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10 Discoveries in the War on Cancer - BIOL 101 Individual Assignment 3

   

Added on  2023-06-08

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BIOL 101
BIOLOGY INDIVIDUAL ASSIGNMENT 3
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BIOL 101
INDIVIDUAL ASSIGNMENT 3 - 10 DISCOVERIES IN THE WAR ON CANCER
1. Virologists are modifying lentiviruses as vectors for carrying proto-oncogenes into
cancer-transformed cells in culture. They are developing this virus for inserting the ras
proto-oncogene directly into its correct location in the genome. The correct ras gene will
already be linked to human DNA on either side of it and complexed with a recombination
enzyme that will insert it into its correct location within the human genome. At the same
time, the recombination enzyme will excise the defective oncogenic form of ras. The
cells in culture should again come under normal hormonal control and require extra-
cellular signals in order to continue dividing. (b) correction of cancer genes, (Cai, Bak
& Mikkelsen, 2014)
2. Malignant brain tumors in adults are fast-growing cancers with median survival rates of
15 months, even with aggressive treatment. Researchers have been searching for genetic
“signatures” (characteristic groups of cancer-causing genes) that could help in defining
the kind of brain tumor the patient has. They hope to be better able to predict the course
of the disease and more accurately design the patient’s course of treatment. a) reduction
of cancer risks, (Park et al., 2017)
3. Tobacco smoking is the leading cause of preventable deaths worldwide. It is a risk factor
for lung cancer and several other types of cancer. Results of analysis of the entire human
gene collection (the “genome”) support some previous findings that a region of human
chromosome number 15 contains one or more genes that are associated with smoking
intensity (the number of cigarettes smoked per day) and the closely related trait of
nicotine dependency. Scanning people’s genomes for these genes will help them to
determine their risk of addiction should they begin smoking tobacco. a) reduction of
cancer risks, (Varella-Garcia, 2010, VanderWeele et al., 2012)
4. Immunologists are working with a mutation (HER2) that is expressed on the surface of
many breast, bladder, pancreatic, and ovarian cancer cells. They have made antibodies
against this mutant surface protein. These antibodies have been covalently bonded to a
“gene expression vector” that makes cells light up when incubated with luciferin from
fire flies. The vector takes the gene for luciferin into the cancer cells. The researchers
have shown that their antibody can accurately find and “light up” cancer cells. Their next
step is to bond the antibody to an expression vector that carries the normal HER2 gene
into mutant cancer cells. (b)correction of cancer genes, (Housman et al., 2014).
5. Immunologists are investigating ways to destroy lymphocytes (white blood cells of the
immune system) that have become cancerous (lymphomas). A current drug Rituximab
contains antibodies that bind to the surfaces of these lymphocytes setting them up for
destruction by the cancer patient’s own immune system. They are currently seeking ways
to modify the antibody’s structure so that it will attract the cancer patient’s “natural
killer” (NK) cells to the lymphocytes. Success of this project will bring a multi-faceted
immune response against lymphomas and hasten destruction (c) destruction of
cancerous tissue, (Goldszmid, Dzutsev and Trinchieri, 2014).
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BIOL 101
6. .Biochemists have discovered a protein kinase enzyme named BRAF that is an important
link in a molecular pathway that causes a cell to divide. Normally, BRAF responds to
signals coming from outside the cell—signals calling for the cell to divide normally
under normal conditions. But there is a mutation in BRAF enzymes that causes it activate
the cell toward division continually. In this way it gives rise to melanomas and thyroid or
ovarian cancers. Biochemists have also found a drug, vemurafenib, which binds
selectively to mutant BRAF totally inactivating it. Cells that have inactivated BRAF
undergo apoptosis—a process that leads to cell death (c) destruction of cancerous
tissue, (NCBI, 2018)
7. Molecular biologists have taken nanoparticle-sized spheres and used them to deliver a
cell-killing toxin from bee venom to tumors in mice, substantially reducing tumor growth
without harming normal body tissues. Nanoparticles are known to concentrate in solid
tumors because blood vessels in tumors show “enhanced permeability and retention
effect” or EPR. Hence substances such as nanoparticles escape more readily from the
bloodstream into tumors and the generally poor drainage of lymph from tumors further
helps trap the particles in tumor tissue (c) destruction of cancerous tissue. (Rady et al.,
2017)
8. Organic chemists are exploring structural variations of the organic compound
avobenzone (1-[4-Methoxyphenyl]-3-[4-tert-butylphenyl] propane-1,3-dione) for
inclusion in sunblock products. Avobenzone is known for its ability to absorb a broad
spectrum of ultra-violet radiations including UVB light (known to enhance the frequency
of basal cell and squamous cell carcinomas [skin cancers]); and UVA rays thought to
increase the frequency of melanoma cancers. New variations in the structure of
avobenzone are hoped to retain the ability to absorb harmful UV radiation while having
an increased stability in the presence of that radiation (a) reduction of cancer risks, (US
Department of Health and Human Services, 2014)
9. Biochemists are analyzing the many, many components of red meat (beef and pork) to
determine which component, if any, will cause increased colorectal cancer rates in mice
when the component is administered orally. Studies have shown that higher colorectal
cancer rates in humans are associated with higher consumption rates of red meat (a)
reduction of cancer risks, (Turner and Lloyd, 2017).
10. Molecular biologists have developed a new sequence of human genes called an ankyrin
insulator sequence. A new corrected or therapeutic gene is placed within this sequence.
Its role is to create an active area on a human chromosome where the new gene can work
efficiently no matter what chromosome it lands on (b)correction of cancer genes,
(Hoban, Orkin and Bauer, 2016).
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