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GI Week 3 > Lecture 22: Tumors of Large and Small Bowel > Flashcards

Lecture 22: Tumors of Large and Small Bowel Flashcards

1
Q

What is the cumulative probability of cancer in UC?

A

18% in 30 years of disease

Duration of disease, grade of dysplasia, DALM and primary sclerosing cholangitis are all risk factors

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2
Q

What are carcinomas?

A

Epithelial

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3
Q

What are sarcomas?

A

Mesenchymal

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4
Q

What are lymphomas?

A

Lymphoid

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5
Q

What is the adenoma carcinoma sequence?

A
  1. normal
  2. adenoma
  3. adenocarcinoma
    DOES NOT apply to neuroendocrine tumors
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6
Q

What is dysplasia?

A 
Defined histologically as that set of nuclear changes which denote that the cell has undergone a neoplastic change 
Only for EPITHELIUM
By definition, an adenoma is composed of dysplastic epithelium and has undergone neoplastic transformation
Histologic features
	i. hyperchromatic nuclei
	ii. irregular nuclear borders
	iii. high N:C ratio
	iv. dysplasia of high, medium or low
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7
Q

For the colon, where must the tumor penetrate in order to be called cancer? Small bowel?

A

Must penetrate the muscularis mucosa into the submucosa
Small bowel = any invasion into lamina propria
Based on when it can metastasize

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8
Q

What is APC?

A

Adenomatous Polyposis Colon cancer
85% of sporadic colon cancer arise from mutations in APC
Knowcking out both APC genes is sufficient to give adenoma
The “gate keeper” of the colon
Wnt pathway is essential to development of tumors (C-Myc)

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9
Q

What happens when there is Wnt signaling?

A

Production of a shitload of beta-catenin

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10
Q

Why do we study the neuroendocrine tumors when they only account for 2% of all malignant tumors?

A

Because 74% of the NETs are in the GI tract

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11
Q

What happens if there is no Wnt signaling?

A

Beta-catenin is degraded in the cytoplasm into toxic monomers

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12
Q

What is the role of beta catenin?

A

Serves as a transcription factor AND as an adhesion molecule (by binding with cadherin)

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13
Q

Normally, what does APC do in the cell?

A

It is part of the Wnt signaling pathway
It combines with the MULTIMERIC form of beta-catenin, thereby keeping the monomeric (and dangerous) form of beta-catenin low

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14
Q

What happens if APC is knocked out?

A

No APC means there is nothing to bind the multimeric B-catenin
Failure to bind multimeric B-catenin = more monomeric B-catenin
Monomeric B-catenin translocates in the nucleus and binds to Tcf (T cell factor)
Monomeric B-catenin and Tcf then upregulate a shitload of genes, one of those being C-MYC

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15
Q

What is the receptor of wnt called?

A

Frizzled

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16
Q

What are the colon cancers that have genetic component?

A
  1. Lynch
  2. FAP (APC gene)
  3. Juvenile
  4. Peutz-Jeghers
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17
Q

What are the percentage of sporadic colon cancers that arise from APC mutations?

A

85%

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18
Q

What are the key characteristics about familial adenomatous polyposis?

A

Germ line mutations in APC gene

The polyp location can first be found in the small bowel, particularly at the ampulla of Vater

19
Q

What is Turcot Syndrome?

A

Aka mismatch repair cancer syndrome
Mutation in MLH1, MSH2, MSH6 and PMS2 (all mismatch repair genes)
GI malignancies and BRAIN tumors
A type of HNPCC and also for FAP

20
Q

What are the key characteristics of Hereditary Non-Polyposis Colon Cancer (Lynch’s)?

A

10-15% of all colon cancers
Have a mutation in DNA mismatch repair genes like MLH1
Develops cancer at an early age because second hit makes progression much faster
Can lead to colorectal adenocarcinoma as well as endometrial malignancies

21
Q

What is the gene that is mutated in HNPCC?

