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G.I & Nutrition > GI Cancers Small Bowel > Flashcards

GI Cancers Small Bowel Flashcards

1
Q

2 most common malignant epithelial tumors in GI tract

A

adenocarcinoma, neuroendocrine tumor

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2
Q

T/F most neuroendocrine tumors are of the GI tract

A

T, not a common kind of tumor but most often is GI

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3
Q

Risk factors for adenocarcinoma in the small bowel/colon

A

age (>50 should screen), diet, environment, obesity, genetics, ibd

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4
Q

Is adenocarcinoma more common in small bowel or colon?

A

colon

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5
Q

By the time you have an adenocarcinoma, most _____ genes have been knocked out.

A

APC

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6
Q

Most common sequence of gene knockouts in adenocarcinoma of colon.

A

85% of colon cancers: point mutation in APC leading to stop codon + 2nd hit of gene rearrangements/loss of chromosome –> 10 years for additional epigenetic/genetic changes before invasive –> metastases (take about 60 years)

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7
Q

_____ are polypoid masses of dysplastic epithelium with no invasion.

A

adenomas

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8
Q

Tx of adenoma

A

resection of adenomatous polyp –> can prevent transformation to adenomatous dysplasia and consequent carcinoma

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9
Q

In the colon, when does adenoma become adenocarcinoma

A

once the polyp invades into submucosa –> no metastatic ability until in that compartment (lymph nodes)

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10
Q

In the small bowel, esophagus, stomach, when does adenoma become adenocarcinoma

A

when it invades the lamina (lymph nodes closer than in colon so can metastasize)

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11
Q

Genetic components of colon cancer

A

35% due to genetic predisposition
Dominant: hereditary nonpolyposis colon cancer, familial APC, juvenile SMAD4/ALK3, Peutz-Jeghers LKB1
Recessive: myh

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12
Q

What part of the colon has the highest susceptibility to adenomas?

A

cecum

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13
Q

Crypt proliferation sequence

A

stem cells proliferate –> repair replication mistakes/get rid of defective cells –> migrate up –> differentiate –> die

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14
Q

Wnt signaling pathway

A

When there is no wnt to bind the frizzled receptor, multimeric beta catenin is phosphorylated by the protein group (apc, axin, gsk3b) –> proteosomal destruction of beta catenin –> reduced monomeric and multimeric beta catenin (these two are in equilbrium)

When wnt binds frizzled receptor, there is no phosphorylation of multimeric beta catenin –> increased level of monomeric beta catenin –> nuclear binding to Tcf –> upregulation of genes like cmyc, etc. involved in proliferation

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15
Q

Which cells in GI tract make wnt?

A

perifibroblastic cells in base of crypt where stem cells reside –> physiologic cell proliferation

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16
Q

Wnt gradient in GI mucosa

A

highest in the base of crypt where stem cells proliferate and lower at the top of the crypt where cells are differentiating

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17
Q

Functions of beta catenin in GI mucosa

A
  1. upregulate proliferation of stem cells

2. bind to intracellular portion of cadherin and involved in cell-cell adhesion

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18
Q

How does colon cancer relate to Wnt?

A

with knockout of APC and other proteins involved in phosphorylation of betacatenin, can have too much beta catenin –> messed up regulation of cell proliferation in crypts –> adenoma + more mutations = cancer

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19
Q

Staging of colon cancer

A

TNM

20
Q

T/F colonoscopy + resection of adenomas reduces risk of colon cancer

A

T

21
Q

Through which molecular classification do 85% of colon cancers arise?

A

chromosomal instability neoplasm (CIN)

22
Q

Through which molecular do 15% of colon cancers arise (the portion that don’t arise b/c of chromosomal instability neoplasms/CIN)?

A

microsatellite instability –> germ line HNPCC/lynch syndrome or CpG island methylation (CIMP)

23
Q

Gains or losses of whole or parts of chromosomes frequently occurring with each cell division resulting in karyotypic cell to cell variability

A

chromosomal instability = CIN

24
Q

Uncontrolled methylation of CpG in promoter region leading to gene activation

A

CIMP= cpg island methylator phenotype

25
Q

Insertions or deletions in areas of di and tri nucleotide repeats.

