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House AMP > Colorectal Cancer > Flashcards

Colorectal Cancer Flashcards

1
Q

Colorectal cancer is a/an ______genous disease classified into different subtypes that have specific morphological and molecular characteristics

Studies have shown _____asing incidence with _______ prognosis

A

hetero

incre; dismal

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2
Q

Colorectal cancer is the _____ most common cancer accounting for ____% of all cancers and _____ most common
cause of (9.4%) of all cancer deaths. Globocan, 2020

A

4th; 10

2nd

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3
Q

Increasing Incidence of CRC
• It’s projected that global incidence will increase by ___% in 2035 with significant rise in the _______ and ______ countries

A

80

young and underdeveloped

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4
Q

Increasing Incidence of CRC

• Review of CRC in Nigeria have also indicated ______asing incidence in with greater proportion in (younger or older?) patients

A

incre

Younger

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5
Q

Age and Gender Prevalence
• The mean ages in most studies in
Nigeria ranged from _____ to ______ years
(average of _____years).

A

39 to 50.7

46.2

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6
Q

Age and Gender Prevalence

• M:F ratio = ——- to _____

• Patients <40years =______ %

A

1.3 to 1.

32.2

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7
Q

Aetiology/Predisposing factors
• CRC is a/an _____genous and _____-factorial disease

A

hetero

multi

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8
Q

Aetiology/Predisposing factors of CRC

• Multiple factors predispose to the disease:
•________ and ______
• host __________ disorders
•__________

A

Environmental & dietary

inflammatory GI

Genetic

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9
Q

Predisposing factors to CRC

Environmental and Dietary factors

• High content of ______ and ______
• Low content of _______________ in
diet
• Low overall __________ and ______ intake
• Low intake _____ micronutrients
• _______ and ______ consumption
• Obesity
•_______ habits

A

red meat and animal fat

un-absorbable fiber

fruits and vegetable

protective

Alcohol and tobacco

Sedentary

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10
Q

Protective factors against CRC

• Use of ______ (_____ ————)
• Vegetables
•______ activity
• _____________________ therapy
•_______ intake

A

NSAIDs; COX 2 inhibitors

Physical

Hormone replacement

calcium

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11
Q

Host inflammatory disorders that predispose to CRC

Inflammatory bowel diseases such as
•________________
•_______ disease
• The risk increases with ______ of the IBD and the ________ of ____________

A

Ulcerative colitis

Crohn’s; duration

extent of colonic involvement

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12
Q

Risk factors- Genetic (Major Familial
syndromes)

2 conditions
Mention them

A

Hereditary non-polyposis coli (HNPCC) syndrome

Familial adenomatous polyposis (FAP) syndrome

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13
Q

Risk factors- Genetic

Hereditary non-polyposis coli (HNPCC) syndrome

Abnormal Genes:
Lifetime cancer risks:
Features:

A

DNA mismatch repair gene MLH1, MLSH2, MSH6, PMS2

50-80%

No polyps, microsatellite instability

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14
Q

Risk factors- Genetic

Familial adenomatous polyposis (FAP) syndrome

Abnormal Genes:
Lifetime cancer risks:
Features:

A

APC gene mutation in on chromosome 5q21.

100% by age , 40yrs

multiple adenomatous polyps throughout the GIT (50-500 polyps)

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15
Q

Classification of CRC Pathology
• CRC is a single disease

T/F

A

F

• CRC is not a single disease but a collection of multiple diseases

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16
Q

Classification of CRC Pathology

• It is highly ______genous and dynamic with multiple ______ and ______ alterations underlying its
pathogenesis.

A

hetero

genetic and epigenetic

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17
Q

Classification of CRC Pathology

• The different subtypes have distinct clinical, morphological, and molecular characteristics which explains the differences in disease outcomes and
response to therapy

T/F

A

T

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18
Q

Classification of CRC : Hereditary or acquired

Hereditary-____-___%
•____ syndrome
•____________ syndrome
• others

Sporadic -____-____%
• Complication of ________________

A

20-30 ; Lynch; Familial Polyposis

70-80; Inflammatory bowel syndrome

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19
Q

Classification of CRC: Anatomic

based on location of the tumour
___________ and _________ colon cancer

A

Right sided

Left sided

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20
Q

Classification of CRC: Molecular

based on the _________________

A

underlying genetic abnormality

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21
Q

Molecular classification

• In CRC, the transformation of colonic mucosa into invasive cancer occurs through __________ or __________ changes
within the genome and epigenome

