Exploring The Kinetics: Bilateral And Unilateral...

1. In 1971, Alfred Knudson Jr. studied the kinetics with which bilateral and unilateral retinoblastomas appeared in children. He determined that the bilateral occurred with one-hit kinetics, whereas the unilateral tumors occurred with two-hit kinetics. Each hit was believed to represent a somatic mutation. This gives reason that cancer is the result of multiple mutations.

2. FTI’s usually function by blocking the enzyme that links the 15 carbon farnesyl lipid group to recently synthesized H- and K-Ras protein molecules. Out of the four Ras proteins (H-, N-, and two K-Ras proteins), H-Ras is the only protein that depends entirely on its farnesyl group for function. N-Ras and K-Ras have alternative lipid groups attached to their C-termini such as geranylgeranyl, which allow them to continue to function as normal. Also, H-Ras oncoprotein is activated in less than 5% of tumor containing Ras oncogenes. This limits the efficacy of any FTIs that might be successively developed. These protein links may explain why FTIs are not effective inhibitors in such cancers as osteosarcoma. To counter this, the next target would be geranylgeranyl and like lipid groups that may attach to these Ras proteins.

3. Diagnosis and death rates are independent of each other. Although the chance of being diagnosed with either of these cancers is low, the fatality of both cancers is high. This difference may be due to how the cancer is formed, whether it’s caused by life style or certain environments. It could also be due to the methods used to diagnose these cancers and the availability of prevention/treatments compared to other known cancers.

4. The normal function of the EGF receptor is to recognize the presence of its associated ligand in the extracellular space and then inform the cell interior of this encounter. In a mutated EGF receptor most of the extracellular domain isn’t there. This trimmed receptor sends out growth stimulatory signals into cells, even if the EGF is not present. This function causes the receptor act as an oncoprotein to drive cell proliferation. Each receptor has its own growth factor ligand or sets of ligands. The binding of the ligand to its receptor initiates multiple biological responses. This includes cell shape, cell survival, and cell motility.

5. Oncogenes are genes that transform normal cells into cancerous cells. Oncogenes occur when there is a mutational activation of proteins that normally promote cell proliferation
Tumor suppressor genes are genes that normally inhibit cell proliferation or promote apoptosis. Tumor suppressor genes code for Tumor suppressor proteins, such as Retinoblastoma protein (pRb) and p53. Tumor suppressor genes (in cancer) function when there is a mutational inactivation of proteins that normally inhibit cell proliferation. If Rb becomes mutated and is not able to prevent cell proliferation, a tumor will eventually grow and form cancer.

6. During the activation of Wnt signaling, GSK-3β firing is blocked and β-catenin is safeguarded from rapid destruction. This causes a large accumulation of β-catenin molecules that travel into the nucleus to activate transcription by binding to Tcf/Lef proteins. The produced multi-subunit transcription factor complexes then activate many significant Wg/Wnt genes, including those encoding critical proteins associated with cell growth and proliferation. High levels in β-catenin have been found to be critical to the formation of colon carcinomas. This can be tested by testing colon cancer tissue and checking for the level of β-catenin expression, this can then be compared to the β-catenin level of normal tissue.

7. Typically, after a β-catenin molecule is synthesized it creates a multiprotein complex with APC and axin. These proteins aid in bringing β-catenin together with is GSK-3β executioner. GSK-3β phosphorylates β-catenin causing it to be tagged by ubiquitylation. Ubiquitylation guarantees the rapid destruction of β-catenin.

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