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MoD-Exam 2 > 7.3 Molecular Basis of Cancer > Flashcards

7.3 Molecular Basis of Cancer Flashcards

1
Q

Gene A is described as being haplosufficient, which would mean what?

A. A gain of function mutation of Gene A would lead to carcinogenesis

B. A loss of function mutation in only one copy of Gene A would lead to decreased activity of the protein it expresses

C. A loss of function mutation in both copies of Gene A would be needed in order for carcinogenesis to occur

D. Non of the above

A

B. A loss of function mutation in only one copy of Gene A would lead to decreased activity of the protein it expresses

Haploinsufficiency

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2
Q

Which of the following is true of carcinogeneisis?

A. The principle targets of cancer causing mutations cannot yet be classified

B. Tumors are not clonal

C. Lethal genetic damage is at the heart of carcinogenesis

D. Carcinogenesis results from an accumulation of complementary mutations that occur in a stepwise fashion overtime

A

Carcinogenesis results from an accumulation of complementary mutations that occur in a stepwise fashion overtime

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3
Q

Which of the following correctly explains driver mutations?

A. Mutations which contribute to the development of malignant phenotypes

B. First mutation that starts a cell on its malignant path

C. There must be an accumulation of driver mutations for cancer to develop

D. One driver mutation is necessary and sufficient for cancer development

E. All except D

F. A and C

A

A and C

A. Mutations which contribute to the development of malignant phenotypes

C. There must be an accumulation of driver mutations for cancer to develop

NOTE: B is describing initiating mutation

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4
Q

Which of the following is a common early step on the road to malignancy that is particularly exmplified in solid tumors?

A. Loss of Function mutations

B. Gain of Gunction mutations

C. Down regulation of apoptosis

D. Acute dysfunction of DNA repair proteins

A

A. Loss of Function mutations

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5
Q

What are the 8 hallmarks of cancer?

GAMA WIIG

A
  1. Growth- self sufficient sans growth signals
  2. Apoptosis- resists
  3. Metastasizes- and invades
  4. Angiogenesis
  5. Warberg effect - switch to aerobic glycolysis
  6. Immortal- able to divide always
  7. Immunity- able to evade immune cells
  8. Growth- ignors growth inhibitory signals
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6
Q

The genetic and epigenetic alterations that lead to the hallmarks can be accelerated by what two things?

A. Genomic instability only

B. Cancer promoting inflammation only

C. Genomic instability and Cancer Promoting inflammation

D. None of the above

A

C. Genomic instability and Cancer Promoting inflammation

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7
Q

Genes that promote self-suffiencient cell growth in cancer cells are called _______, and the unmutated counterparts are called ___________.

A

Genes that promote self-suffiencient cell growth in cancer cells are called oncogenes, and the unmutated counterparts are called proto-oncogenes.

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8
Q

Here’s a chart potentially worth looking at, but we’ll make specific questions for ones that continuously show up in the chapter

A

Keep reading x3

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9
Q

Which of the following seems to be the most frequently mutated oncogenic pathway in human neoplasms?

A. G-protein coupled receptor

B. RTK pathway

C. JAK/STAT pathway

D. Notch pathway

E. TGF-B/SMAD

A

B. RTK pathway

Receptor Tyrosine Kinase pathway

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10
Q

Understand this pathway, the signal transducers, and the oncoproteins.

A

3 times

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11
Q

Which of the following options correctly explains why we are able to assume RAS mutations in tumors can substitute for tyrosine kinase activaity?

A. RAS mutations always lead to direct inhibition of tyrosine kinase activity

B. RAS mutations can cause selective inhibition of tyrosine kinase activity

C. Tyrosine kinase activating mutations are almost always absent when RAS mutations are found in the tumor

D. Tyrosine kinase activating mutations are almost always absent when RAS mutations are found in the tumor cell, or at least the dominant tumor clone

A

D. Tyrosine kinase activating mutations are almost always absent when RAS mutations are found in the tumor cell, or at least the dominant tumor clone

NOTE: C is right, but that little addition of D, makes it the most right option

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12
Q

What is the most common abnormality involving proto-oncogenes in human tumors?

