Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MS1 Spring > CABCO > Flashcards

CABCO Flashcards

1
Q

Are alterations in cell cycle regulation that increase cell proliferation sufficient for carcinogenesis and tumorigenesis?

A

No, other mutations are needed for premalignant cells to acquire traits and behaviors that lead to invasiveness and metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the two most desirable therapeutic outcomes when treating cancerous cells?

A

Apoptosis or permanent cell cycle arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

It takes how many hours for most human cells to complete the cell cycle?

A

24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the shortest phase in the cell cycle? The longest?

A

Shortest: mitosis (~1 hour)

Longest: S phase (1/3 to 2/3 cell cycle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the difference between an inactive CDK and an active CDK?

A

Inactive has no cyclin + a T-loop blocking the active site containing ATP

Active has cyclin bound + phosphorylated T-loop does not block the active site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In what phase of the cell cycle are CDKs not active?

A

G0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What cyclin-CDK complexes are present in mid G1?

A

Cyclin D-Cdk 4

Cyclin D-Cdk 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What cyclin-CDK complexes are present in late G1?

A

Cyclin E-Cdk 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What cyclin-CDK complexes are present in S phase?

A

Cyclin A-Cdk 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What cyclin-CDK complexes are present in M phase/mitosis?

A

Cyclin A-Cdk 1

Cyclin B-Cdk 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What kinase phosphorylates mitotic CDK-cyclin complexes with an inhibitory phosphate?

A

Wee1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What kinase phosphorylates mitotic CDK-cyclin complexes with an activating phosphate?

A

CDK Activating Kinase (CAK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What phosphatase removes inhibitory phosphate from the mitotic CDK-cyclin complex?

A

Cdc25

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does an activated mitotic CDK-cyclin complex phosphorylate?

A

Histones, mitotic spindle proteins, lamins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes degradation of mitotic cyclins and cohesion proteins holding metaphase chromosomes together?

A

Anaphase Promotion Complex (APC)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What transcription factor does Rb protein regulate?

A

E2F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What checkpoint is Rb present in?

A

G1/S phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe Rb/E2F interaction

A

Active Rb is bound to E2F, inactivating it

An active G1-Cdk can phosphorylate Rb, inactivating it and releasing E2F. E2F is now free to increase S-phase gene transcription and produce the needed Cyclins (A and E) at this stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the function of the Cip/Kip family of proteins? Name them.

A

Bind and inactivate dimeric complexes of cyclin D-Cdk4/6, cyclin A-Cdk2 or Cyclin E-Cdk2

p21, p27, and p 57

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the function of the INK4 family? Name them.

A

Bind and inactivate Cdk4 and Cdk6 kinases

p15, p16, p18, and p19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What two CDK inhibitors regulate the G1/S transition?

A

p16 and p27

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Ras increases the transcription of what proto-oncogene?

A

Myc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does Myc increase the expression of?

A

Entry into S phase via increased Cyclin D, decreased p27, and increased E2F synthesis & activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does p53 do (in general terms)?

A

Arrest the cell cycle and cause apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where are most oncogenic point mutations in p53?

A

The DNA binding domain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Is p53 active when phosphorylated or dephosphorylated?

A

Phosphorylated

Inhibits Mdm2 from binding and tagging p53 for degradation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does it mean to describe p53 mutations as “dominant negative”?

A

The mutant allele overrides the normal allele

p53 is normally a tetramer and it cannot bind to DNA properly if half of the tetramer is damaged/unable to bind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does p53 activate the intrinsic pathway of apoptosis?

A

Via BCL2 family of proteins & cytochrome C release from the mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What types of cells do tumors contain?

A

Cancerous AND normal cells (they need the nutrients that normal cells provide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What type of cancer cell is relatively rare and has a high replicative potential that can effectively “seed” new tumors?

A

Cancer stem cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How many viruses are associated with human cancers?

A

7

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What percentage of human cancers are due to viruses?

A

20%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the most common STD in the US?

A

HPV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How many HPV strains are classified as high-risk?

A

12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the two HPV strains that cause the majority of cervical cancers?

A

HPV16 and HPV18

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What type of tissues does HPV normally infect?

A

Skin or mucosa (genital tract, oral, nasal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What two low-risk strains of HPV cause 90% of all genital warts

A

HPV6 and HPV11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How many genes does a papilloma virus typically have?

A

8-10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What does HPV transmission require?

A

A microabrasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What does HPV’s E7 protein do?

