Download docx Molecular Mechanism

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Major Molecular Mechanisms That Contribute to the Development of Retinoblastoma
Retinoblastoma is a protein containing tumor suppressors that perform essential roles in
the destructive mechanism of the cell cycle and the progression of the tumor. Retinoblastoma
(pRb) blocks the manifestation of S-phase and the growth of cells. Genes carrying tumor
suppressors exist in two broad groups: caretaker and promoter genes whereby, promoters are
tumor suppressors similar to RB and p53 (Yajnik et al. 27). It is noteworthy that tumor
suppressor genes protect cells from certain steps in the process of cancer acquisition. When antioncogene genes transform, their functioning reduces, thus leading to the formation of cancer
about various genetic modifications.
In 1971, Knudson projected a model named 'Two-hit hypothesis' that aimed at
establishing the difference between nonhereditary and hereditary forms in the development of
retinoblastoma. The design emphasized that various molecular mechanisms could help in the
identifying the phenotypic differences between the hereditary and nonhereditary retinoblastoma.
The study established that heritable retinoblastoma tumors rely on the mutation of RB1 gene that
takes place in the germinal cells; thus, the tumors are hereditary (Lamlum, et al. 1071).
Formation of tumors only happens when the additional somatic mutation happens in retinal cells.
The development of retinoblastoma involves the biallelic RB1 gene inactivation in a
single retina cell due to germ line mutation, double somatic mutations where there is a
manifestation of sporadic diseases, and an extra-somatic hit in transmissible diseases. Genomic
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instability and unrestrained cell division can result if tumor suppressors in retinoblastoma are
lost. Moreover, formations of malignant retinoblastoma tumors require additional mutations.
Oncogenes are the mutant alleles of the proto-oncogenes, and consequently, single allele
mutation of a proto-oncogene can result in cellular alterations considered to be dominant (De
Leon 47). Additionally, for a transformation to occur, all alleles contained in suppressor genes
must be modified to facilitate the occurrence of a conversion.
Genes regulating apoptosis can be dominant or they may seem to function like suppressor
genes that exist as caretaker and promoter genes. RB and p53 are the customary tumor
suppressors, and when these genes mutate, a transformation happens whereby cellular
proliferation breaks are freed. Genome integrity emanates from caretaker genes that are
responsible for processes like the DNA repair. However, it should be noted that caretaker genes
do not control the spread of cells directly, but they can help in the mutation of other genes due to
their ability to repair DNA damages (Levitt and Ian 186).
The other molecular mechanism is the cell proliferation. The increase of cells is the rapid
growth of particular genes in a cell. Normally, cells contain several normal genes that participate
in the normalization of the growth process. In this regard, the mutation of some of these types of
genes can happen to configurations that support the proliferation of free cells. Mutated and
cancer-causing genes are known as oncogenes, whereas proto-oncogenes are the usual kinds of
these genes. Oncogenes stimulate the proliferation process, while tumor suppressor genes alter
the cell proliferation process. Further, the mutation processes that transform proto-oncogenes
regularly intensify encoded protein happenings.
Cyclin D gene transcription factor is the other molecular mechanism involved in the
phenomenon in question. An overexpressed or amplified versions proto-oncogene cancers help
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in encoding Myc. In situations where normal cells should halt proliferation, the presence of
surplus quantities of Myc can prompt the proliferation process to take place.
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Works Cited
De Leon, M. Ponz. "Oncogenes and tumor suppressor genes." Familial and Hereditary Tumors.
Springer Berlin Heidelberg, 1994. 35-47.
Lamlum, Hanan, et al. "The type of somatic mutation at APC in familial adenomatous polyposis
is determined by the site of the germline mutation: a new facet to Knudson's' two-hit
hypothesis." Nature Medicine 5.9 (1999): 1071-1075.
Levitt, Nicola C., and Ian D. Hickson. "Caretaker tumor suppressor genes that defend genome
integrity." Trends in molecular medicine 8.4 (2002): 179-186.
Yajnik, Vijay, et al. "Dock 3 tumor suppressor gene." U.S. Patent Application No. 10/480,330.