A. Translocation mutation of RAS

B. Point mutation of RAS

C. Fusion mutation of RAS

D. Overexpression of RAS

E. Amplification of RAS

A

B. Point mutation of RAS

NOTE: Nearly 15-20% of human tumors express mut RAS protein

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13
Q

While nearly 15-20% of human tumors express mutant RAS, some cancer types have an even higher frequency. Which of the following has 90% frequency of RAS point mutations? Bonus: Which have 50% or 30%?

A. Colon, endometrial, and thyroid cancer

B. Lung adenocarcinomas and myeloid leukemia

C. Panceratic adenomas and Cholangiocarcinomas

D. None of the above

A

C. Panceratic adenomas and Cholangiocarcinomas

50%- colon, endometrial, and thyroid

30%- lung adenocarcinomas and myeloid leukemia

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14
Q

Decreased functioning of which of the following would most likely lead to an increase in RAS activity seen in many cancers like Familial Neurofibromatosis Type 1?

A. MAPK and PI3T/Akt

B. RAS-GTP binding

C. GAP

D. cyclin D

A

C. GAP

NOTE: GAP is GTPase-activating proteins, which is encoded by NF1 tumor suppressor gene. A LoF in NF1 leads to the inherited cancer syndrome Familial Neurofibromatosis Type 1

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15
Q

In almost 100% of hairy cell leukemias, 60% of melanomas, and 80% of benign nevi, mutations in BRAF have been detected. BRAF mutations would allow activation of which of the following without external signaling?

A. RAS

B. PI3K/Atk

C. MAPK

D. mTOR

A

MAPK

NOTE: BRAF is a serine/threonine protein kinase that sits atop the MAPK cascade

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16
Q

Phosphorylation of Akt by PIK3 leads to increased activity of which of the following?

A. mTOR a nutrition status sensor that turns on lipid and protein synthesis

B. BAD a pro-apoptotic substrate

C. FOXO a promotor of apoptosis

D. None of the above

A

A. mTOR a nutrition status sensor that turns on lipid and protein synthesis

NOTE: phosphorylated Akt inhibits BAD and FOXO, which also adds to the ability of a tumor cell to ignore death signals

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17
Q

What is the tumor supressor gene that responsible for regulating PI3K, whose LoF mutation is often implicated in the devlopment of endometrial carcinomas?

What is the tumor suppressor gene that’s responsible for synthesizing GAP, a protein that helps deactivate RAS, whose LoF mutation is often discoverable in Familial Neurofibromatosis Type 1?

A

What is the tumor supressor gene that responsible for regulating PI3K, whose LoF mutation is often implicated in the devlopment of endometrial carcinomas?

PTEN

What is the tumor suppressor gene that’s responsible for synthesizing GAP, a protein that helps deactivate RAS, whose LoF mutation is often discoverable in Familial Neurofibromatosis Type 1?

NF1

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18
Q

In chronic myelogenous leukemia and acute lymphoblastic leukemias the ABL gene is translocated to the BCR gene, where the BCR gene’s ability to self-asociate with ABL is sufficient for activating the tyrosine kinase activity of ABL. What is the route of translocation of ABL to become ABL-BCR?

A. Chromosome 9 to chromosome 20

B. Chromosome 20 to chromosome 9

C. Chromosome 19 to chromosome 22

D. Chromosome 9 to chromosome 22

A

Chromosome 9 to chromosome 22

NOTE: Fusion of an oncogenic tyrosine kinase to a self-associating non-tyrosine kinase is a common mechanism of cancer

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19
Q

T/F: ABL-BCR inhibitors have been a nice designer drug for therapies for CML patients (chronic myeloid leukemia), due to the oncogene addiction of the CML tumor cells

A

True

NOTE: signalling of ABL-BCR is required for CML proliferation and survival

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20
Q

MYC activates the expression of genes involved in all of the following EXCEPT?

A. Warburg effect

B. Cell growth through cyclin D expression

C. Ribosome assembly needed for protein synthesis via rRNA expression

D. Telomerase expression

E. Reprogramming somatic cells into pluripotent stem cells

F. All of the above are actually correct

A

All of the above are actually correct

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21
Q

WBurkitt Lymphoma usually develops from a chromosomal translocation that involves what gene?

A. MYC

B. NMYC

C. Both MYC and NMYC

D. None of the above

A

MYC

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22
Q

What are two major checkpoints of the cell cycle?

A

G1/S transition

G2/M transition

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23
Q

Gain of function mutation in what two genes most often promotes G1/S transition?