• -so-called _______ and ________ hypothesis

A

an accumulated somatic or inherited

multi-hit and multi-step

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22
Q

Tumour Cancer Genome Atlas, TCGA,

____________(___%)

____________(___%)

____________(___%)

A

Hyper mutated; 13

Ultramutated; 3

Chromosomal instability;84

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23
Q

Consensus Molecular Subtype

___________(_____%)

___________(_____%)

___________(_____%)

___________(_____%)

___________(_____%)

A

MSI: immune; 14

Canonical; 37

Metabolic ;13

Mesenchymal ;23

Mixed features;13

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24
Q

Tumour Cancer Genome Atlas, TCGA : Consensus Molecular Subtype

__________ = _________

__________ = ___________

A

Hypermutated; CMS1 : MSI immune

Chromosomal instability; canonical, metabolic, and mesenchymal

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25
Q

Anatomical location of:

MSI immune
Canonical
Metabolic
Mesenchymal

A

Right sided colon
Left sided colon and rectum
No predominance
Typically diagnosed at more advanced stages

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26
Q

Prognosis and survival of:

MSI immune
Canonical
Metabolic
Mesenchymal

A

Good prognosis but poor survival after relapse

Good survival after relapse

Intermediate survival

Worst overall and relapse-free survival

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27
Q

Treatment plan for :

MSI immune
Canonical
Metabolic
Mesenchymal

A

Likely benefit from immune checkpoint blockade

Anti-EGFR therapies likely effective , may respond to oxali-platin based regimens

Likely resistant to anti-EGFR therapies

Maybe responsive to antiangiogenic therapies and perhaps more sensitive to irinotecan-based regimens

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28
Q

Colorectal carcinogenesis
• The mechanisms that underlie
development of CRC have been
described as a “multi-hit, multi-stage”
phenomenon in which
•__________ mutations (alterations or changes) occur in ______ genes, after exposure to ___________ of
environmental and dietary risk factors.

A

several

multiple

multiple hits

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29
Q

Colorectal carcinogenesis

These mutations occur at (same or different?) stages and result in increasing _______________ from normal _____proliferative epithelium,
to _________,__________ and then finally _________

As the tumour grows, it is prone to _________ that confer on it, _________________ potential

A

Different

phenotypic abnormality; hyper

small adenoma, large adenoma

invasive cancer; more mutations

metastatic potential

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30
Q

3 Major Pathogenetic Pathways in CRC
Pathology

___________
_______________
______________

A

Chromosomal instability

Hypermutated (microsatellite instability)

Serrated pathways

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31
Q

Chromosomal instability
Hypermutated (microsatellite instability)
Serrated pathways

Sporadic:
Hereditary:

A

80%; FAP 1%

15%; Lynch syndrome 3-4%

10-20%

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32
Q

Chromosomal instability

_______ activation

__________ inactivation

(Early or Late?) abnormalities of _____ pathway

A

Oncogen

Tumor surpressor gene

Early abnormalities of WNT

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33
Q

Hypermutated (microsatellite instability)

Defective ___________________

A

DNA mismatch repair

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34
Q

Serrated pathways

Overlapping with ________________

Mutation in _______ or _______ leading to ________ of ______ pathway

A

CIN and MSI

KRAS or BRAF

hyper activation of
MAPkinase

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35
Q

Chromosomal instability

_____________________ sequence

•________ ————

A

Adenoma→Carcinoma

Classical adenocarcinoma

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36
Q

Hypermutated (microsatellite instability)

_______ differentiated tumour

•_____________ lymphocytes

A

Poorly

Tumour infiltrating

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37
Q

Serrated pathways

Premalignant lesions-

• Traditional _________ (TSA) and
•_____________ adenomas/______

A

serrated adenomas

Sessile serrated

polyps

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38
Q

The adenoma-carcinoma mode of
mechanism of pathogenesis

• This implies that ———————————————————————-

A

some carcinoma of the colon arise
from adenoma

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39
Q

The adenoma-carcinoma mode of
mechanism of pathogenesis

There is cumulative alteration in the genome which results in→ increasing _____,______ of _______ & ______ potential
of the tumour→carcinoma

A

size, level of dysplasia

invasive

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40
Q

Microsatellite instability pathway

• characterized by genetic abnormalities in the _________________ genes

• It is responsible for ____-____% of sporadic colorectal cancers

A

DNA mismatch repair

10-15

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41
Q

_____________ is the main pathway in Hereditary non-polyposis coli cancer syndrome (HNPCC syndrome).

A

Microsatellite instability pathway

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42
Q

Microsatellite instability pathway

Cancer occurs in ______ colon, tends to be _________ and in (younger or older?) age.

