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Biology 101 flashcards
0
Q

Name the 6 hallmarks of cancer

A 
Self sufficiency in growth signals
Insensitivity to inhibitory signals
Evasion of apoptosis
Limitless replicative potential
Sustained angiogenesis 
Potential for metastasis/invasion
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1
Q

Name two BONUS hallmarks of cancer

A

Modified energy metabolism

Immune escape

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2
Q

What phase of cell signal is most critical for development of neoplastic phenotype?

A

G0-G1 transition (aka R point, restriction point)

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3
Q

Define anoikis

A

Cell suicide occurring when cell loses integrin-mediated attachment to ECM.

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4
Q

Describe the forces that shift the oxygen hemoglobin dissociation curve

A

Temperature
PCO2
H+
2,3DPG

Increases shift right, decreases shift left

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5
Q

Ki67

  • putative function?
  • clinical utility
  • change throughout cell cycle
A

Function unknown: ribosomal RNA synth?
Only expressed in proliferating cells
Located in nucleolus during interphase, moves to perichromosomal location during mitosis.

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6
Q

AgNOR

  • stands for?
  • what are the two main proteins?
A

Argyrophilic staining of Nucleolar Organizing Regions

Nucleolin and nucleophosmin

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7
Q

What is the Philadelphia chromosome?

  • disease its associated with
  • rearrangement
  • drug target
A

CML
9 and 22 translocation
Gleevec

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8
Q

Identify the most correct statement in regards to the cancer stem cell hypothesis.

a. All cancer cells have the potential to self-renew, proliferate indefinitely and differentiate to give rise to more differentiated tumor cells
b. Only a minority of cancer cells has the potential to self-renew, proliferate indefinitely and differentiate to give rise to more differentiated tumor cells
c. Every cancer stem cell is fated to form new metastasis
d. Terminally differentiated cells are the only cells of origin in most cancers

A

Answer: b

Explanation:

a. This is incorrect because not all cancer cells have the potential to self-renew, proliferate, or differentiate
c. Not every CSC is fated to form a new metastasis (p. 299)
d. Somatic stem and progenitor cells are likely to be the cell or origin in some (perhaps most) cancers, but some terminally differentiated cells, which can be much longer-lived than previously assumed, may have sufficient time to acquire oncogenic mutations in a stepwise fashion, allowing them to evade apoptosis and senescence, proliferate independently of microenvironmental signals, and reactivate their self-renewal potential.

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9
Q

In regards to targeting cancer stem cells, identify the most correct answer in regards to the type of cancer, the targets, and the interventions used for treatment.

a. Breast carcinoma: VEGF, Hedgehog, BMPR2: Perifosine, Cyclopamine, Gemcitabine
b. Melanoma: AKT, NOTCH, IL-4: Rapamycin, Gamma-secretase inhibitor
c. Pancreatic carcinoma: BMPR2, NF-κβ, MHC and NK ligands: Parthenolide, Bevacizumab
d. Acute myeloid leukemia: mTOR, CD44, CD47: Rapamycin, Anti-CD44 antibody, Anti-CD-47 antibody

A

Answer: d

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10
Q

You have isolated some cells that you believe are cancer stem cells (CSCs) from a human breast cancer sample. When injected into an immunocompromised mouse, a tumor is formed. According to the CSC hypothesis, what additional piece of information is necessary to prove these are CSCs?

a. Identify the new tumor’s metastatic potential
b. Confirm genotype and phenotype heterogeneity is identical to the original tumor
c. Remove cells from the xenograft and successfully implant into a different host
d. Determine that the tumor is resistant to all cytotoxic chemotherapy
e. Successfully regrow the tumor in a growth factor-deficient media

A

Answer: b

CSCs are characterized by their ability to generate tumors upon serial transplantation in immune deficient animals AND their ability to recapitulate the genetic and phenotypic heterogeneity of the original tumor.

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11
Q

Which of the following types of mice would be most successful for xenotransplantation (e.g., least likely to reject the xenograft)?

a. Irradiated mice
b. Athymic nude mice
c. SCID mice
d. NOD/SCID mice
e. NSG mice

A

Answer: e

These are listed from earliest to most recent, with NSG mice being the newest and preferred option. NSG mice (aka NOD/SCID/IL2Yγ-/- mice) lack NK-cell activity as well as B- and T-cell activity.