A. Cyclin B and E with CDK6

B. Cyclin D and CDK4

C. CDKI and Cyclin D

D. None of the above

A

cyclin D and CDK4

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24
Q

What 3 tumor suppressor genes normally inhibit G1/S progression?

A

p16

RB (retinoblastoma)

TP53

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25
Q

Read this

A

x3

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26
Q

Know this too and look at other flash cards for testing

A

x3

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27
Q

RB function is compromised in 2 ways. One of those ways is a LoF that involves the RB alleles. What is the other way that is due to either a GoF of cyclinD/CDKs or LoF of CDKIs?

A. Rapid shift from active HYPERphosphorylated state to inactivated HYPOphosphorylated state

B. Rapid shift from active HYPOphosphorylated state to inactivated HYPERphosphorylated state

A

B. Rapid shift from active HYPOphosphorylated state to inactivated HYPERphosphorylated state

Remember RB is a tumor suppressor and it should NOT be HYPER when active

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28
Q

In what state is RB inactivated, allowing E2F to be released and the cell cycle able to progress forward?

A. HYPERphosphorylated

B. HYPOphosphorylated

A

HYPERphosphorylated

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29
Q

What oncogenic virus utilizes it’s E7 protein to bind RB and make it functionally inactive even in its HYPOphosphorylated state?

A. Simian Virus 40

B. Polymavirus

C. HPV

D. Adenovirus

A

C. HPV

NOTE:

Simian Virus 40 and Polymavirus use large T-antigens

Adenovirus uses E1A protein

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30
Q

A loss of function mutation on which of the following chromosomes is most likely to cause a mutation in TP53?

A. Chromosome 13q14

B. Chromosome 17p13.1

C. Chromosome 11p15

D. None of the above

A

Chromosome 17p13.1

NOTE: Chromosome 13q14 is RB

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31
Q

People with an inherited TP53 mutation are said to have what syndrome where there is a 25-fold chance of developing cancer before the age of 50?

A. Familial Retinoblastoma

B. Cowdmens syndrome

C. Li-Fraumeni syndrome

D. None of the above

A

Li-Fraumeni syndrome

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32
Q

What two proteins are released inresponse to DNA damage or hypoxia, and posttranslational phosphorylation of p53 and MDM2 disrupts p53s degredation by MDM2, allowing for p53 to accumulate?

A. ATM and ATR

B. ATM and p14/ARF

C. ATR and p14/ARF

D. p14/ARF

A

ATM

ATR ( AT and Rad3)

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33
Q

Which of the following is released during oncogenic stress (lots of MAPK and PIK3/Akt activity), and binds MDM2 to displace and allow accumulation of p53?

A. ATM and ATR

B. ATM and p14/ARF

C. ATR and p14/ARF

D. p14/ARF

A

p14/ARF

NOTE: p14/ARF is encoded by the CDKN2A tumor suppressor gene

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34
Q

How does p53 induce transient cell cycle arrest?

A. Early in the G1 phase, transcription of CDKN1A gene is promoted which encodes the CDKI, p21

B. Late in the G1 phase, transcription of CDKN1A gene is promoted which encodes the CDKI, p21

C. Transcription of proteins like Bax and Puma

D. Mechanism is unclear

A

B. Late in the G1 phase, transcription of CDKN1A gene is promoted which encodes the CDKI, p21

35
Q

How does p53 induce senescence?

A. Early in the G1 phase, transcription of CDKN1A gene is promoted which encodes the CDKI, p21

B. Late in the G1 phase, transcription of CDKN1A gene is promoted which encodes the CDKI, p21

C. Transcription of proteins like Bax and Puma

D. Mechanism is unclear

A

D. Mechanism is unclear

36
Q

How does p53 induce apoptosis?

A. Early in the G1 phase, transcription of CDKN1A gene is promoted which encodes the CDKI, p21

B. Late in the G1 phase, transcription of CDKN1A gene is promoted which encodes the CDKI, p21

C. Transcription of proteins like Bax and Puma

D. Mechanism is unclear

A

C. Transcription of proteins like Bax and Puma

NOTE: intrinsic (mitochondrial) pathway

37
Q

T/F: p53 is inactivated by viral oncoproteins like HPV’s E6

A

True

38
Q

Adenomatous Polyposis Coli (APC) is the gatekeeper of colonic neoplasia, which develops when there is a germinline mutation on what loci that results in APC LoF?