• There is Increase incidence of ______ and ________ cancer

A

proximal; mucinous

Younger

endometrial and ovarian

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43
Q

In Microsatellite instability pathway

Presence of preceding polyps.

T/F

A

F

No preceding polyps.

44
Q

Microsatellite instability pathway
abnormality may be inherited or sporadic

T/F

A

T

45
Q

microsatellites

Are ______ (small or large?) ( DNA or RNA?) sequences scattered in the genome and are (fixed or variable?) in
number for an individual

They are _____________ during DNA
replication

A

repetitive; small; DNA

Fixed

prone to errors

46
Q

microsatellites

are located in the _____ or _______ region of genes involved in ______ of _______

A

coding or promoter

regulation of
cell growth

47
Q

microsatellites

The mutations occur within hMLH1,
hMSH2, hMSH6, hPMS1 or hPMS2. hMLH1 & hMSH2 are the most common
T/F

A

T

48
Q

Diagnosis of CRC

_________ is taken to obtain ___________ for _______ diagnosis

A

Biopsy; tumour tissue; histological

49
Q

_________ and ________ are the commonest site of CRC in Nigeria

A

Rectum and sigmoid colon

50
Q

Morphology -MACROSCOPY

Site:

_________ and _________ colon

_______ and _________ colon

_________ colon

A

caecum and ascending

Rectum and sigmoid

Descending

51
Q

Macroscopy: Right sided, Caecal
tumour- ___________

Macroscopy: Left sided colon cancer __________________

A

fungating

annular constricting

52
Q

Morphology: Right sided, Caecal
tumour-fungating

In (proximal or distal?) colon (right sided tumour), they grow as:

• ______________ mass along ______ of the _______ and ______ colon
• Obstruction is ( common or rare?)
• (Acute or Chronic?) blood loss

A

Proximal

Polypoid fungating

one wall; caecum & ascending

Rare; chronic

53
Q

Left sided colon cancer: annular constricting

In (proximal or distal?) colon (lt. sided tumour) are:

•________,_________ lesion that produces a _______-_____ constriction of the bowel

• Obstruction and bleeding per ______ are (common or rare?)

A

Distal

annular, encircling

napkin-ring

rectum; common

54
Q

Microscopy: WHO Histologic classification of CRC

___________

___________(_____) adenocarcinoma

_____________ carcinoma

A

Adenocarcinoma

Mucinous (colloid)

Signet-ring cell

55
Q

Microscopy: WHO Histologic
classification of CRC

Adenocarcinoma –most _________ , (poorly or well?) formed glands

Mucinous adenocarcinoma (> ____ % ________)

Signet-ring cell carcinoma (> ____ % __________)

A

common; well

50; mucinous

50; signet-ring cells

56
Q

Microscopy of CRC

 _________ carcinoma
__________ carcinoma
________ carcinoma
 ________ carcinoma
 ___________ carcinoma
 Others

A

Squamous cell

Adenosquamous

Medullary; Small cell

Undifferentiated

57
Q

Small cell carcinoma

Aka
_____ grade ___________ carcinoma

A

high

neuroendocrine

58
Q

Microscopy of CRC

__________ is the most common, with significant proportion of (poor or good?) prognostic types

A

Adenocarcinoma

Poor

59
Q

Colonic adenocarcinoma

(poorly or well?) differentiated

_____ gland formation

T__

A

Poorly

no

3

60
Q

Histologic grading of CRC

Grade 1- _____ differentiated

Grade 2 - _______ differentiated

Grade 3 - ________ differentiated

A

Well

Moderately

Poorly

61
Q

Size of primary tumor

Tis- carcinoma insitu

T1-tumour invades _________

T2-tumour extends to ___________
but ____________

T3-tumor is ________________ into ________

T4-(directly or indirectly?) _______________________

A

submucosa

muscularis propria

not penetrating through

penetrating through muscularis propria
into subserosa

Directly invades surrounding
structures/organs

62
Q

TNM- Nodal metastasis (N)

