Expression of a truncated allele of the Apc tumor suppressor causes intestinal tumors with a low rate of chromosomal instability (CIN). Increasing the rate of CIN suppresses tumor growth without inhibiting tumor initiation in both the small intestine and colon, suggesting that increasing CIN is a useful chemotherapeutic strategy.

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Background MicroRNAs (miRNAs) represent a novel class of single-stranded RNA molecules of 18–22 nucleotides that serve as powerful tools in the regulation of gene expression. They are important regulatory molecules in several biological processes. Main body Alteration in the expression profiles of miRNAs have been found in several diseases. It is anticipated that miRNA expression profiling can become a novel diagnostic tool in the future. Hence, this review evaluates the implications of miRNAs in various diseases and the recent advances in miRNA expression level detection and their target identification. A systematic approach to review existing literature available on databases such as Medline, PubMed, and EMBASE was conducted to have a better understanding of mechanisms mediating miRNA-dependent gene regulation and their role as diagnostic markers and therapeutic agents. Conclusion A clear understanding of the complex multilevel regulation of miRNA expression is a prerequisite to explicate the origin of a wide variety of diseases. It is understandable that miRNAs offer potential targets both in diagnostics and therapeutics of a multitude of diseases. The inclusion of specific miRNA expression profiles as biomarkers may lead to crucial advancements in facilitating disease diagnosis and classification, monitoring its prognosis, and treatment. However, standardization of methods has a pivotal role in the success of extensive use of miRNA expression profiling in routine clinical settings.

Chromosomal instability (CIN) is a hallmark of cancer. While low levels of CIN can be tumor promoting, high levels of CIN cause cell death and tumor suppression. The widely used chemotherapeutic, paclitaxel (Taxol), exerts its anticancer effects by increasing CIN above a maximally tolerated threshold. One significant outstanding question is whether the p53 tumor suppressor is required for the cell death and tumor suppression caused by high CIN. Both p53 loss and reduction of the mitotic kinesin, centromere-associated protein-E, cause low CIN. Combining both genetic insults in the same cell leads to high CIN. Here, we test whether high CIN causes cell death and tumor suppression even in the absence p53. Despite a surprising sex-specific difference in tumor spectrum and latency in p53 heterozygous animals, these studies demonstrate that p53 is not required for high CIN to induce tumor suppression. Pharmacologic induction of high CIN results in equivalent levels of cell death due to loss of essential chromosomes in p53+/+ and p53−/− cells, further demonstrating that high CIN elicits cell death independently of p53 function. Implications: These results provide support for the efficacy of anticancer therapies that induce high CIN, even in tumors that lack functional p53.

OBJECTIVE: Elevated plasma lipid levels are believed to be probable cause of endothelial cell dysfunction. We planned to measure the changes in the lipid levels in patients of PIH (pregnancy induced hypertension) and compare it with that of normotensive pregnant females. MATERIALS & METHODS:We studied 804 pregnant women. 624 patients studied were of PIH and 180 patients were healthy pregnant women. Lipid levels were estimated in these pregnant women. RESULTS: We found a significant rise in the serum lipid levels in the PIH patients group as compared to normotensive pregnant females, which were highly significant (P<0.001) except changes in LDL (P>0.05) and total cholesterol. Amongst the different lipoprotein ratios, TC: HDL, LDL: HDL, TG: HDL, and HDL: VLDL ratios were found highly significant (p<0.001) in PIH patients group. CONCLUSION: It is essential that blood lipid concentrations be estimated in pregnant women during antenatal care since it could be useful in early diagnosis and prevention of obstetric complications such as PIH. INTRODUCTION:Pregnancy induced hypertension is recognized since ancient times. It has been described in reviews of Thiagarajha and Chesley 1 .Hypertension after 20 weeks of pregnancy in a woman with edema and proteinuria without previous history of hypertension is called pregnancy induced hypertension (PIH). When associated with proteinuria, the disorder is termed pre -eclamptic eclampsia/ toxemia and when present without protein in the urine, it is called transient hypertension or gestational hypertension 2 . Raised blood pressure is present in 5% of entire pregnancies, in 10% of primiparous women and 20 -25% of women with pervious history of chronic hypertension. It is the major cause of fetomaternal morbidity and mortality 3 .When blood pressure rises in pregnancy with significant protein in the urine, it is called pre-eclampsia. It may occur from 20 weeks of pregnancy. It can also occur upto 6 weeks post partum. Delivery of the placenta is the ultimate treatment. It may affect both fetal and mother survival 4 .Eclampsia is a dangerous complication of pregnancy with a sudden onset and has the features of developing tonic -colonic seizures in a patient who has pre -eclampsia. With increasing age, the risk of developing PIH increases 5 .