A

Activates cell cycle progression by binding to Rb

Rb is normally bound to E2F to inhibit cell-cycle progression. E7 binds Rb very tightly, allowing uncontrolled actions of E2F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What does HPV’s E6 protein do?

A

E6 blocks apoptosis by inducing p53 degradation

E6 complexes with cellular E6AP and this complex can bind to p53 and cause its degradation in the proteosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

The combination of HPV’s E6 and E7 proteins are oncogenic because…?

A

Their actions result in uncontrolled proliferation AND loss of the ability of the cell to kill itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Do most people with HPV get cancer?

A

No, most people clear the virus over time. A small percentage get cancer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the key step in the transition from benign cervical lesion to invasive cervical cancer?

A

Circular HPV DNA becomes linear and inserts into the host’s genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What protein is lost in the transition from circular HPV DNA to linear? This protein normally keeps E6 and E7 in check

A

E2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are koilocytes?

A

Cells in the cervical epithelium full of 1000s of HPV viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How do you treat persistent HPV infections not associated with abnormal cell changes?

A

You don’t

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the three FDA-approved HPV vaccines?

A

Ceravix, Gardasil, Gardasil 9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What cells of the epithelium does HPV first infect?

A

Basal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What component of the HPV capsid do most of the vaccines target?

A

L1 protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What enzyme has increased activity in Chronic Lymphocytic Leukemia?

A

Bruton’s tyrosine kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Can capacitated patients refuse life-sustaining treatment?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Can patients use advanced directives to refuse life sustaining treatment when they become incapacitated?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the ethical and legal difference between withholding and withdrawal of life sustaining treatment?

A

There isn’t one

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

When are advanced directives legally enforceable?

A

When a patient loses decisional capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Can ordinary power of attorney be used for decision-making for incapacitated patients?

A

No, only a durable power of attorney continues through incapacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Define neoplasia

A

general process of new growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Define neoplasm

A

A new growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Define cancer

A

general term for all malignant tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Are tumor and malignancy synonymous?

A

No

Tumor = neoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Name of benign and malignant tumors affecting squamous epithelium?

A

Benign: squamous papilloma

Malignant: squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Name of benign and malignant tumors affecting glandular epithelium

A

Benign: adenoma

Malignant: adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Name of benign and malignant tumors affecting surface epithelium?

A

Benign: papilloma

Malignant: papillary carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Name of benign and malignant tumors affecting smooth muscle

A

Benign: leiomyoma

Malignant: leiomyosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Name of benign and malignant tumors affecting striated muscle?

A

Benign: Rhabdomyoma

Malignant: Rhabdomyosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Name of benign and malignant tumors affecting blood vessels?

A

Benign: Hemangioma

Malignant: Angiosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Name of benign and malignant tumors affecting fat?

A

Benign: Lipoma

Malignant: Liposarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Name of benign and malignant tumors affecting cartilage?

A

Benign: chondroma

Malignant: chondrosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Name of benign and malignant tumors affecting bone?

A

Benign: osteoma

Malignant: osteosarcome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Name of benign and malignant tumors affecting fibroblasts?

A

Benign: fibroma

Malignant: fibrosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Name of benign and malignant tumors affecting melanocytes?

A

Benign: nevus

Malignant: malignant melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Name of benign and malignant tumors affecting totipotent germ cells?

A

Benign: mature teratoma

Malignant: immature teratoma (teratocarcinoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Name of benign and malignant tumors affecting lymph nodes/bone marrow?

A

Benign: low grade lymphoma

Malignant: high grade lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Six steps in the invasion-metastasis cascade?

A
  1. Local invasion
  2. Intravasation into blood/lymphatic vessels
  3. Transit in vessel
  4. Arrest/extravasation into distant tissue
  5. Micrometastasis formation (small nodules)
  6. Colonization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the first transformation cancer cells must make in order to complete metastasis?

A

Epithelial to mesenchymal transition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Is metastasis an efficient or inefficient process?

A

Very inefficient

Less than 0.01% of cancer cells in circulation develop into metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Define hypertrophy

A

Increase in tissue mass without cellular proliferation (aka increase in cell size)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Define hyperplasia

A

Increase in tissue mass due to an increase in cell number

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Define metaplasia

A

A reversible change in which a differentiated cell type is replaced by another cell type. Most common in mucosal/epithelial surfaces

Usually happens in response to a stimulus

Becomes a problem when stimulus/irritant continues and produces genetic changes leading to autologous growth and cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What are four types of non-neoplastic growth & differentiation?