Nx— regional nodes _______________
N0—_____ regional node metastasis
N1-metastasis in _____ nodes
N2-metastasis in ________ nodes

A

cannot be assessed

no

1-3

4 or more

63
Q

Staging- distant metastasis (M)
• Mx- metastasis __________
• M0- _____distant metastasis
• M1-distant metastasis_______

A

cannot be assessed

No

present

64
Q

Screening for CRC
• ___________________ test (FOBT)
• _______________________ test (FIT)
• ______________________________ (DCBE),
•_______________

A

Faecal occult blood

Faecal Immunochemical

Double contrast barium enema

Colonoscopy

65
Q

Clinically majority show no
symptoms for several years. Later,

Left sided tumour–(distal)

•______/______ bleeding
•Change in _______
• _______ left lower abdominal discomfort

•______,______,______

A

Occult/frank

bowel habit

Crampy

Malena, diarrhoea,
constipation

66
Q

Right side tumour-Proximal

fatigue,weakness,
____________ anemia,
__________ if bulky

A

iron deficiency

bleeding

67
Q

Colon Polyps

Are _________ of tissue into lumen

May be __________

A

Raised outgrowth

pre-cancerous

68
Q

Removal of colon polyps can prevent colon cancer

T/F

A

T

69
Q

Hyperplastic Polyp

• (Benign or malignant?)

• Common in ________ colon

• (Normal or Abnormal?) cellular structure, ____ dysplasia

A

Benign

rectosigmoid; normal

no

70
Q

Most common type of polyp is ???

A

Hyperplastic Polyp

71
Q

Hyperplastic Polyp

Classically have a “________” or _______ pattern

Usually ________ screening is required after biopsy

A

saw tooth; serrated

no special

72
Q

Adenomatous Polyp

Dysplastic with ________ potential

A

malignant

73
Q

Adenomatous polyp

By shape:

______ and ______

A

Sessile

Pedunculated

74
Q

Adenomatous polyp

By histology:

______ and ______

A

Tubular

Villous

75
Q

Sessile vs. Pedunculated

Sessile: (broad or narrow?) base attached to _____

Pedunculated: attached via _______

A

Broad ; colon

stalk

76
Q

Tubular vs. Villous

Tubular
• (Most or least?) common subtype (___%+)
•________ epithelium forming ______

A

Most; 80

Adenomatous; tubules

77
Q

Tubular vs. Villous

Villous
• (more or less?) common type
• Often (sessile or pedunculated?)
• (Short or Long?) projections extending from surface
• (Low or High?) risk of development into colon cancer

A

Less; sessile

Long; High

78
Q

Polyp Symptoms

Almost always (asymptomatic or symptomatic?)

Screening ________ done for detection

A

asymptomatic

colonoscopy

79
Q

Polyp Symptoms

Large polyps may cause bleeding
• Usually (visible or not visible?) in stool (“______”)
• Basis for screening with _______________ testing

A

Not visible ; occult

fecal occult blood

80
Q

High Risk Polyps

Likely to develop into _____
• _______ histology
•Dysplasia grade
• Determined by pathologist
• “______ grade dysplasia” = ↑ risk

A

cancer; Villous

High

81
Q

Patient likely to develop more polyps
• Metachronous adenoma: new lesion ~ _________ after prior
• >___ cm in diameter = ↑ risk
•_______ of polyps = ↑ risk

A

six months

1

Number

82
Q

Juvenile Polyps

(Benign or Malignant?) tumors ( _________ ) that occur in (children or adults?)

• Usually in _______
• Usually (sessile or pedunculated?)