A

MLH1 (MSH2, MSH6, PMS2 or the mismatch repair genes in general)

22
Q

What is CIN?

A

Chromosmal instability neoplasm
-gains and or losses of whole or parts of chromosomes
Occurs with each cell division resulting in karyotopic cell to cell variability

23
Q

Why can CIN be deleterious?

A
  1. Leads to Fork collapse (breaks, recombination)
  2. Puts stress onto DNA replication by
    i. decreased dNTP pool
    ii. DNA damage blocking replication
    iii. Inaccessibility due to tertiary structure
24
Q

What is MSI?

A

Microsatellite instability

Insertions or deletions in areas of di and tri nucleotide repeats

25
Q

What is CIMP?

A

CpG Island Methylator Phenotype

Uncontrolled methylation of CpG in promoter region leading to gene inactivation

26
Q

Why is CIMP deleterious?

A

Methylation of cytosine in CpG islands in promoter regions is a normal control mechanism for blocking transcription
Thus, HYPERmethylation states may shut off key genes

27
Q

What are the key characteristics of FAP/Gardners/Turcot’s?

A

An Adenoma
Polyp = ampulla of vater and has HUNDREDS of polyps
100% development to carcinoma if left untreated
FAP has no extraintestinal manifestations
Gardner’s and Turcots both have manifestations (in head/brain)

28
Q

What is HNPCC associated with?

A

Lynch can lead to colorectal adenocarcinoma (CRC) AND endometrial malignancies
So HNPCC can be associated with outside shit!

29
Q

So HNPCC can be associated with outside shit!

A
  1. Multi-torre syndrome
    -sebaceous lesions/GI malignancies
  2. Turcot’s syndrome
    -brain tumors
    Can also be medulloblastomas (for FAP)

Turcot’s syndrome is the same name for TWO DIFFERENT THINGS!!

30
Q

What is microsatellite instability due to?

A

MSI is due to the DNA mismatch errors which are particularly prone to occur in sequences of di/tri nucleotides
-can be germline or sporadic

31
Q

What is the significance of CpG island methylator phenotype?

A

This is SPORADIC most of the times
Example: MLH1 is methylated by a BRAF V600E mutation
Hypermethylation will turn of MLH1 sporadically (10% germline gene mutations, but methylation = sporadic)

32
Q

What is significant about MYH mutations?

A

A base excision repair gene

Can lead to adenomas Iook like FAP)

33
Q

What is a polyp?

A

A protrusion in the lumen of the GI tract
Etiologies are numerous
Can come from any tissue while mostly being epithelial

34
Q

What is the most common small polyp?

A

Hyperplastic polyp

35
Q

What are the types of polyps?

A
  1. pedunculated (stalk)
  2. sessile (flat)
    Can also separate into tubular vs. villous and stalk vs. flat
36
Q

What are the characteristics of hyperplastic polyps?

A 
Represent 90% of polyps
Found in colon
NOT DYSPLASTIC
NO propensity for carcinomas so it is benign as shit 
No need for surgery
37
Q

What are characteristics inflammatory and filiform polyps?

A

Results from repair of inflammation (UC and CD)

Not dysplastic and no cysts

38
Q

What are juvenile polyps?

A

Come about from SMAD4 mutations

No propensity for carcinoma

39
Q

What is the most common polyp in the pediatric population?

A

Juvenile polyp

40
Q

What is Juvenile polyposis?

A

Multiple juvenile polyps
Definite increased risk of cancer = 10%
Very rare
Comes from SMAD4

41
Q

What is SMAD4 associated with?

A

Juvenile polyposis

42
Q

What is a peutz-Jegher polyp? Significance

A

Hamartomatous
Can present as Peutz-Jegher syndrome (has black specks on lips and mouth)
BENIGN if no syndrome
If syndrome, then has some propensity for carcinoma progression

43
Q

What are benign etiologies of bumps?

A
  1. brunner gland
  2. lipoma
  3. leiomyoma (esophagus)

GI Week 3 (11 decks)

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