A
  1. Reparative proliferation (granulation tissue)
  2. Hypertrophy
  3. Hyperplasia
  4. Metaplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Characteristics of benign neoplasms?

A

Autonomous growth that is slow and progressive

Growth by expansion NOT invasion

Encapsulation/clear demarcation from normal tissue

Cells with high degree of differentiation/preserved architecture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Define ectopic

A

Normal tissue in abnormal location

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Define hamartoma

A

normal tissue components in an abnormal/disorganized configuration (“at home”)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Define choristomas/heterotopia

A

Normal tissue but in the wrong place

Ex: normal pancreatic tissue ectopically present in the wall of the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Define polyp

A

Grossly visible growth projecting from a surface, often a mucosal surface

General term. Can be hyperplastic (non-neoplastic), benign, or malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Define hyperplastic polyp

A

Most common type of colonic polyp; lacks malignant potential . Has “saw-tooth”/serrated/tufted appearance

In many organs/locations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Is benign neoplastic growth reversible?

A

“the process is not generally considerable reversible”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What does “oma” mean?

A

Tumor (no distinction between benign or malignant though!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is Von Hippel-Lindau Syndrome?

A

Autosomal dominant genetic condition characterized by visceral cysts, benign masses, and the potential for malignant transformation in multiple organ systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Clinical features of Von Hippel-Lindau Syndrome?

A

Eye tumor, brain tumor, kidney tumor, adrenal gland tumor, pancreatic tumor, Cafe Au Lait spots, CVS (strokes and heart attacks)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Most common type of disease-causing mutation?

A

Single point mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Three ways proto-oncogenes are converted into oncogenes?

A
  1. Point mutation
  2. Gene amplification
  3. Chromosomal rearrangement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What does Ras bind in its active state? Does this induce or inhibit cell growth?

A

GTP

Induces cell growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What oncogene in responsible for Neuroblastoma? What is its mechanism from proto-oncogene to oncogene?

A

N-myc

Amplification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

How do Burkitt lymphoma tumor cells appear on H&E?

A

Round, homogenous, and display a high mitotic rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Chromosomal translocation responsible for Burkitt lymphoma?

A

8 and 14 (14q has new IgH-myc gene)

Places the myc gene adjacent to IgH enhancer/promoter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Chromosomal translocation responsible for Chronic Myelogenous leukemia (CML)?

A

9 and 22 (9q has new Bcr-Abl gene)

Bcr-Abl is a constitutively active tyrosine kinase that leads to cell growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What drug inhibits Bcr-Abl function?

A

Imatinib (Gleevec)

Binds into the ATP site of Bcr-Abl and inhibits tyrosine kinase functionality

Gleevec is a synthetic ATP mimic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Effect of mutations on tumor suppressor genes?

A

Inactivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Effect of mutations on oncogenes?

A

Activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

First tumor suppressor gene identified?

A

Rb

13q

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Main job of Rb?

A

“Molecular policeman” of the cell cycle: serves as a guard at the G1/S transition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is the most commonly mutated gene in human cancer?

A

p53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

95% of p53 mutations are found where?

A

point mutations in the DNA-binding domain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

The cancer cell phenotype is (dominant or recessive) to the normal cell phenotype?

A

Recessive

per cell fusion experiment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Are viral oncogenes derived from viral or host genomes?

107
Q

Define log cell kill

A

A given dose kills a fixed percentage of cells

Note: established in vitro, not in vivo

108
Q

Define dose dependent

A

Different depending on whether or not the agent is cell cycle specific

109
Q

The growth fraction of tumor cells depends on what?

A

The size of the tumor

As tumor size increases, growth fraction decreases

110
Q

When is chemotherapy most effective?

A

When cell turnover is highest

111
Q

When is cell turnover highest?

A

When tumor volume is below the level of detection (10^9 tumor cells)

112
Q

Log cell kill effect depends on the tumor ______ at diagnosis

113
Q

What results in the best chance of cure?

A

Dose intensity - the concept that the highest dose at the most frequent intervals will result in the best chance of cure

114
Q

If a tumor has a stable growth fraction, a given dose of drug will kill what?

