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Oncology > 13 & 14 - Colon Cancer > Flashcards

13 & 14 - Colon Cancer Flashcards

1
Q

Third most common cancer in the USA

A

Colon Cancer

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2
Q

Leading cause of cancer death in non-smokers

A

Colon cancer

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3
Q

Majority of colorectal cancers

A

Sporadic

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4
Q

Risk in general population of colorectal cancer

A

6 - 8%

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5
Q

Risk for those with personal history of colorectal neoplasia

A

15% - 20%

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6
Q

Risk for those with IBD

A

15% - 40%

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7
Q

Risk for those with Lynch Syndrome

A

80%

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8
Q

Risk for those with FAP

A

100%

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9
Q

Strongest risk factor for colorectal cancer in general population

A

Age

Upswing begins at 50

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10
Q

Other risk factors for CRC

A 
High red meat diet
Prior history of adenoma or cancer
Family history of adenoma or cancer
High fat diet
smoking
obesity
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11
Q

Protective factors for CRC

A 
High physical activity
Aspirin/NSAID use
High vegetable/fruit diet
High fiber diet
High folate/methionine diet
High calcium intake
postmenopausal hormone therapy
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12
Q

First degree family history of CRC

A

Shift screening 10 years earlier

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13
Q

Hereditary Colorectal Cancer Syndromes

A

Familial Adenomatous Polyposis (FAP)
Lynch Syndrome
Both involve germline inheritance of gene mutations
Autosomal dominant

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14
Q

Sporadic Cancer

A

Tumor initiation 30 - 50 years
Tumor progression 10 - 20 years
Carcinoma 6% risk - mean age 66 years

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15
Q

FAP

A

Tumor initiation 5 - 20 years
Tumor progression 10 - 20 years
Carcinoma 100% risk - mean age 40 years

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16
Q

Lynch Syndrome

A

Tumor initiation 30 - 50 years
Tumor progression 1 - 3 years
Carcinoma 80% risk - mean age 40 years

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17
Q

Clinical Features of FAP

A 
1% of all CRC
100 - 1000s of adenomas
APC gene mutations
Risk of extracolonic tumors (desmoids, duodenal cancer, thyroid, brain)
Risk of CRC 100% if untreated
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18
Q

Congenital Hypertrophy of the Retinal Pigment Epithelium (CHRPE)

A

Associated with FAP

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19
Q

Desmoid Tumor

A

Fibrous, non-malignant, obstruction is greatest risk
Surgery increases their risk.
They grow back bigger.

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20
Q

Diagnosis of FAP

A

APC gene mutations in >90% with classic polyposis
Family history: AD inheritance
Prevalence 1/8000
De novo mutations - 30% of carriers have no family history

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21
Q

Management of FAP

A

Sigmoidoscopy at 10 - 12 years and every 2 years to assess polyp burden
Colectomy
Upper GI surveillance for adenomas
Genetic counseling

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22
Q

Lynch Syndrome

A 
Most common hereditary CRC syndrome
5% of all CRC
Defective DNA mismatch repair
Mutations in MLH1, MSH2, MSH3, PMS2
Lifetime risk of CRC = 70 - 80%
Risk is markedly lower if we begin colonoscopies early
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23
Q

Lynch Syndrome - Clinical Features

A 
Striking family history (multiple generations)
Early (but variable) age at CRC diagnosis (mean 45 years)
Multiple primary cancers
Extracolonic cancers:
Endometrium
Ovary
Urinary tract
Stomach
Small bowel
Sebaceous carcinomas of skin
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24
Q

Lynch Syndrome - Mechanism

A

Failure of mismatch repair (MMR) genes

Microsatellite instability

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25
Q

Lynch Syndrome - Amsterdam Criteria

A 
Three or more CRC diagnoses in a family
Two or more generations
1 case is a first degree relative of the other two
One is affected by age 50
FAP excluded
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26
Q

Lynch Syndrome - Revised Bethesda Guidelines

A

CRC

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27
Q

Lynch Syndrome Screening Recommendations

A

Colonoscopy starting at age 20 - 25, repeat every 1 - 2 years
Transvaginal ultrasound & endometrial aspirate annually starting at age 25 - 35