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12
Q

Identify a type of cancer in which most of the malignant cells are tumor-initiating cells (TICs).

a. Acute myeloid leukemia
b. Colorectal carcinoma
c. Malignant melanoma
d. Glioblastoma
e. Mammary carcinoma

A

Answer: c

Explanation: T&H, page 307-8. The cancer stem cell hypothesis was criticized when TICs were commonly identified in melanomas. About 1 in 4 unselected melanoma cells could form a xenograft. Alternatively, TICs are rare in epithelial cancers and leukemia.

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13
Q

Which of the following immunophenotype would be expected for a suspected cancer stem cell?

a. CD44-/CD24+/CD3-/CD31-
b. CD44+/CD24-/CD3-/CD31-
c. CD133-/CD24+/CD3+/CD31-
d. CD133-/CD24-/CD3-/CD31+

A

Answer: b

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14
Q

Which of the following is the correct definition of totipotent?

a. Ability of stem cells to differentiate into any cell
b. Ability of a cell to differentiate into several different types of cells
c. Ability of a cell to differentiate into one other type of cell
d. Ability of a differentiated epithelial cell to transform to have a mesenchymal phenotype

A

Answer: a

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15
Q

Which of the following most accurately describes Paget’s “seed and soil” theory?

a. It is the concept behind a technique, SS Technique, used to identify cancer stem cells.
b. A normal cell within its respective organ is the seed and the surrounding stroma represents that “soil”. Under the right stromal environment the cell may transform into a malignant cell and form a tumor.
c. The stromal cells within an organ represent the “seeds” and the organ represents the “soil”
d. Cancer cells represent the “seeds” and the organs represent the potential “soil” for seeds to implant and develop into a tumor

A

Answer: d

16
Q
  1. Which of the following is/are upregulated during epithelial to mesenchymal transition?
    i. desmin
    ii. metalloproteinases
    iii. vimentin
    iv. E-cadherin

a. i, iv
b. ii, iii, iv
c. iii, iv
d. i, ii, iii

A

Answer: d.
Explanation: desmin is associated with reorganization of the cytoskeleton. MMPs are associated with degradation of the surrounding ECM. Vimentin is associated with migration through the local environment.

17
Q

Which of the following cell surface marker phenotypes would help identify the cell expressing it as a cancer stem cell?

i. CD34++/CD38-
ii. CD34+/CD38+
iii. CD133+
iv. CD45+

a. i, iii, iv
b. i, iii
c. ii, iii, iv
d. iii, iv

A

Answer: b.

18
Q

Which of the following are characteristic of normal and cancer stem cells?

i. Ability to efflux water soluble flurorescent dyes such as Hoechst 33342
ii. Retention of lipophilic fluorescent dyes such as PKH26 even after several passages in culture
iii. Fluorescing in the presence of propidium iodide
iv. Fluorescing in presence of a dye that requires liberation by aldehyde dehydrogenase

a. i, iii
b. i, iii, iv
c. i, ii, iv
d. ii, iii

A

Answer: c.

(i) (ii) and (iv) are expected of normal and cancer stem cells. PI is membrane impermeable and should only be taken up by leaky (ie dead) cells. See p. 302

19
Q

The mechanism of action of cyclopamine is:

a. Inhibition of mTOR pathway
b. Inhibition of the NOTCH pathway
c. Inhibition of the Hedgehog pathway
d. Inhibition of the AKT pathway
e. CD44 antibody
A

Answer: C

20
Q

Which of the following have been associated with epithelial-to-mesenchymal transition?

i. TGF-β
ii. Fas
iii. Wnt
iv. PDGF
v. caspase 8

a. I, ii, iii
b. I, iii, iv
c. ii, iii, iv
d. iii, iv, v
e. ii, iv, v

A

Answer: b.

21
Q

Which of the following is TRUE regarding cell proliferation in tumors?

a. The rate of cell proliferation in tumors is typically greater than that in rapidly proliferating normal tissues (bone marrow, intestine).
b. The low growth fraction of tumors is the key contributor to chemotherapy resistance.
c. The unlimited population of stem cells within a tumor contributes to its ability regenerate after cytotoxic treatment.
d. The rate of cell proliferation is exponentially higher than the rate of cell death.
e. Tumor cells further from blood vessels have a higher rate of proliferation to meet their nutrient requirements.

A

Answer: b
a) Tumor cell proliferation is generally less than cells of normal renewing tissues. c) Tumor cells likely have a limited amount of stem cells for regeneration. d) The rate of cell production is only marginally higher than the rate of cell death (the rate of cell death is 75-90% of the rate of production). e) Tumor cells further from blood vessels have a lower rate of proliferation, which further contributes to their chemotherapy resistance.

