PHA 6852 University of Florida Molecular Biology Questions

Description

Using any means of research available (texts, online, etc), briefly explain how defects in mitochondrial function may contribute to development and progression of cancer [3]
Locate and read the following article, then answer the related questions: Keller ET, Fu Z, Yeung K, Brennan M. (2004).
Raf kinase inhibitor protein: a prostate cancer metastasis suppressor gene. Cancer Lett, 207(2): 131-137.
What strategy ensures that passage through the cell cycle is unidirectional and irreversible? What mechanism underlies this strategy? [3]
What is the wee phenotype? What mistiming of the cell cycle does it reflect? What protein activities can cause this phenotype? [3]
What are the mechanisms that regulate the distribution of the correct number of “normal” chromosomes to daughter
cells? [3]
Describe how the phosphorylation state of proteins regulates passage through critical points in the cell cycle [3]
How might overexpression of cyclin D1 foster loss of cell cycle control? [2]
Explain the significance of telomerase expression in cancer cells [2]
Myc activation in quiescent cells is sufficient to induce cell cycle entry in the absence of growth factors – T / F [1]
What protein is encoded by the SIS oncogene, and why might this product be of particular interest to those studying promotion of cell growth? [2]
Briefly describe the difference between carcinomas and sarcomas [2]
According to the Hanahan and Weinberg paper:

In its inactive state, RKIP is (unphosphorylated / phosphorylated) and binds to activated Raf, inhibiting its
ability to (activate / inactivate) MEK [2]
List the two main mediators of stress-induced apoptosis in cancer cells after treatment with chemotherapeutic drugs [2]