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28
Q

Asymptomatic, no risk factors

A 
Start screening at age 50
Colonoscopy
Flexible sigmoidoscopy
CT colonography
Double contrast barium enema
Fecal stool tests (Guaiac-based fecal occult blood test or fecal immunohistochemical test) - Can't detect polyps, though...
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29
Q

Screening for patients risky enough to warrant colonoscopy

A 
History of adenomas
History of CRC
Family history of adenomas
Family history of CRC
IBD
Hereditary CRC Syndromes
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30
Q

Right colon symptoms

A

Occult bleeding
Obstruction
Anemia
Abdominal Mass

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31
Q

Left colon symptoms

A 
Gross bleeding
Obstruction
Anemia
Change in bowel habits
Pain
32
Q

Metastatic CRC Spread

A

Lymphatics:
Mesenteric nodes
Virchow’s nodes

Hematogenous spread:
Liver via portal circulation

33
Q

Types of polyps

A

Adenomas
Serrated sessile polyps
Hyperplastic polyps

34
Q

Adenomas

A

True pre-malignant lesions that have a risk for developing cancer
Blue means dysplasia
Lack of surface maturation
Proliferation extends to surface

35
Q

Hyperplastic polyps

A 
Benign
Pink
Saw tooth shape of surface epithelium
Normal surface maturation
No dysplasia
Proliferation restricted to crypts
36
Q

Pedunculated Adenomas

A

Nice stalk

Easier to excise than sessile

37
Q

Sessile Adenomas

A

Gotta resect

38
Q

Polypectomy is effective/curative if

A

Stalk margin has normal colonic mucosa
No lymphatic/vascular invasion
Tumor is not poorly differentiated

39
Q

Dysplastic Crypt

A

Earliest sign of an adenoma/adenocarcinoma to come
Never catch it at this point
If you can catch it (probably via familial setting) you can cure it before ever forming a polyp

40
Q

WNT Pathway

A

At rest, WNT is inactive
APC destroys beta catenin
WNT signaling prevents APC’s action and beta catenin remains intact. Proliferation!

41
Q

FAP - with regard to WNT pathway

A

Always on!
You don’t even need WNT.
It is a problem with APC
Beta Catenin never gets degraded!!

42
Q

Key protein in sporadic cases

A

Always MLH1 - but not due to a mutation

It is epigenetics! The promoter is methylated!

43
Q

MSH2 deficiency - Sporadic or Lynch?

A

LYNCH!!!

44
Q

2 Molecular categories of CRC

A

Microsatellite Instability

Chromosombal Instability

45
Q

CRC - Microsatellite Instability

A

Nucleotide-level mutations
Hypermutated (many at high frequency)
15% of CRC

Leads to HNPCC/Lynch (Germline Mutation of MLH1, MSH2, MHS6, PMS2, MMR genes)
OR
Leads to Sporadic MSI+ (Epigenetic silencing of MLH1 by hypermethylation of its promotor region)

46
Q

CRC - Chromosomal Instability

A

More macro genetic mutations
Non-hypermutated (low frequency)
85% of CRC

Leads to FAP (Germline mutation of APC gene)
OR
Leads to Sporadic CIN (Acquired mutations of APC, p53, DCC, KRAS, LOH)

47
Q

What genetic testing do we do on all cases of CRC?

A 
KRAS
BRAF
PIK3CA
MMR
Lynch
48
Q

TNM Classification (Tumor Node Metastasis) - Tumor

A

T - Primary Tumor
Tx - Primary tumor cannot be assessed
T0 - No evidence of primary tumor
Tis - Carcinoma in situ (intraepithelial or intramucosal invasion of lamina propria)
T1 - Tumor invades submucosa (start to develop risk of invasive tumor/metastatic invasion)
T2 - Tumor invades muscularis propria
T3 - Tumor invades through muscularis propria into subserosa or into pericolic/perirectal fat
T4 - Tumor directly invades other organs or structures and/or perforates the visceral peritoneum

49
Q

TNM Classification (Tumor Node Metastasis) - Node

A

N0 - No regional lymph node metastasis
N1 - Metastasis in 1 to 3 regional lymph nodes
N2 - Metastasis in 4 or more regional lymph nodes