A. Chromosome 11p15

B. Chromosome 17p13.1

C. Chromosome 13q14

D. Chromosome 5q21

A

Chromosome 5q21

39
Q

APC is a component of which of the following signaling pathways where it inhibits the proto-oncoprotein Beta-catenin?

A. RAS

B. Notch

C. WNT

D. None of the above

A

WNT

40
Q

Germline mutation of PTEN results in what syndrome?

A. Neurofibromatosis Type 1 an AD disorder associated with higher risk of neurofibromas and malignant peripheral nerve sheath

B. Cowdens syndrome an AD disorder association with higher risk of breast cancer and endometrial cancer

C. Gorlin syndrome an AD disorder associated with increased risk of basal cell carcinoma and medulloblastoma

D. von Hippel Lindau syndrome an AD disorder associated with higher risk of renal cell carcinoma and pheochromocytoma

A

B. Cowdens syndrome an AD disorder association with higher risk of breast cancer and endometrial cancer

41
Q

Germline mutation of NF1 results in what syndrome?

A. Neurofibromatosis Type 1 an AD disorder associated with higher risk of neurofibromas and malignant peripheral nerve sheath

B. Cowdens syndrome an AD disorder association with higher risk of breast cancer and endometrial cancer

C. Gorlin syndrome an AD disorder associated with increased risk of basal cell carcinoma and medulloblastoma

D. von Hippel Lindau syndrome an AD disorder associated with higher risk of renal cell carcinoma and pheochromocytoma

A

A. Neurofibromatosis Type 1 an AD disorder associated with higher risk of neurofibromas and malignant peripheral nerve sheath

42
Q

Germline mutation of VHL results in what syndrome?

A. Neurofibromatosis Type 1 an AD disorder associated with higher risk of neurofibromas and malignant peripheral nerve sheath

B. Cowdens syndrome an AD disorder association with higher risk of breast cancer and endometrial cancer

C. Gorlin syndrome an AD disorder associated with increased risk of basal cell carcinoma and medulloblastoma

D. von Hippel Lindau syndrome an AD disorder associated with higher risk of renal cell carcinoma and pheochromocytoma

A

D. von Hippel Lindau syndrome an AD disorder associated with higher risk of renal cell carcinoma and pheochromocytoma

43
Q

Germline mutation of PTCH1 results in what syndrome?

A. Neurofibromatosis Type 1 an AD disorder associated with higher risk of neurofibromas and malignant peripheral nerve sheath

B. Cowdens syndrome an AD disorder association with higher risk of breast cancer and endometrial cancer

C. Gorlin syndrome an AD disorder associated with increased risk of basal cell carcinoma and medulloblastoma

D. von Hippel Lindau syndrome an AD disorder associated with higher risk of renal cell carcinoma and pheochromocytoma

A

C. Gorlin syndrome an AD disorder associated with increased risk of basal cell carcinoma and medulloblastoma

44
Q

The cancer cells engagement of glucose uptake and conversion to lactose (fermentation) via the glycolytic pathway, even in the presence of a lot of oxygen, is called what?

This behavior is also seen in what normal tissue type?

A

The Warburg Effect

aka Aerobic Glycolys

growing embryonic tissue

45
Q

Metabolic reprogramming required of a tumor cell to cause the Warburg effect is carried out by 3 major pathways: MYC, PI3K/Akt, and RTK activity. All of the following describe the effects of PI3K/Akt, EXCEPT which 2 things? Bonus: Identify the pathways carry out the 2 outliers options.

A. Upregulates glucose transporters and glycolytic enzymes

B. Shunts mitochondrial intermediates to lipid biosynthesis

C. Stimulates factors that are needed for protein synthesis

D. Phosphorylates the pyruvate kinase isoform M2

E. Drives gene expression that supports anabolic metabolism and cell growth, including expression of glycolytic enzymes and glutaminase

A

D. Phosphorylates the pyruvate kinase isoform M2

RTK activity

E. Drives gene expression that supports anabolic metabolism and cell growth, including expression of glycolytic enzymes and glutaminase

MYC

46
Q

What apoptotic pathway is most frequently disabled in cancer?

