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GI > Cancer: Small Bowel & Colon > Flashcards

Cancer: Small Bowel & Colon Flashcards

0
Q

What are the common benign GI tumors?

A

(1) leiomyoma
(2) lipoma
(3) neuroma
(4) Schwannoma

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1
Q

What malignant GI tumors are derived from epithelial cells?

A

(1) adenocarcinoma

(2) neuroendocrine tumor

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2
Q

J: This refers to clonal, polypoid mass of dysplastic epithelium with no invasion.

A

What is an adenoma?

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3
Q

In the colon, when is an adenoma considered cancer?

A

When it invades the submucosa.

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4
Q

In the small bowel, when is an adenoma considered cancer?

A

When it invades the lamina propia.

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5
Q

What gene is reliably mutated in adenomas?

A

APC gene.

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6
Q

What percentage of cases of colorectal cancer are due to genetic predisposition?

A

35%.

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7
Q

What are the genetic variants of colon cancer and the genes associated to them?

A

(1) hereditary nonpolyposis colon cancer (DNA mismatch repair)
(2) familial adenomatous polyposis colon cancer (APC)
(3) juvenile (Smad4, Alk3)
(4) Peutz-Jeghers (LKB1)

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8
Q

What happens to the GI epithelium in the absence of Wnt signaling?

A

(1) Beta-catenin is phosphorylated by the complex of APC, AXIN and GSK-3b.
(2) The phosphorylated beta-catenin is degraded.
(3) No cell proliferation.

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9
Q

What happens to the GI epithelium in the presence of Wnt signaling?

A

(1) Wnt binds to the Frizzled receptor.
(2) Phosphorylation of beta-catenin is inhibited.
(3) The monomeric beta-catenin accumulates in the cytoplasm and acts as a transcription factor (in conjunction with Tcf) for genes involved in cell proliferation.

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10
Q

Where in the epithelial architecture is Wnt most prevalent?

A

In the base of the crypts.

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11
Q

What happens if APC is knocked out?

A

Since beta-catenin cannot be phosphorylated, the cell is in a constitutively proliferative state.

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12
Q

What is the first step done when an adenoma is discovered?

A

Surgically remove it.

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13
Q

What is CIN?

A

Chromosomal instability. Gains or losses of whole or parts of chromosomes, frequently occurring with cell division resulting in karyotypic cell-to-cell variability.

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14
Q

What is CIMP?

A

CpG island methylator phenotype. Uncontrolled methylation of CpGs in promoter regions, leading to gene inactivation.

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15
Q

What is MSI?

A

Microsatellite instability. Insertions or deletions in areas of di- and trinucleotide repeats. This can lead to slippage during DNA replication.

16
Q

What are sources of DNA replication stress?

A

(1) decreased dNTP pool
(2) DNA damage, blocking replication
(3) inaccessibility due to tertiary structure

Can lead to fork collapse, breaks, recombination, CIN.

17
Q

What are the 4 major genes associated with DNA mismatch repair?

A

MSH2, MSH6, MLH1, PMS2.

18
Q

What results from the oxidation of guanine?

A

8-hydroxyguanine (8-OH-G), which is recognized as thymine by DNA replication enzymes.

19
Q

In what 3 ways can problems associated with guanine oxidation be solved?

A

(1) removal of 8-OH-G from the nucleotide pool (MTH1)
(2) removal of 8-OH-G once incorporated into the DNA (OGG1)
(3) removal of mis-incorporated adenine (MYH)

20
Q

What condition is associated with a germ line mutation in the APC gene?

A

Familial adenomatous polyposis.

21
Q

In FAP, what segments of the GI tract are at a particularly increased risk of adenocarcinoma?

A

The small bowel. Dysplasia can occur in the stomach, but the risk of gastric cancer is not increased.

22
Q

What are some extra-intestinal manifestations of an APC gene mutation?

A

(1) desmoid tumors
(2) osteomas
(3) CNS tumors

23
Q

What disorder is characterized by germ line mutations to DNA mismatch repair genes?

A

Hereditary non-polyposis coli.

24
Q

J: This refers to the presence of HNPCC and sebaceous lesions.

A

What is Muir-Torre syndrome?

25
Q

What is Turcot’s syndrome?

A

The presence of GI malignancies and brain tumors. Either:

(1) HNPCC and glioblastomas
(2) FAP and medulloblastomas

26
Q

What mutation is common in colon cancers due MSI caused by hypermethylation of promoters (rather than a germ line mutation)?

A

BRAF V600E.

27
Q

What is the most common small GI polyp?

A

Hyperplastic colon polyp.

28
Q

Is a polyp an adenoma?

A

No.

29
Q

J: These GI polyps are not dysplastic or cystic and frequently result from the repair of inflammation.

A

What are inflammatory polyps?

30
Q

J: This GI polyp is not dysplastic and is associated with Smad4 mutations.

A

What is a juvenile polyp?

31
Q

Does the presence of a juvenile polyp indicate an increased cancer risk?

A

Not singly. Multiple polyps, juvenile polyposis, carries a 10% increased risk.

32
Q

J: This GI polyp is characterized by arborizing smooth muscle.

A

What is a hamartomatous polyp?

33
Q

What is Peutz-Jegher’s syndrome?

A

An autosomal dominant condition characterized by:

1) mucocutaneous melanin pigmentation
(2) hamartomatous polyps
(3) increased risk of cancer (not strictly in GI

GI (39 decks)

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