50
Q

TNM Classification (Tumor Node Metastasis) - Metastasis

A

M0 - No distant metastasis

M1 - Distant metastasis

51
Q

Stage 1 Colorectal Cancer

A

25% of CRC
Cancer has grown through mucosa and invades muscularis
Treatment - Surgery to remove the tumor & some surrounding lymph nodes
5-year Survival 90%
Once you reach 5 years, recurrence is unlikely

52
Q

Stage 2 Colorectal Cancer

A

30% of CRC
Cancer grows beyond muscularis of the colon or rectum, but has not spread to lymph nodes
Treatment (colon) - Surgery +/- adjuvant chemo
Treatment (rectal) - Sugery, radiation, chemo

53
Q

Stage 3 Colorectal Cancer

A

25% of CRC
Cancer has spread to regional lymph nodes
Treatment (Colon) - Surgery and adjuvant chemo
Treatment (Rectal) - Surgery, radiation & Chemo
Survival - 40% to 80%

54
Q

Stage 4 Colorectal Cancer

A

20% of CRC
Cancer has spread to other areas of the obdy
Treatment - Chemotherapy, surgery to remove mets (liver/lung) in carefully-selected patients
Survival - Evolving

55
Q

CRC Prognosis Depends on

A

Histo (poor differentiation, vascular invasion)
Depth of invasion
Nodal involvement
Genetic alterations: -18Q LOH (bad), MSI (good)

56
Q

CRC Treatment

A

Surgery (Stage 1, 2, 3) - Try to remove isolated mets
Radiation (Rectal cancer) - Prevent local recurrence
Pharmaceuticals (Stage III Node+ and IV)

57
Q

CRC Pharmaceuticals

A

5-Fluorouracil
Irinotecan
Oxaliplatin

58
Q

5-Fluorouracil

A

Pyrimidine antimetabolite

59
Q

Irinotecan

A

Topoisomerase I inhibitor

Prevents re-ligation after cleavage of DNA by Topoisomerase I

60
Q

Oxaliplatin

A

Alkylating agent

Causes formation of bulky DNA adducts

61
Q

Irinotecan - Side Efects

A

Alopecia

GI toxicity

62
Q

5-Fluorouracil - Side Effects

A

Gi toxicity

63
Q

Oxaliplatin - Side Effects

A

Neuropathies

Cold tingly

64
Q

CRC Biologics

A 
Bevacizumab
Regorafenib
Aflibercept
Cetuximab
Panitumumab
65
Q

Bevacizumab

A

Ab against VEGF-A

May block angiogenesis and also stabilize leaky vasculature

66
Q

Regorafenib

A

Multi-targeted TKI

67
Q

Aflibercept

A

Binds to circulating VEGF
Costs $11,000/month
Prolongs survival by 1.4 months

68
Q

Cetuximab

A

Antibodies against EGFR

KRAS mutation means this drug won’t work!!

69
Q

Panitumumab

A

Antibodies against EGFR

KRAS mutation means this drug won’t work!!

70
Q

Bevacizumab Toxicities

A 
Bleeding
Thrombosis
Hypertension
Wound healing complications
Half life of about 3 weeks, wait at least 2 half lives before major surgery
71
Q

Cetuximab & Panitumumab Toxicities

A

Horrible rash

Rash predicts better outcome though so haaaayyy

72
Q

Types of cancers with a LOT of mutations

A 
Melanoma
Lung Cancer
Bladder Cancer
Esophagus
Colorectum

Mostly associated with toxins

73
Q

CTLA4

A

On T Cells
Brake on the immune system
Prevents T Cells from attacking body

PD1 is another receptor that does the same thing

74
Q

Who responds to PD1 inhibitors?

A

Mismatch Repair cancers!

Tumors with a ton of mutations!!

75
Q

Survival for those with metastatic disease

A

Systemic chemo - 3 years
Sometimes treat neoadjuvantly
If the metastases are “limited” you can CURE!

76
Q

Can you resect a liver met? - Criteria

A

Ability to resect all evident disease
Ability to leave a sufficient hepatic remnant (at least 2 contiguous remaining segments, adequate inflow and outflow, adequate hepatic volume and function) - >20% desirable

Oncology (23 decks)

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