A

A fixed percentage of tumor cells regardless of the tumor mass

** he stressed this in class **

115
Q

Define palliative chemotherapy

A

Chemotherapy given to patients with metastatic/incurable cancer with the intent of prolonging life or alleviating symptoms

116
Q

Define curative chemotherapy

A

Chemotherapy, almost always combination of drugs, given with the intent of inducing remission and curing the patient

Used with testicular cancer, lymphomas, leukemia, and a few solid tumors

117
Q

Define adjuvant chemotherapy

A

Chemotherapy given after a local procedure (surgery or radiotherapy) with the intent of eradicating microscopic metastases

Commonly used in breast cancer, colon cancer, and selected other tumors

*** Patients generally do not have clinically detectable metastases

118
Q

Define neoadjuvant chemotherapy

A

Chemotherapy given when a tumor is large/unresectable with the intent of making it more amenable to local therapy and at the same time treating the subclinical metastatic diseases

119
Q

What is the order of gene mutations seen in colon cancer progression?

A
  1. APC/B-catenin
  2. K-RAS
  3. p53
120
Q

Two categories of molecular changes seen in colon cancer development?

A
  1. Genomic changes/genetic (chromosomal instability or microsatellite instability)
  2. DNA methylation/epigenetic
121
Q

In which part of the colon are hyperplastic polyps most common?

A

Left colon

Result from decreased cell turnover; no malignant potential

122
Q

What are three types of adneomas/neoplastic polyps found in the colon?

A
  1. Tubular adneoma
  2. Villous adneoma
  3. Sessile serrated adenoma
123
Q

Define tubular adenoma

A

small, pedunculated, “tubular glands,” and often have a stalk

Nucleus appears elongated

124
Q

Define villous adenoma

A

larger, long, slender villi

Has a wide base and grows as a sessile (“attached along the base of lesion”) rather than as a pedunculated lesion with a long stalk

125
Q

Define sessile serrated adenoma

A

Similar to hyperplastic polyps but crypt dilation and budding into the lamina propria (wider base)

126
Q

In which portion of the colon are sessile serrated adneomas most commonly found?

A

Right colon

127
Q

What precedes the development of macroscopic polyp (adenoma)?

A

An aberrant crypt focus (ACF)

128
Q

What are the precursor lesions in Familial Adenomatous Polyposis (FAP)?

A

aberrant crypt foci (ACF)

129
Q

Outside of the colon, where do lesions typically present in those with FAP?

A

Retinal lesions, gastric & duodenal polyps, desmoid tumors

130
Q

What is Gardner syndrome?

A

FAP, osteomas, skin cysts

131
Q

What is Turcot syndrome?

A

FAP, brain tumors

132
Q

What germline mutation is present in people with FAP?

A

APC gene

** know this!!!

133
Q

What does APC regulate?

A

B-catenin

When Wnt signaling is present, APC is constantly degraded and B-catenin signaling is always “on”

This leads to constitutive proliferation

134
Q

What precursor lesions are present in patients with Lynch Syndrome (HNPCC)?

A

Tubular adenomas (but smaller and flatter)

135
Q

Median age of CRC diagnosis in HNPCC? FAP?

A

HNPCC: 60

FAP: 35-40

136
Q

Where is CRC most commonly present in those with Lynch Syndrome?

A

right colon

137
Q

People with Lynch Syndrome are at a higher risk for what other cancers?

A

Endometrial, small bowel, ovarian, gastric and ureteral

138
Q

What is the distinctive histology present in Lynch Syndrome?

A

Mucinous and “medullary/solid” differentiation

139
Q

Germline mutations in Lynch Syndrome?

A

hMLH1, hMSH2, hPMS1, hPMS2, hMSH6

140
Q

What gene is methylated/silenced in SSA adenomas?

141
Q

Which side of the colon has more goblet cells?

142
Q

Which side of the colon has more Paneth cells?

A

Right side

143
Q

Most common neoplastic polyp?

A

Tubular adenoma

144
Q

Favorite places for colon cancer metastasis?

A

Lymph nodes, liver, lungs, and bones

145
Q

What cancer(s) are associated with Epstein-Barr virus?

A

Nasopharyngeal carcinoma

Burkitt lymphoma

146
Q

What cancer(s) are associated with human herpes virus type 8 (HHV8)?

A

Kaposi sarcoma

147
Q

What cancer(s) are associated with Human T-cell leukemia/lymphoma virus (HTLV-1)?

A

T-cell leukemia/lymphoma

148
Q

What cancer(s) are associated with Human T-cell leukemia/lymphoma virus (HTLV-2)?

A

Hairy cell leukemia (very weak association)

149
Q

What cancer(s) are associated with HPV 16 & 18?

A

Cervical, head & neck cancers

150
Q

What cancer(s) are associated with Hepatitis B & C?

