Developing B cells that fail to make productive D to J heavy-chain rearrangements on both homologous chromosomes a. die by apoptosis in the bone marrow b. will rearrange heavy-chain loci multiple times until a productive rearrangement is made c. undergo clonal proliferation d. upregulate expression of transcription factors E2A and EBF e. fail to rearrange V to DJ.

When the antigen-presenting cells binds to the T-cell, it will cause the T-cell to increase the amount of a protein called perforin, which is secreted to kill nearby cells. Which of these could INCREASE the amount of a functional perforin proteins produced?       a.   Increased methylation of DNA near the site of the gene       b.   Increased binding of a repressor, that decreases the binding affinity between TFIID and DNA       c.   Increased production of a small RNA that is complementary to perforin mRNA       d.   Increased O-linked glycoslyation of perforin proteins in the Golgi

Which of the following statements concerning p53 is NOT correct? O a. p53-dependent transcription of target genes leads to cell cycle arrest or cell death (apoptosis). O b. O C. Loss of p53 function results in loss of checkpoint controls. Loss of p53 function creates an environment that is permissive for genome instability--that is, more damaged cells with chromosome aberrations and mutations survive and propagate. d. p53 is a tumor suppressor protein which is largely responsible for protecting cells from cancer- causing DNA-damaging agents.

People who inherit two copies of the BRCA1 mutation are not born with cancer, and some of them never end up developing cancer. Give a possible explanation for why a mutation in a single gene does not always lead to cancer.

Which of the following would inhibit the function of the JAK-STAT Pathway? Multiple answers    A. Inhibition of protein import into nucleus   B. The Ser/Thr kinase inhibitor Staurosporine   C. Treat cells with Interferon   D. Inhibitors of SH2 domain interactions   E. Drug that causes dimerization of STAT3

T-cell receptor diversity is controlled by O b. O c. 1 O d. e. DNA recombination during mitosis in T-cells DNA recombination during prophase of meiosis II DNA recombination during prophase of meiosis l proteasomal degradation of viral proteins proteasomal degradation of host proteins

Explain in general what is meant by a proto-oncogene and how they are involved in the formation of a tumor

Please answer subquestions 1.a and 1.b   Question 1.a: A mutation in MAPK makes it constitutively active. If cells are treated with the control treatment (no EGF)                             will be observed. When cells are treated with EGF                            will be observed. A. No proliferation; proliferation B. Proliferation; proliferation C. No proliferation; no proliferation D. Proliferation; no proliferation   Question 1.b: In order to prevent a specific event (step),  from occurring in a pathway (e.g, the phosphorylation of MAPKK), you should target the                             portion of the cascade with an inhibitor. A. Downstream B. Extracellular C. Nuclear D. Upstream

If a centrocyte does not interact with antigen and engage CD40 shortly after its derivation, then Select one: a. it recommences somatic hypermutation b. it undergoes apoptosis C. it moves back into the dark zone of the germinal center and switches its isotype d. its surface immunogloblulin levels decrease and proliferation recommences.

A mutated gene that transforms a normal cell into a tumor cell is called a   a. oncogene.   b. neoplasm.   c. carcinoma.   d. checkpoint gene.   e. proto-oncogene.