A

MSI = microsatellite instability

26
Q

CIN arises from collapse of what DNA feature?

A

fork collapse due to DNA replication stress (decreased dNTP pool,DNA damage blocking replication, inaccessibility due to tertiary structure) leads to breaks and recombination and missing bits of chromosomes

27
Q

CIMP arises from what DNA feature?

A

methylation of cytosine in CpG islands in promoter regions is normal but when hypermethylated, can shut off key genes

28
Q

Microsatellite instability arises from what DNA feature?

A

normally di and trinucleotide repeats but are prone to slippage leading to deletions via premature stop codons or formation of loops

29
Q

How does DNA mismatch repair work?

A

in areas of microsatellite instability, there is a set of MSH and PMS proteins that recognize the errors and repairs them –> hypermethylation or germline hits can knock these guys out

30
Q

How does base excision repair work?

A

Guanine can be easily oxidized to look like thymidine –> can disrupt the DNA being made–> MTH1 can remove OH-G from the nucleotide pool and OGG1 can remove it once incorporated into DNA and MYH can remove misincorporated A on complementary strand

  • recessive germline hits can knock these guys out
31
Q

How does familial adenomatous polyposis occur?

A

germ line APC mutation + somatic hit = Knudson two hit hypothesis –> multiple small bowel adenomas –> each could become a cancer over 10 years –> results in a really high risk of cancer at an early age + extraintestinal manifestations (note that fundic gland polyps don’t increase their risk of gastric cancer)

*rare

32
Q

3 common extraintestinal manifestations of FAP

A

desmoid tumors, osteomas, CNS Turcot’s syndrome

33
Q

Which hits are required in hereditary non-polyposis colon cancer?

A

original hit in DNA mismatch repair + 2 hits in APC + cancer hits

34
Q

What mismatch repair genes are implicated in HNPCC?

A

hMLH1,2,6 and PMS2 –> lynch syndrome

35
Q

T/F HNPCC are linked to other malignancies

A

T –> colorectal adenocarcinoma, endometrial, ovarian, pancreatic, etvc

36
Q

Muirr-Torre Syndrome

A

HNPCC w/ sebaceous lesions + GI malignancy

37
Q

Turcot’s Syndrome

A

GI+brain: GI tumors and GBM (HNPCC) or GI tumors and medulloblastoma (FAP)

38
Q

Is there a germline mutation that can lead to hypermethylation in states in colon cancer?

A

no –> in the course of tumor evolution can sporadically acquire the changes necessary to become cancer

39
Q

which gene _____ is highly mutable in microsatellite instability repair processes.

A

hMLH1 –> 90% due to promoter hypermethylation –> BRAFV600E is a common mutation in these cases but not germline cases

40
Q

IHC for mismatch repair proteins

A

MSH2 and MLH1

41
Q

Which gene is commonly mutated in excision repair?

A

myh –> missense mutations leading to somatic transversions –> recessive, caucasian, multiple adenomas like FAP (but no germline mutations in FAP)

42
Q

Which colon polyps have no malignant potential?

A

hyperplastic colon polyps (kras)

43
Q

Are inflammatory/filiform polyps dysplastic?

A

no

* occur due to IBD repair or sporadically

44
Q

What is a juvenile polyp?

A

Most common polyp in pediatrics and is due to SMAD mutations –> usually not individual risky for malignancy …

however, juvenile polyposis which is due to germline SMAD4 mutations has a definite increased risk of cancer

45
Q

What gene mutations are responsible for 50% of Peutz-Jegher’s Syndrome and how does the syndrome present?

A

STK11/LKB1 –> mucocutaneous melanin pigmentation, hamartomatous polyps in GI tract, increase risk of all cancers (95%)

46
Q

What mutations lead to epithelial tumors with neuroendocrine differentation?

A

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G.I & Nutrition (43 decks)

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