A. Intrinsic (mitochondrial) pathway

B. EXtrinsic pathway

A

A. Intrinsic (mitochondrial) pathway

47
Q

In more than 85% of follicular B-cell lymphomas which of the following is overexpressed due to a translocation of chromosome 14q32 to 18q21?

A. Bax and Puma

B. BCL2

C. MCL-1

D. All of the above

A

B. BCL2

NOTE: MCL-1 is in the BCL2 family, and often the cause of drug resistant tumors as the drugs generally target intrinsic pathway

48
Q

T/F: All cancers contain cellls that are immortal and have limitless replicative potential

A

True

49
Q

What are the 3 interralting factors that are critical to a cancer cell’s immortality?

A
  1. Evasion of senecence
  2. Evasion of mitotic crisis
  3. Capcaity for self renewal
50
Q

Which of the following would most likely aid in a cancer cell’s ability to evade senscence?

A. RB in a hyperphosphorylated state

B. upregulation of p53 and p16/INK4

C. RB in a hypophosphorylated state

D. None of the above

A

C. RB in a hypophosphorylated state

51
Q

TElomerase activity is the key to which critical component in the cancer cells ability to be immortal?

A. Evasion of senscence

B. Evasion of mitotic crisis

C. Self-renewing capcity

A

B. Evasion of mitotic crisis

52
Q

Self renewal

A

Again, outloud

53
Q

A solid tumor that use to be 2mm, has recently grown to be 4 mm in diameter. Which of the following abilities must the tumor cells have aqcquired in order to reach the new status of growth?

A. Angiogenesis

B. The Warberg Effect

C. TElomerase activity

D. None of the above

A

Angiogenesis

A solid tumor cannot enlarge beyond 1-2mm in diameter

54
Q

The metastatic cascade is divided into two phases. What is phase 1?

What is phase 2?

A

Phase 1: Invasion of ECM

Phase 2: Vascular dissemination, homing of tumor cells, colonization

55
Q

Loosening up tumor cell-cell interactions is the first step in invasion of the ECM by tumor cells. The mechanisms in this step are carried out mostly by which of the following substances?

A. Proteases like MMP, cathepsin D, urokinase plasminogen activator

B. Stromal cells like fibroblasts and inflammatory cells

C. Integrins

D. Cadherins

A

D. Cadherins

NOTE: loss of E-cadherin function is commonly seen in epithelial tumors, adenocarcinomas of the colon, stomach, and breast

56
Q

ECM degredation is step 2 of the invasion of ECM by tumor cells, and the mechanism is carried out by which of the following cell types?

A. Fibroblasts

B. Inflammatory cells

C. Resident macrophages

D. Stromal cells

E. Tumor cells

F. All of the above

A

E. All of the above

  • tumor cells can secrete proteolytic enzymes, or induce stromal cells to elaborate proteases
57
Q

The gelatinase MMP9 cleaving Type IV collagen and stimulating the release of VEGF is an example of which of the following steps of invasion of ECM by tumor cells?

A. Step 1: loosening up tumor cell-cell adhesions

B. Step 2: ECM degredation

C. Step 3: Attachment to new ECM components

D. Step 4: migration and invasion

A

B. Step 2: ECM degredation

58
Q

The binding of hepatocyte growth factor (scatter factor) to tyrosine kinase MET on tumor cells is a mechanism of what step in ECM invasion?

A. Step 1: loosening up tumor cell-cell adhesions

B. Step 2: ECM degredation

C. Step 3: Attachment to new ECM components

D. Step 4: migration and invasion

A

D. Step 4: migration and invasion

59
Q

Locomotion of tumor cells through contraction of actin cytoskeleton is usually stimulated by which of the following?

A. Collagen and laminins

B. Tumor cell derived cytokines

C. Growth factors like IGF I and II

D. Hepatocyte growth factor (scatter factor) binding tyrosine kinase MET on tumor cells

E. All of the above

A

B. Tumor cell derived cytokines

NOTE: While A-D all provide locomation, B was specified in a way to make it seem like it was the most direct player…I could be wrong

60
Q

Targeted therapies that are against which of the following components would theoretically cause a decrease of tumor migration in lymphoid tissue?