22
Q

Which of the following characteristics is likely predictive of a poor outcome in cancer patients?

a. Acidic intracellular pH
b. Elevated interstitial fluid pressure
c. Downregulation in PERK and IRE-1 signaling
d. Upregulation of VHL protein
e. Low levels of CA9 and GLUT-1

A

Answer: b
. a) Although extracellular pH is often acidic (and correlated with a poor outcome), intracellular pH is typically normal or basic. b) Elevated IFP is caused from a build-up of fluid in the extracellular space due to a lack of functional lymphatics and abnormal/leaky blood vessels. This predicts a poor outcome for some solid tumors in humans. c) PERK and IRE-1 signaling mediate the unfolded protein response, which promotes adaptation to hypoxic stress. Therefore, defects in UPR would result in intolerability to hypoxia. d) VHL is responsible for ubiquitination of HIF-1α and HIF-2α, leading to their degradation. e) CA9 and GLUT-1 are target genes of HIF and should be increased in hypoxic tumors.

23
Q

Match the tumor suppressor gene with its correct downstream target.

a. Tuberous sclerosis 1 (TSC) : upregulation of mTOR
b. PTEN : inhibition of AKT1
c. Rb : increased activity of p21
d. p53 : downregulation of NRF2
e. p53 : decreased glutathione production

A

Answer: b
Loss of tumor suppressor genes increases oxidative stress. Their usual mechanisms include the following: a) TSC inhibits mTOR; b) PTEN inhibits AKT1 and subsequently the FOXO transcription factor; c) Rb apparently does a bunch of things that was not worth mentioning in the chart; d&e) p53 increases NFR2 (via p21) and stimulates glutathione production (via GLS2).

24
Q

In humans, many internal tumors are unlikely to be detected until they grow to approximately what weight? And tumors of this size will contain approximately how many cells? Identify both answer choices.

a. 1 kg, ~ 1012 cells
b. 10 g, ~ 1010 cells
c. 1 g, ~ 109 cells
d. 0.25 g, ~ 103 cells

A

Answer: c
A tumor containing approximately 109 cells will have undergone approximately 30 doublings in volume prior to clinical detection (because of cell loss, this will involve more than 30 consecutive divisions of the initial cell). After 10 further doublings in volume, the tumor would weigh approximately 1 kg (1012 cells), a size that may be lethal to the host. Thus, the range of size over which a tumor is detectable clinically represents a rather short and later part of its total growth history.

25
Q

Identify the true statements in regards to the Warburg effect in tumor cells.

i. Observed in tumor cells even under normal oxygen concentrations
ii. The only identified etiology for aerobic glycolysis in tumor cells is because of functional mitochondrial defects, which occur very commonly in tumors
iii. occurs when glucose is converted to lactate and secreted from the cell, rather than being completely oxidized to CO2 via oxidative phosphorylation in the mitochondria
iv. glycolysis does not have the capacity to generate ATP at a higher rate compared to oxidative phosphorylation
v. glycolytic metabolism arises as an adaptation to the hypoxic conditions that develop during the early avascular phase of tumor growth , as it allows for ATP production and maintenance of homeostasis in the absence of oxygen

a. i, iii, v
b. i, ii, iii
c. ii, iv
d. i, ii, iii, iv, v

A

Answer: a

Explanation:

ii. Initial work by Warburg focused on the concept that tumor cells develop defects in mitochondrial function; however, functional mitochondrial defects in tumors are rare, and most tumor cells retain the capacity for oxidative phosphorylation and continue to consume oxygen at rates similar to those observed in normal tissues.
iv. As an explanation for the shift towards aerobic glycolysis is included the concept that glycolysis has the capacity to generate ATP at a higher rate compared to oxidative phosphorylation, so it could be advantageous as long as glucose supplies are not limited

26
Q

Identify the oncogenic protein that can enhance glutamine metabolism at several levels in the proliferation cycle and render tumor cells highly dependent on exogenous glutamine.

a. PTEN
b. MYC
c. MITF
d. Bcl-2

A

Answer: b
Explanation: One factor that plays a major role in regulating glutaminolysis is the oncogene MYC. Thus MYC promotes not only proliferation but also the production of the macromolecules and reducing power required for cell growth and division. MYC increases glutamine uptake by directly increasing the expression of the glutamine transporters SLC5A1 and SLC7A1. Furthermore, MYC indirectly increases the level of glutaminase 1 (GLS1), the first key enzyme of glutaminolysis, by repressing the expression of microRNAs-23a/b, which function to inhibit GLS1.

27
Q

Identify the true statement regarding HIF (hypoxia-inducible factor):

a. HIF1-alpha is constitutively expressed; HIF1-beta is synthesized only in the presence of hypoxia
b. The hypoxia threshold for HIF activation is tissue oxygenation of approximately 8%
c. Hypoxia-induced radiation resistance occurs at approximately the same level of hypoxia that triggers HIF activation
d. HIF expression is inactivated in oxygen-rich states via ubiquitination of HIF-1alpha

A

Answer: d.
(a) HIF1-alpha is oxygen sensitive; HIF1-beta is constitutively expressed (b) Tissue threshold of approximately 2% oxygen (c) It takes more mild hypoxia to trigger HIF activity than it does to induce radiation resistance

28
Q

Which is the correct statement regarding tumor hypoxia?

a. A tumor’s size is predictive of the level of hypoxia within it
b. Immunohistochemistry is the test of choice to identify oxygenation at the cellular level
c. Tumors typically undergo perfusion-limited hypoxia while diffusion-limited hypoxia is typically confined to non-neoplastic tissue
d. The oxygenation threshold for HIF activation threshold is higher in neoplastic tissue than in normal tissues.

A

Answer: b.
(a) weak correlation between size and hypoxia; hypoxia is not always worst at core of tumors. (c) Tumors can experience both; normal tissues should not experience diffusion limited hypoxia if tissue blood supply is unaltered. (d) Should be approximately similar for normal and neoplastic tissues

29
Q

What percent of cells are expected to be in S phase in most human solid tumors?

a. 1-2%
b. 3-15%
c. 20-27%
d. 30-45%

A

Answer: b

30
Q

Which of the following when increased can induce autophagy?

i. HIF1
ii. Fas
iii. mTOR
iv. Fad
v. UPR

a. i, ii, iii
b. i, iii, v
c. ii, iii, iv
d. iii, iv, v
e. ii, iv, v

A

Answer: B

31
Q

How does the PI3K pathway affect aerobic glycolysis?

a. upregulation of AKT1 that causes downstream increases in ATP
b. AKT1 activates mTOR by dephosphorylating TSC2
c. PI3K is activated by PTEN
d. AKT1 signaling upregulates fork-head box subfamily O (FOXO) resulting in increase of glycolytic capacity
e. AMPK is a potent activator of the AKT1 pathway
A

Answer: A

32
Q

Which of the following are CORRECT regarding endoplasmic reticulum stress secondary to hypoxia?

i. Response to stress is mediated by three sensors: PERK, IRE-1, and ATF6
ii. PERK activation leads to downstream decreases in protein synthesis
iii. IRE-1 and ATF6 lead to mechanisms that support adaptation and recovery from ER stress
iv. increased ATF4 expression is a positive prognostic indicator in canine lymphoma
v. Defects in PERK and IRE-1 signaling result in cell survival during hypoxia

a. I, ii, iii
b. ii, iii, iv
c. iii, iv, v
d. I, iii, v
e. ii, iv, v

A

Answer: A

Explanation: IV) expression of ATF4 is upregulated in perinecrotic regions of human tumors; this has not been reported as a prognostic indicator in animals V) defects in PERK and IRE-1 lead to increased cell death during hypoxia

33
Q

Which of the following statements are true regarding mTOR?

i. Hypoxia inhibits mTOR signaling
ii. mTOR signaling stimulates autophagy
iii. mTOR inhibition generally reduces metabolic activity
iv. mTOR inhibition promotes tolerance to hypoxia

a. i, ii
b. ii, iii
c. i, iii, iv
d. ii, iii, iv

A

Answer: c

  • inhibition of mTOR stimulates autophagy
  • inhibition of mTOR promotes tolerance to hypoxia and reduces metabolic activity. Agents that inhibit mTOR could result in an increase in the proportion of viable hypoxia cells and as a consequence reduce the effectiveness of other therapies.
34
Q

Which of the following is true regarding the unfolded protein response (UPR)?

a. UPR occurs secondary to mitochondrial disruption
b. UPR occurs secondary to hypoxia
c. UPR is induced by extracellular acidosis
d. UPR has been associated with an improved prognosis in most human tumors

A

Answer: b

Basic Science (11 decks)

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