A

Hepatocellular carcinoma

151
Q

What are examples of AIDS-defining cancers?

A

Kaposi sarcoma, non-hodgkin lymphoma, invasive cervical cancer

152
Q

What are examples of cancers that can develop in persons with HIV infection while they are being treated with HAART?

A

Hepatocellular carcinoma, anal cancer, hodgkin lymphoma

Note: NON-hodgkin lymphoma is an AIDS-defining cancer. Don’t let Winter trick you!!!

153
Q

What is Post-transplant lymphoproliferative disorder (PTLD)?

A

A neoplasm that can develop after organ transplantation due to immunosuppression (linked to EBV B-cell infection)

154
Q

List the three tumor markers Winter gave in his presentation

A

M-spike, PSA, CEA

155
Q

What type of lymphocyte do we need for tumor resistance?

156
Q

What is “cancer immunoediting”?

A

Cancer cells that escape immune system recognition are able to survive and proliferate

“selective outgrowth of antigen-negative variants”

157
Q

What are three ways tumors escape immune recognition?

“Greased pig phenomenon”

A
  1. Loss of MHC 1 due to TAP or proteasome mutation
  2. Loss of adhesion molecule expression
  3. Lack of B7 expression (no co-stimulus -> leads to T Cell anergy
158
Q

How do tumor cells prevent killing by NK cells?

A

They express other MHC 1 molecules that prevent this

just missing the MHC 1 class that T cells interact with

159
Q

What two cytokines do tumors secrete that suppresses the immune system?

A
  1. TGF-beta
  2. IDO enzyme

Both of these suppress CD4 and CD8 cells

160
Q

What does TGF-beta activate?

A

Tregs (CD4+, CD25+, FoxP3+)

161
Q

What do Tregs secrete?

A

TGF-beta, IL-10 (also suppresses immune response!), and IDO

162
Q

How can a tumor cell induce apoptosis in a CD8 T cell?

A

Tumor Fas-ligand binds to CD8 Fas and causes apoptosis of CD8 cell

163
Q

What two tissues lack lymphatics?

A

Brain and gonads

164
Q

How do tumor cells mask themselves?

A

With connective tissue and glycocalyx molecules

165
Q

What does Anti-CD22-pseudomonas toxin do?

A

It is a toxin-labeled antibody that binds to CD22 on tumor cells. The tumor cell internalizes the receptor-Ab conjugate and dies

Causes remission in 2/3 of hairy cell leukemia patients

166
Q

How can antibodies be used to attack tumor cells?

A

Monoclonal antibodies that make it easier for NK cells to find the tumor cells

Toxin, radiation or drug-labeled antibodies

167
Q

Does immunizing cancer patients with tumor proteins mixed with bacterial adjuvants work?

A

Nope, largely ineffective

168
Q

What are Immune Stimulatory Complexes (ISCOMs)?

A

lipid micelles containing tumor antigen

APCs take up these ISCOMs and present the antigens to CD8 t cells. Now they’re activated and looking for tumor cells

169
Q

What are Lymphokine-activated killers (LAKs)?

A

mononuclear cells are isolated from peripheral blood and given IL-2 (T cell growth factor!). Enhanced CD8 t cells & NK cells are infused back into the patient

170
Q

What are Tumor-Infiltrating lymphocytes (TILs)?

A

Lymphocytes and NK cells are isolated from a tumor and given IL-2 (T cell growth factor!). Enhanced CD8 t cells & NK cells are infused back into the patient

171
Q

What is KRAS?

A

Proto-oncogene GTPase

Oncogenic form is stuck in the “on” position with GTP

172
Q

What are “CAR-T cells”?

A

Chimeric antigen receptor modified T cells

A patient’s t cells are modified to include a receptor that targets tumor cell antigen

Structure is a single chain fragment that is mostly variable region

173
Q

What kind of malignancies have CAR-T cells been effective in treating?

A

Hematologic

174
Q

How can CAR-T cells be made effective against solid tumors?

A

Diapedesis into the solid tumor needs to be increased

This can be done by re-engineering CD6 (5HS) to increase transit into the tumor

175
Q

What are immune checkpoint inhibitors?

A

Normally, T-cell signaling can lead to down-regulation of T-cell actions; this can be via CTLA4-B7 or PD1-PDL1 interactions

Monoclonal antibodies, aka checkpoint inhibitors, can be developed that bind to PDL1, PD1, and CTLA4 and stop this down regulation

176
Q

What immunologic toxicities are caused by anti-PD1/anti-PDL1 monoclonal antibodies?