A. CD95

B. CD44

C. CD14

D. CD21

A

B. CD44

NOTE: CD44 is found on T cells and some solid tumors, and adheres to hyaluronate on high endothelial venules

61
Q

While most metasteses occur in the 1st capillary ed available to the tumor, not every cancer follows this rule due to tropisms. Of the following tumors, which of them is their most frequent route of metastases?

A. Prostate –> bone

B. Bronchogenic –> liver and bone

C. Neuroblastoma –> adrenals

D. None of the above are correct

A

A. Prostate –> bone

NOTE:

BRonchogenic –> adrenals

Neuroblastoma –> liver and bone

62
Q

Some tumor cells are able to make metastatic sites a more hospitalble environment. Which of the following correctly characterizes how breast cancer cells make bone a better metastatic site?

A. Secretion of PTH related hormone stimulates osteoclasts to make RANK-L, which can be used to activate osteoblasts to degrade bone matrix

B. Secretion of RANK-L from stimulates osteoblasts to make PTH related hormone, which can be used to activate osteoclasts to degrade bone matrix

C. Secretion of PTHRH stimulates osteoblasts to express RANK-L, which can be used to activate osteoclasts to degrade bone matrix

D. SEcretion of IGF and TGF-B allows breast cancer cells to degrade bone matrix

A

C. Secretion of PTHRH stimulates osteoblasts to express RANK-L, which can be used to activate osteoclasts to degrade bone matrix

63
Q

Which of the following correctly characterizes the clonal evolution model as an explanation for why some tumors metastasize and others dont?

A. Inherent metastatic gene expression in tumor cells

B. Inherent metastatic gene expression in tumors in necessary, but not sufficient and requires additional genetic evolution

C. The right tumor has to be produced in the correct location

D. Genetic instability allows the cancer cell to acquire a gene pattern sufficient for metastasis

A

D. Genetic instability allows the cancer cell to acquire a gene pattern sufficient for metastasis

NOTE:

A is “metasitic signature”

B is a combo of clonal evolution model and metasttic signature

64
Q

What are the two candidates for metastatic oncogenes that primarily function to promote epithelial-to-mesenchymal transition (EMT) through downregulation of E-cadherin?

A. SNAIL and TWIST

B. SNAIL and Notch

C. Shh and Htt

D. TWIST and Shh

A

A. SNAIL and TWIST

NOTE: this has been documented mainly in breast cancers

65
Q

Look at this chart, be aware of the examples

A

x3

66
Q

Antibodies against which of the following can be used to target B-Cell lymphomas, and also normal B-Cells?

A. MAGE

B. CEA (carcinoembryonic antigen) and AFP (a-fetoprotein)

C. CD20

D. E7 and E6 proteins

E. CD30

A

C. CD20

NOTE: CD30 is related to T cell lymphomas and TNF

67
Q

Which of the following immune cells are likely the first line of defense against tumor cells as they can kill without prior sensitization?

A. CD8+ T cells

B. NK lymphocytes

C. Macrophages

D. Neutrophils

A

B. NK lymphocytes

68
Q

Secretion of which of the following is most instrumental in promoting the callobratory effects of macrophages, NK cells, and CD8 T cells against tumors?

A. IL-2 and IL-15

B. IL-2 and IFNy

C. IFNy

D. TNFa

A

C. IFNy

NOTE: IFNy is secreted by NK cells and CD8 T cells to activate macrophages

IL-2 and IL-15 activate NK cells

69
Q

Upregulation of all of the following receptors by tumor cells would lead to the inhibition or destruction of T cells, EXCEPT?

A. CTLA-4

B. PD-L1

C. PD-L2

D. CD28

A

CD28

CD28 is found on APCs and engagement is needed for complete T cell activation

A-C are all inhibitory factors found on APCs that tell T cells to kill themselves

70
Q

Hereditary Nonpolyposis Colon Cancer syndrome results from defects in a family of genes involved in which of the following DNA-repair mechansims?

A. Mismatch repair

B. Nucleotide Excision Repair

C. Recombination repair

A

A. Mismatch repair

NOTE: Germline mutations in MHS2 and MLH1 are common for about 30% of HNPCC syndrome

71
Q

Microsatalite instability are tandem repeats of 1-6 nucleotides found throughout the genome at variable lengths and distribution. These occurences are hallmarks of mutations in which of the following DNA-repair mechanisms?

