PubMed · 12110734
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Joseph S Pagano. 2002-07-11. Viruses and lymphomas.. https://doi.org/10.1056/nejmp020056
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BACKGROUND: Abnormalities of cell numbers and apoptosis have been observed in renal failure. As uncontrolled expression of c-myc is known to induce apoptosis, we thought that polymorphism in the other myc gene, L-myc gene, which is structually similar to c-myc and reported to be expressed in the kidney, may have a role in the induction of apoptosis and thus have role in chronic renal failure. The aim of this study was to investigate the relationship between the distribution of L-myc genotypes and renal failure. METHODS: In the present study we examined 101 chronic renal failure patients who had either live or cadaveric renal transplants and 105 healthy individuals, for L-myc gene polymorphism by polymerase chain reactions and restriction fragment length polymorphism techniques. RESULTS: Among our patient group, the distribution of the LL, LS, and SS genotypes was 24% (n=25), 71% (n=71), and 5% (n=5), respectively, versus 41% (n=43), 47% (n=49), and 12% (n=13) in our control group. The distribution of genotypes was significantly different between our patients and the control group (chi2=12.281; P=.002). The frequency of the S allele was significantly higher in the patient group (chi2=6.122; P=.013). CONCLUSION: Our study showed that having an S allele in the L-myc gene may increase the risk of renal failure.
In recent twenty years, the incidence of lung cancer has increased quickly in our country. Till now, the morbidity and mortality of lung cancer have occupied the top of the cancers. Early diagnosis is the most important key to increase the five-year survival rate. This review is attempted to summarize the early hereditary events during the development of lung cancer, mainly including the mutation of p53 gene, the abnormal methylation of the promoter area of p16 gene, the loss of heterozygosity of 3p, 8p, 9p, 5q, etc. The purpose is to seek the biological markers during the development of lung cancer to provide theoretical basis for treatment of lung cancer.
Prostate cancer, like most other solid tumors, represents a heterogeneous entity consisting of a mixture of androgen-dependent and androgen-independent cells. Although proliferation of prostate tumor cells is often initially androgen-dependent, the inevitable development of androgen-insensitivity in late-stage prostate cancer renders androgen-suppressing treatments ultimately ineffective. Non-hormonal chemotherapy induces apoptosis in actively proliferating cells and is typically of little value, since prostate cancer demonstrates very slow growth kinetics. Objective response rates of < 10% and no improved survival rates have been observed in several hundred clinical studies using both experimental and approved chemotherapeutic agents. An improved understanding of the molecular mechanisms responsible for the onset of the disease, as well as the factors that control the proliferation of prostate cancer cells, have identified key changes in gene expression during cancer progression, especially from androgen-dependent to androgen-independent status. Manipulation of the genes implicated in disease progression represent an important approach for therapeutic intervention. This review summarizes recent progress that has been made with the use of antisense technology with various chemistries to modify gene expression, a strategy that seems to hold great promise for prostate cancer therapy.