A

Immune-related adverse reactions (irARs) like pneumonitis, diarrhea/colitis, vitiligo, T1DM, thyroid changes, etc

177
Q

What does CD47 do?

A

It’s a protein present on tumor cells that binds to SIPalpha on macrophages and says “don’t eat me!”

An anti-CD47 monoclonal antibody can bind to CD47 and increase macrophage phagocytosis

178
Q

What type of biopsy just gives cells?

A

Fine needle

179
Q

What type of biopsy gives architecture and allows more tests to be performed?

A

Core needle biopsy

180
Q

What type of biopsy is the gold standard for initially assessing image detectable lesions in the breast?

A

Core needle

181
Q

What percentage of biopsies should require open surgical biopsy?

182
Q

What is en bloc resection?

A

Removing the cancer with a rim of normal tissue

Well-established benefit in clinical trials for most cancers

183
Q

What is the “gold standard” trial for breast cancer surgery? What did it show?

A

NSABP B-06

Mastectomy = lumpectomy + radiation

Lumpectomy with radiation is better than without

184
Q

In which types of cancer surgeries is laparoscopic technique not an accepted surgical treatment?

A

Ovarian, adrenal, thyroid, uterine

OAT U

185
Q

Screening is best understood as _______ _______?

A

Therapeutic intervention

186
Q

Possible good outcomes of screening?

A

Decreased morbidity and mortality

187
Q

Possible bad outcomes of screening?

A

Side effects, labeling with a diagnosis, false positives & negatives, over-diagnosis

188
Q

Sources of bias in screening?

A

Selection bias, lead-time bias, and length-time bias

189
Q

What is “up staging”?

A

Introduction of a new staging modality such as CT, PET, or surgical staging that gives one more accurate staging

190
Q

What is the Will Rogers effect?

A

New staging makes it look like the survival is better for each stage but really patients have just migrated from one stage to another

All stages of the disease look better, but the overall population has the same survival

191
Q

What is the number needed to screen?

A

The number of individuals you would need to screen to achieve one additional desirable outcome

1/Absolute risk reduction

he said this was an exam question!!!

192
Q

How do you calculate absolute risk reduction?

A

Control Event Risk - Experimental Event Risk = ARR

193
Q

What is fallacy of division?

A

What is true for the group is true for each individual

194
Q

What is fallacy of composition?

A

What is true for an individual is also true of the group

195
Q

Majority of cancer survivors are over what age?

196
Q

What percentage of children with cancer will be cured?

197
Q

What are late effects of cancer treatment?

A

Complications that occur or persist more than 5 years from the end of therapy

They are unrecognized toxicities that are absent or subclinical at the end of therapy but manifest later

Ex: growth & development abnormalities, infertility, psychosocial effects, problems with vital organ function, etc

198
Q

What are long-term effects of cancer treatment?

A

Side effects or complications of treatment that begin during treatment and continue beyond the end of treatment

ex: lymphedema, malabsorption, loss of voice

199
Q

Which cancer treatment method has systemic effects?

A

Chemotherapy

200
Q

What are the culprits of cardiac toxicity following cancer treatment?

A

Radiation

Anthracycline-type chemotherapy (Doxorubicin)

Tyrosine kinase inhibitors (Pazopanib, Sunitinib, Nilotinib)

Monoclonal antibodies (Trastuzumab, Bevacizumab)

201
Q

How long after anthracycline-therapy is cardiac risk elevated?

202
Q

The risk of second cancer is highest for who?

A

Those diagnosed at a younger age

because their bodies are growing/DNA is active when initial treatment is occurring

203
Q

When is the risk for a second cancer highest?

A

Within first 5 years after initial cancer but risk persists beyond 10 years from diagnosis

204
Q

What can be viewed as a cell cycle disease?

205
Q

What three phases/blocks of treatment are used to treat childhood leukemia?

A

Induction, consolidation, maintenance

206
Q

What were the downsides of craniospinal radiation used in the 1970s to treat leukemia?

A

Myelosuppression, growth issues, altered intellectual and psychomotor function, endocrine abnormalities

207
Q

What treatment combination was found to be equivalent to brain radiation?

A

Intensive systemic chemotherapy and intrathecal therapy combined

(intrathecal therapy was less effective than radiation when less intensive chemo was used)

208
Q

What is the Goldie Coldman hypothesis?

A

Intensive cytoreduction leads to fewer surviving tumor cells to undergo mutation & lead to resistance

“If mutations are chance events during cell division, having more cells around increases the risk of mutation leading to resistance.”

