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28 Cards in this Set

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four things APC regulates
1. amount of free B-catenin
2. microtubule assembly
3. regulatory role in apoptosis
4. progression of G1 to S
APC gene mutation happens from germ line trunkation and effects care taker genes "caretaker efect"
sporadic polyps which result in acquired mutation affects what genes
gatekeeper "gatekeeper effect"
how does B-catenin effect differentiation and transcription
decreases differentiation and increases transcription
how does the APC mutation effect B-catenin
its associated protein is unable to bind B-cat or microtubules leading to an increase in B-catenin in cells
how does a decrease in B-catenin affect apoptosis
increases
how does B-catenin affect microtubules
makes them faulty leading to less efficient mitosis
three types of neoplasms that may result from APC mutation
Tubular adenoma (benign - colon polyp)
adenocarcinomes (w/ mixed glandular + neuroendocrine differentiat
what inhibits B-catenin's effect on transcription and causes apoptosis
NSAIDS
cells capable of producing peptides that can function as hormones or paracrin mediators
neuroendocrine cells
grade of typical carcinoid
low
grade of malignant carcinoid
intermediate
grade of sm. neuroendocrine carcinoma
high
grade of lg neuroendocrine carcinoma
high
Notch promotes the differentiation into what kind of neuroendocrine cells
exocrine
Delta promotes the differentiation into what kind of neuroendocrine cells
endocrine
how does notch effect Hes
stimulates
how does notch effect bHLH
inhibits
notch has what effect on the cell cycle
causes cell cycle arrest
how does SHH effect the development of pancreatic progenitor cells
does not effect - it stimulates the making of intestinal cells
how migh one develop insulinoma (tumor producing insulin)
w/o notch - increase in ngu - endocrine fate - glucagon cells appear first then insulin and somatostatin
excess ACTH is may be produced by a tumor (e.g in SCCL) and cause what syndrome
Cushings
organoid pattern
a carcinoid marked by a 3D clusters surrounded by blood vessels
non-neoplastic bronchial dialtion, benign endocrine proliferation, and dysplasi
Bronchiectasia
what causes facial flushing
carcinoid syndrome
what is a significant regulator of carcinoid development
notch

notch activates Hes-1 which activates p48 which leads to exocrine fate.

if notch is inhibited then you have an increase in endocrine fate and could possibly develop insulinemia
the two ways inflammation contributes to carcinogenesis
1. generation of promutagenic reactive oxygen species
2. increased cell turnover
Ulcerative colitis (autoimmune)
Hepatitis C
chronic pancreatitis
peptic ulcer disease
may lead to malignancy due to
inflammation
virus that through binding mimics mutatio nor delection of Rb and p53 genes
HPV