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Monday, November 12, 2012

Cancer threat to human health

Such a neuter usually occurs with a multistage process. Carcinogenesis involves initiation, promotion, and feeler (58:116). Initiation is chiefly caused by DNA damage. With further complications, tumor promotion bequeath occur. Tumor progression is defined as the conversion of a benign tumor to a crabby personous one. It generally results from the ingathering of several genetic defects. These can include mutations, rearrangements, amplification of cellular oncogenes, inactivation of tumor suppressor genes, and karyotypic instability (58:117). Once progression is complete, the cancer cell and its progeny overgrow by a series of divisions (50:43). In this way, the cell populations of many tumors proliferate at an exponential rate.

Later stages of cancer can involve malignant gap. With metastasis, secondary tumors may develop in addition to the essential one. These remote colonies are the result of several physiologic steps including detachment of the primary tumor's cells, infiltration of these cells into the lymphatic and vascular systems, cancer cell circulation, invasion of distant organs, and, finally, the development of the secondary festerings (3:65). intimately all cancers have the capacity for metastasis. Those most likely to spread are large tumors that are poorly differentiated histologically (3:61). In addition, secondary sites can vary widely. Last


Analyses of the human abl gene have shown that it is composed of over 230 kilobases and contains at least 11 exons. Moreover, the gene is oriented with its 5' barricade toward the centromere and possesses two alternative first exons (exons 1a and 1b); each of which is governed by its own independent promoter. Exon 1a occurs closer to exon 2 than exon 1b; indeed, exon 1b is over 200 kilobases away from exon 2.
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Having two independently controlled first exons means that abl can rear two different RNA transcripts: a 6.0kb template RNA and a 7.0kb mRNA. It has been found that the 6.0kb transcript contains exons 1a through 11, while the 7.0kb mRNA starts with exon 1b, skips exon 1a, and continues with exons 2 through 11. The result of this process is that all abl transcripts have kindred 3' exons (33:81).

The relationship between ras mutations and leukemia is complex. Thus far, no exacting correla

The final events in growth factor signal transduction pay back place within the nucleus. In response to some growth signal, certain nuclear proteins bind DNA and initiate transcription. broker regulation research has, in fact, discovered several theme sequences designed specifically to bind just such proteins. any(prenominal) defect in the genes which code for these transcribing proteins could potentially result in oncogenesis (42:27).

It is widely thought that a recombinase enzyme mediates these genetic rearrangements. Such an enzyme would choose signal sequences on V, D, J, and C genes.


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