing the drug can then make people better. Seen with FLUTAMIDE, an anti-androgen that suddenly acts as an AGONIST instead of an ANTAGONIST (definitely seen in prostate cancer).

BCR-able mutates a lot. Dasininitib is the new drug for people failing imininatib. KNOW E255V mutation.
so, in the future, we're going to want to sequence the mutations in individual's tumors and design individual therapy. what's the problem with this?
each person's tumor contains lots of cells, and each can have its OWN mutations. no two patients have the same mutations.
if solid tumors represent a chaos of diferent mutations (even within one patient and especially between metatastatic sites in one patient), what's a strategy to deal with this?
maybe cancer stem cells? traditional chemotherapy spares stem cells, generally. maybe VEGF - stromal targets, not tumor, not prone to mutation and escape. Alpha particles.
what's an anti-androgen to be familiar with?
he mentioned flutamide a bunch.

seen patients go off the drug and have it save their lives. likely due to a mutation in the testosterone receptor that turned flutamide into a tumor driver.
how can resistances to treatment be discovered?
mapping mutations using sophisticated sequencing and 3d modeling software. though because tumors are heterogenous, later stage cancers may develop lots of tumor resistance strategies.
why are one kind of tumor (brain, pancreas, etc) complicated? what can be done to make it understandable?
it's been found that each different "kind" of cancer is really the result of dozens of separate mutations.

one brain cancer may be completely different from another, even if they're both glioboastomas.

each person's cancer is a different disease.

though it's been found that there are only so many pathways that can be messed with (around 12), meaning that you can begin to make sense of it.

also, targeting stem cells (if they're really driving cancers) might make be the trick to all of it.