•Cause (painful or painless?) rectal bleeding

• Often “____________”

A

Benign; hamartomas

children; rectum

pedunculated; painless

auto-amputate

83
Q

Juvenile polyposis syndrome
•(Single or Multiple?) (usually >___) polyps
• ____eased risk of cancer
• Surveillance ______

A

Multiple

10

Incr

colonoscopy

84
Q

Cyclooxygenase-2 expression is ____eased in colon cancer

A

Incr

85
Q

Chromosomal Instability Pathway

“Adenoma-Carcinoma sequence”
•Sequence of genetic events seen in colon cancer. Leads to colon cancer over many years
• Progression probably takes ____-____ years
• “_______” mutations occurs with aging
•More common in _____ sided tumors
•Descending colon, sigmoid, rectum

A

10-40

Somatic

left

86
Q

APC (____________________) protein/gene

Is a __________ gene

It Prevents ________ of ________ that activates __________

A

Adenomatous polyposis coli

Tumor suppressor

accumulation of β-catenin

oncogenes

87
Q

Chromosomal Instability Pathway
Step 1: APC mutation

• Loss of APC → ↑_______ → _______ activation
• Leads to increased risk for ______

A

β-catenin; oncogene

polyps

88
Q

Chromosomal Instability Pathway

Step 2: K-RAS mutation

• Aberrant _________ Leads to ___________ formation

A

cell signaling

adenoma polyp

89
Q

K-RAS mutation is a ____________

A

Proto-oncogene

90
Q

Chromosomal Instability Pathway
Step 3: p53

• Loss of p53 _________ gene leading go Tumor ________
•

A

tumor suppressor

cell growth

91
Q

Chromosomal Instability Pathway

Step 1:__________ causes a ______
Step 2:____________ leads to ______
Step 3: ________ ends in _____

A

APC mutation; high risk colon

KRAS mutation; polyps formation

Loss of P53; colon cancer

92
Q

FAP
Familial Adenomatous Polyposis

(Autosomal or X-linked?) (dominant or recessive ?) disorder

_______ mutation of ____ gene (chromosome ____)

(Always or sometimes?) (_____%) progresses to colon cancer

A

Autosomal dominant

Germline; APC; 5q

Always ; 100

93
Q

FAP
Familial Adenomatous Polyposis

Treatment: _________(____)

A

Colon removal (colectomy)

94
Q

Microsatellite Instability pathway can arise without polyps

T/F

A

T

Microsatellite Instability can arise “de novo” without polyp

95
Q

microsatellite?
•usually (coding or non-coding?)

• (Same or Different?) density as/from other DNA

• (Same as or Separate from?) other genetic material in testing (“satellites”)

A

Non coding

Different

Seperate from

96
Q

a stable microsatellite

•Successive cellular divisions:
_____________ microsatellites

•Each person has unique, ___________ of microsatellites

• Different person-to-person; same for each individual

A

same length

“stable” length

97
Q

_________ enzymes resolve base errors

A

Mismatch repair

98
Q

Examples of Mismatch repair enzymes

E.g: _____,_______,_______,_______ etc

A

MLH1, MSH2, MSH6, PMS2

99
Q

Microsatellite Instability

__________ can lead to accumulation of errors . This can occur in ________ in cancer cells
Result is ______________

A

Gene mutations

microsatellites

microsatellite instability

100
Q

Microsatellite Instability

•_____ testing
• Different _____ of microsatellites in tumor cells vs other cells
• Indicates ______________ dysfunction

A

PCR

length

mismatch repair enzyme

101
Q

Colon Cancer Screening

CEA (______________)
Tumor marker
(Elevated or depressed?) in colon CA and other tumors (pancreas)

(Poor or excellent?) sensitivity/specificity for screening

A

Carcinoembryonic Antigen

Elevated

Poor

102
Q

Colon Cancer Screening
CEA

Patients with established disease
• CEA level correlates with ________
• Elevated levels should return to baseline after ________
• Can be monitored to ________

A

disease burden

surgery

detect relapse

103
Q

HNPCC
_____________ Cancer/ _____ Syndrome

Inherited mutation of ___________

Leads to colon cancer via __________

• About ____% lifetime risk

A

Hereditary Non-Polyposis Colorectal ; Lynch

DNA mismatch repair enzymes

microsatellite instability ; 80

104
Q

Colon Cancer Screening

HNPCC

• Arise with pre-existing adenoma
T/F

A

F

Arise with out pre-existing adenoma

105
Q

HNPCC

Usually ______-sided tumors

Also increased risk of:
•_________ cancer , Other cancers (ovary, stomach, others)

A

right

Endometrial

106
Q

HNPCC

Classic case
• Patient with ______ sided colon CA
• (Single or Multiple?) ___________ members also with cancer

A

right

Multiple

1st family

107
Q

__________ cancer is most common non-colon malignancy

A

Endometrial

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