209
Q

Combination of what three induction phase drugs brought remission rates to greater than 95%?

A

Vincristine + steroid + asparaginase

Note: anthracycline could be added to further improve remission rates but its highly toxic

210
Q

What is the criteria for standard risk pediatric leukemia patients? High risk?

A

Standard: between 1 and 10 years old; WBC less than 50,000/mL

High: Over 10 and WBC greater than 50,000/mL

211
Q

How many leukemia cells are left after induction phase treatment? Why?

A

~ 10 billion

They persist due to resistance, sanctuary sites, quiescent state (were not dividing when chemo was given)

212
Q

What are two improvements of post-induction therapy?

A
  1. Intensifying therapy of slow responders (if minimal residual disease is left then increase therapy)
  2. Identifying low/high risk subgroups through cytogenetics (i.e. Philadelphia chromosome, MLL rearrangements, hypoploidy, etc)
213
Q

What is the Norton Simon hypothesis?

A

Cells remaining post-induction are relatively/absolutely resistant; late/delayed intensification (new agents) may be beneficial here

He gave the example of a second round of induction and consolidation treatments (dexamethasone + anthracycline (low risk) or doxorubicin (high-risk)

214
Q

Has the introduction of new chemotherapy agents played a large or small role in pediatric leukemia outcome improvements?

A

Small role

Major improvements came via clinical trials assessing traditional drugs

215
Q

Disease-free survival rate for Ph+ Acute Lymphoblastic Leukemia with chemotherapy alone and with BMT from sibling?

A

Chemo: 20%

BMT from sibling: 60%

216
Q

What gene is expressed in Ph-like acute lymphoblastic leukemia?

A

R8

Note: their outcomes are inferior to those who are actually Ph+

217
Q

What is the single best criterion of malignancy?

A

Metastasis

218
Q

What is the most common benign neoplasm of the female breast?

A

Fibroadenoma

219
Q

What is the most common benign tumor of the salivary glands?

A

Pleomorphic adenoma

220
Q

What features reflect a lack of cell differentiation/become more prominent in malignant tumors?

A
  1. Variation in cell size (pleomorphism)
  2. Increased nuclear size (higher N:C ratio)
  3. Increased DNA content & irregular nuclear borders
  4. Large nucleoli
  5. Increased mitoses
  6. Abnormal mitoses
221
Q

In what type of cancer do we see Reed-Sternberg cells (“owl eyes”) on H&E?

A

Hodgkin Lymphoma

222
Q

In what type of tumor do we see multipolar mitotic figures?

A

Wilms tumor

223
Q

In what type of cancer will we see keratin?

A

Squamous cell carcinoma

224
Q

If a cancer cell is TTF+ and CK7+, what type of cancer is it?

A

Adenocarcinoma

225
Q

If a cancer cell is p63+, what type of cell is it?

A

Squamous cell carcinoma

226
Q

What two organs are most commonly involved with metastatic cancer?

A

Lungs and liver

227
Q

What property (or finding) gives a tumor the potential opportunity for metastasis?

A

Invasion through the basement membrane (gaining access to blood vessels or lymphatics)

228
Q

What is the most common general type of human cancer?

229
Q

What are the two main types of carcinoma?

A

Squamous cell carcinoma and adenocarcinoma

230
Q

How common are sarcomas?

A

Less than 1% of all human malignant tumors

231
Q

When are tumor cells most chemo-sensitive?

A

When they are small and have a high growth fraction

232
Q

What is growth fraction?

A

The fraction of tumor cells that are actively dividing

233
Q

What does the Norton-Simon hypothesis predict?

A

Greater log-kill in smaller tumors due to rapid growth and supports chemotherapy in the postoperative setting

234
Q

Five forms of cancer immunotherapy?

A
  1. Bone marrow transplant
  2. Monoclonal antibodies
  3. Cancer vaccines
  4. Checkpoint inhibitors
  5. CAR T cells
235
Q

What is a dendritic cell vaccine?

A

Its used to enhance a patient’s T cell immunity

Dendritic cells are pulsed with tumor antigens and then injected into the patient. DCs present tumor antigen to the patient’s T cells and then tumor-specific T-cells are activated

236
Q

Most common malignancy in children?

A

B-cell acute lymphoblastic leukemia (ALL)

237
Q

What are three targets of targeted therapy?