A. Mismatch repair

B. Nucleotide Excision Repair

C. Recombination repair

A

Mismatch repair

72
Q

Patients with Xeroderma Pigmentosum are at an increased risk to develop skin cancer due to mutations in which of the following DNA repair mechanisms?

A. Mismatch repair

B. Nucleotide Excision Repair

C. Recombination repair

A

B. Nucleotide Excision Repair

all it takes is a loss of 1

73
Q

All of the following diseases result due to defects in DNA repair via Homologous Recombination, and these autosomal recessive diseases have resulting hypersensitivities to certain types of radiation. Which one of these is hypersensitive to DNA-crosslinking agents and also is associated with BRCA2 mutations?

A. Bloom syndrome

B. Fanconi anemia

C. Ataxia-Telangiectasia

D. A and C

A

B. Fanconi anemia

74
Q

All of the following diseases result due to defects in DNA repair via Homologous Recombination, and these autosomal recessive diseases have resulting hypersensitivities to certain types of radiation. Which one of these is hypersensitive to ionizing radiation?

A. Bloom syndrome

B. Fanconi anemia

C. Ataxia-Telangiectasia

D. A and C

A

A and C

Bloom syndrome

Ataxia-Telangiectasia

75
Q

Which of the following is the most common mechansim for activation of proto-oncogenes?

A. Point mutation

B. Deletions

C. Gene Amplification

D. Chromosomal Translocations

A

D. Chromosomal Translocations

76
Q

Which of the following is true of Deletions, a type of nonrandom chromosomal abnormality?

A. Contributes to carcinogenesis by overexpression of oncogenes or generation of novel fusion proteins with altered signalling capacity

B. Most often causes loss of tumor suppressor gene and occasionally proto-onvogene activation

C. Increases the expression and function of oncogenes

D. None of the above are correct

A

A. Contributes to carcinogenesis by overexpression of oncogenes or generation of novel fusion proteins with altered signalling capacity - Chromosomal translocation

B. Most often causes loss of tumor suppressor gene and occasionally proto-onvogene activation

C. Increases the expression and function of oncogenes- gene amplification

D. None of the above are correct

77
Q

Which of the following miRNAs can be described as an oncomiRNA, and has been shown to promote epithelial to mesenchymal transitions which contribute to invasiveness and metastatsis?

A. miRNA-15 and miRNA-16

B. miRNA-200

C. miRNA-150

D. All of the above

A

B. miRNA-200

78
Q

Which of the following miRNAs can be described as an oncomiRNA, whose overexpression has beendocumented in many B-cell lymphomas, and also contributing to indirect upregulation of genes that promote proliferation like MYC?

A. miRNA-15 and miRNA-16

B. miRNA-200

C. miRNA-150

D. All of the above

A

miRNA-150

79
Q

Deletions of which miRNA(s) are most frequently seen in Chronic Lymphocitic Leukemia, and whose loss leads to upregulation of anti-apoptotic BCL-2?

A. miRNA-15 and miRNA-16

B. miRNA-200

C. miRNA-150

D. All of the above

A

A. miRNA-15 and miRNA-16

80
Q

DICER is a gene that encodes endonucleases responisible for processing and producing functional miRNAs. GErmline defects in DICER are often seen in which of the following?

A. Chronic Lymphocytic Leukemia

B. Upregulation of anti-apoptotic BCL-2

C. B cell lymphomas

D. Rare Familal development of a collection of neoplasms like Ovarian and Testicular cancers

A

D. Rare Familal development of a collection of neoplasms like Ovarian and Testicular cancers

NOTE: DICER, like miRNA-15 and -16 are seen to have tumor suppressive roles/influences

81
Q

T/F: lncRNAs are seen to have regulatory activity of chromatin “writers” and histone modification, and thus have a role in controlling gene expression

A

True

82
Q

Carcinogenesis often occurs in a step-wise fashion that always begins with what event occuring at what chromosome?

And while the events in between can happen in a random order, we always see it end with what event occuring what chromosome?

A

Beginning

Inactivation of tumor supresor APC

5q21

End

Loss of TP53

17p13

Want to download/make cancer? A PC update starts at 5:21 and ends with losing 53 Toilet Paper rolls at 1713, because its a shitty upload

83
Q

Here is the multi-step carcinogenesis as documented by an experiment investigating colon cancer

A

x3

MoD-Exam 2 (11 decks)

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