Question

Question 156

Which of the following is not among the 4 most commonly mutated genes in pancreatic cancer?

1. KRAS
2. p16 gene
3. TGFb eta
4. SMAD4

Question 164

Pancreatic Ductal Adenocarcinoma (PDAC) tumors typically arise from (choose all that apply):

1. tumorigenic pancreatic stellate cells
2. neoplasms derived from ductal cells
3. neuroendocrine cells
4. grade 3 intraepithelial neoplasms

Question 170

A drug that inhibits the interaction between PD and PDL-1 would be classified as a(n)

1. NSAID
2. checkpoint inhibitor
3. adoptive cell transfer inhibitor
4. cytokine-mediated chemotherapeutic agent

Question 60

Chronic inflammation has been observed to play a role in promoting which of the following?

1. tumor cell proliferation
2. tumor cell genetic mutations
3. angiogenesis
4. metastasis
5. All of the above.

Question 73

Which of the following is not a common symptom of pancreatic cancer?

1. lower back pain
2. jaundice
3. bloody stools
4. diabetes
5. obstructed bile duct

Question 82

CD8+ and CD4+ activation can be inhibited when ______________ on tumor cells cause:

1. MHC receptors ; a downregulation of Programmed Death (PD) ligand expression on T cell membranes
2. Programmed death ligand (PDL-1) molecules ; a downregulation of Akt/PI3K-mediated growth/proliferation
3. T cell ; the activation of NK cells
4. None of the above.

Answer 1

Q156) KRAS oncogene, especially KRAS2 is responsible for pancreatic cancer, about in 90% of cases. This gene is located in the chromosome arm 12p and functions as a GTPase involved in intracellular signalling. Impair in KRAS2 GTPase will result in the activation of downstream signalling and thereby increasing cell proliferation.

Q164) pancreatic ductal adenocarcinoma (PDAC) tumours typically arise from neoplasms derived from ductal epithelial cells.

Q170) drug that inhibits the interaction between PD and PDL-1 is classified as checkpoint inhibitor. They are function as tumour suppressing factor by blocking the interaction. These kinds of checkpoint blockers are rapidly becoming a promising cancer therapeutic approach having limited side effects.

Q60) chronic inflammation plays a critical role in the tumour cell proliferation and modulating the immune response. Several inflammatory mediators such as, TNF-alpha, IL-6, TGF-beta and IL-10 have shown to participate in both initiation and progression of cancer.