A
  1. Oncogenic signaling pathways (EGF, MAP kinase, BCR-ABL)
  2. Angiogenesis (VEGF)
  3. Apoptotic machinery (HDAC, proteasome inhibitors)
238
Q

What is a basket trial for precision medicine?

A

Genomic aberrations are recurrent across multiple organ sites & the presence of a specific mutation may be more predicative of drug response

aka people with similar mutations, not necessarily in the same organ, are enrolled to see if a treatment approved in another disease will work for their disease or a rare one

239
Q

What is an umbrella trial?

A

Evaluates many treatments (aka many “treatment arms”) within the same cancer type

240
Q

What is a super-umbrella trial?

A

Captures umbrella trial AND basket trial under on super umbrella. Lots of arms that people go be assigned

Downside is that patients could be eligible for multiple arms or that the trial may require a large number of drugs and biomarkers

241
Q

What are SERMS? Example of one?

A

Selective Estrogen Receptor Modulators

Ex: Tamoxifen

242
Q

What is the cause of non-small cell lung cancer?

A

EGFR is aberrantly activated (oncogene)

Activation due to overexpression of receptor or mutations that cause constitutive activation of receptor tyrosine kinase activity

“oncogene addiction”

243
Q

What receptor is overexpressed in 25-30% of patients with metastatic breast cancer?

A

HER-2/neu (human epidermal growth factor receptor 2)

244
Q

95% of Chronic Myelogenous Leukemia (CML) are associated with what?

A

The Philadelphia chromosome t(9;22)

Joins BCR locus on chromosome 22 with the ABL locus on chromosome 9 to make the mutant tyrosine kinase BCR-ABL

245
Q

What type of mutation is found in 60% of melanomas?

A

BRAF mutations

BRAF is a component of the MAP kinase pathway that transmit growth-stimulatory signals from the cell surface to the nucleus

246
Q

90% of BRAF mutations affect a single amino acid residue. What is it?

247
Q

What is the equation for how x-rays interact with matter?

A

High energy x-ray + water —-> H20^+ + e^-

H20^+ quickly decays into H+ and OH* (free radical)

Free radical causes DNA damage

DNA damage leads to cell death

248
Q

When do we see the biologic effects of DNA damage after radiation?

A

Days to weeks after the lethal event

Most cells do not show evidence of radiation damage until they attempt to divide

249
Q

DNA damage can be lethal and ______?

A

Sublethal

Sublethal damage can be repaired

250
Q

Do cancer cells take longer or shorter to repair than normal cells?

A

Longer

Fractionating radiation dosage takes advantage of this! The same small dose is applied over multiple exposures so less damage is caused to normal cells & they can repair themselves

251
Q

What are the two different types of radiation used?

A
  1. Teletherapy (external beam RT) - photon therapy/x-rays, most common
  2. Bracytherapy (internal RT) - radiation implants, ingested radioactive pills, intravascular radiation injections
252
Q

What is 3D conformal RT?

A

3D conformal radiation therapyis a cancertreatmentthat shapes theradiation beams to match the shape of the tumor

253
Q

What is intensity modulated radiotherapy (IMRT)?

A

Divided into various beamlets; varying intensities allow you to conform to the shape and carve out things you don’t want to hit like the spinal cord

254
Q

What is Stereotactic Body Radiation (SBRT) or Stereotactic Ablative Radiotherapy (SABR)?

A

Administration of very high doses of radiation, using several beams of various intensities aimed at different angles to precisely target the tumor

SBRT is typically used to treat small, well-defined tumors

255
Q

What are the goals of CT simulation?

A

Immobilization and reproducibility

256
Q

In which age group is cancer the #1 cause of death?

257
Q

Are most cancer cytotoxic agents specific or nonspecific?

A

Nonspecific

258
Q

Hereditary cancer gene in Familial Melanoma?

259
Q

Hereditary cancer gene in Li Fraumeni Syndrome?

260
Q

Hereditary cancer gene in Familial Gastric Cancer?

261
Q

The occurrence of translocations as a sole karyotypic event in carcinomas are common/uncommon?

A

Uncommon

Generally associated with loss of heterozygosity, specific gene mutations, or aberrant patterns of expression

262
Q

Tumors of ______ origin are often associated with translocations thought to be causally related to the development of the neoplasia

A

mesodermal

263
Q

What was the first therapeutic target?

264
Q

What type of non-small cell lung cancer has the worst survival: squamous or adenocarcinoma?

A

Squamous

Most of the research and treatment effort has been focused on adenocarcinoma

MS1 Spring (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions