Neoplasia/Cell Cycle Flashcards
(16 cards)
Which statement is false regarding antitumor immune effector mechanisms?
a. Macrophages require tumor antigen-specific priming by dendritic cells
b. Natural Killer cells bind to tumor cells lacking MHC molecules and release lytic granules to activate apoptosis
c. Macrophage antitumor activation is stimulated by IFN-γ
d. Cytotoxic lymphocytes are primary effector cells of adaptive antitumor immune response
e. CD4+ T lymphocytes release IL-2 which stimulates CD8+ T lymphocyte proliferation
a, Robbins and Cotran, 8th ed, pg. 319-320
Macrophages anti-tumor activity is stimulated by what?
a. IL-5
b. IL-4
c. Interferon-y (IFN-y)
d. Tumor necrosis facter (TNF)
e. IL-2
c, IFN-y pg 306 Mcgavin 5th edition
A missense mutation that changes a codon for on amino acid into a codon for a different amino acid has been identified in what gene in German shepherd dogs with hereditary multifocal renal cystadenocarcinoma and dermatofibrosis?
a. NF1
b. Birt-Hogg-Dube (BHD)
c. BRCA 1
d. RET
e. MEN1
b, BHD pg 312-313 Mcgavin 5th edition
Which growth factors can endothelial cells of tumor blood vessels produce that can stimulate the growth of tumor?
a. platelet-derived growth factor and interleukin 1
b. Transforming growth factor alpha and IL-4
c. Von-Willabron factor and factor 8
d. VEG-1 and VEG-2
e. IL-2 and IL 5
a, Pathologic Basis of Veterinary Disease McGavin, Zachary 2007 p. 273
JAK2 mutations are involved in the pathogenesis of which of the following neoplastic processes?
a. polycythemia vera
b. primary myelofibrosis
c. hepatocellular adenoma
d. A and B
e. A, B, and C
e, Robbins, 8ed, 2010, p. 284 and NEJM January 2013 (368:2) p.161
Which of the following cyclin-dependent kinases allows cells to progress through the G1 restriction point?
a. CDKN1A-D
b. CDK4
c. CDK2
d. CDKN2A-C
e. CDK1
b, Robbins, 8ed, 2010, p. 286
Which of the following statements about p53 is FALSE?
a. MDM2 and MDMX stimulate its degradation
b. Transcription of MDM2 can be up-regulated by p53
c. p53 activates transcription of the mir35 family of miRNAs
d. p53 mediated cell-cycle arrest occurs mainly due to transcription of CDKN1A (p21)
e. GADD45 can be induced by p53
c. Robbins, Pathologic Basis of Disease, 8th ed. p. 290-292. p53 activates transcription of the mir34 family of miRNAs
Which of the following statements about exosomes in neoplastic lesions is FALSE?
a. They are bilayered membrane-bound nanovesicles
b. Commonly used molecular markers include surface tetraspanins, CD9, CD81, CD63 and MHC class II
c. Contents can include signal proteins, lipids, miRNAs and functional mRNAs
d. They can facilitate metastasis via inducing expression of VEGFbeta, TNF alpha and HIF1alpha
e. They release cytokines to stimulate antigen presenting cells, including dendritic cells
e. Am J Pathol. 2014. Vol. 184. p. 28. Abstract plus p. 30 (molecular characteristics) p. 33 (immunity) p.36 (angiogenesis). They DECREASE activity of APCs, including DCs, via increasing pStat3 and increasing IL-6 expression (p. 33)
Which statement is INCORRECT regarding invasion and metastasis?
a. Macrophages at tumor periphery can supply MMP to foster local invasion.
b. Increased expression of E-cadherin is established as an antagonist of invasion and metastasis.
c. IL-2 is produced by cancer cells to activate macrophages.
d. Snail, slug, twist, and Zeb1/2 orchestrate epithelial mesenchymal transition during embryogensis.
e. Mesenchymal stem cells in tumor stroma have been found to secrete CCL5 which stimulates invasive behavior.
c, (IL-4 is produced by cancer cells to activate macs) Hanahan D, Weinbeg RA: Hallmarks of Cancer: The next Generation. Cell 144, 2011
Which statement about reprogramming energy metabolism as an emerging hallmark of cancer is FALSE?
a. Ras and hypoxia together are necessary to increase levels of HIF2α to upregulate glycolysis.
b. Cancer cells largely limit their metabolism to glycolysis.
c. There is upregulation of GLUT1 to increase glucose import into the cytoplasm.
d. Glycolytic fueling has been shown to be associated with activated RAS.
e. Both Ras and hypoxia can also independently increase levels of HIF1α to upregulate glycolysis.
a, Hanahan D, Weinbeg RA: Hallmarks of Cancer: The next Generation. Cell 144, 2011
All of the following are TRUE of MYC, except:
a. expressed in virtually all eukaryotic cells
b. belongs to the immediate early response genes and is rapidly induced when dividing signals are received
c. MYC is amplified in some cases of breast, colon, lung, and many other carcinomas
d. orchestrates the orderly progression of cells through the various phases of the cell cycle
e. MYC is a transcription factor which can act to reprogram somatic cells into pluripotent stem cells
d, Robbins and Cotran, 8th Ediditon, 2010, pg. 284-5
Which of the following resist epithelial-to-mesenchymal transition (EMT) by phosphorylating SNAIL and marking it for degradation by proteasomes?
a. GSK3
b. IκB
c. KLF17
d. miR205
e. podoplanin
a, Cell, volume 139 (5), pg 871-90
p53 causes cell cycle arrest mainly by enhancing transcription of which CDK inhibitor?
a. p21
b. p57
c. p18
d. p15
e. p19
a, R anc C, p. 292
Normally, when DNA repair is unsuccessful, p53 directs cell death by activation of which component?
a. p21
b. GADD45
c. Cyclin D
d. BAX
3. p16INK4a
d, PBVD, p. 317
Which of the following prevents G1/S transition?
a. Hyperphosphorylated RB
b. Histone methyltransferase
c. E2F transcription factors
d. Cyclin D
e. Cyclin E
b, Robbins and Cotran 8th ed, p288-289
The following cyclin-CDK complexes is active in the G2-M transition phase of the cell cycle:
a. CyclinD-CDK4
b. CyclinD-CDK6
c. CyclinE-CDK2
d. CyclinA-CDK2
e. CyclinB-CDK1
e, Robbins and Cotran, p:285
