Molecular Biology: Open Access

Cancer, a highly morbid and mortal disease, which shows properties of metastasis thereby tumours formation at a distant site has been in the last decade been probed and overwhelmingly researched and has been shown to have two significant emerging hallmarks in the pathogenesis of metastasis which are (a) Reprogramming Energy Metabolism (REM) and (b) Evading Immune Destruction (EID). REM has the ability to reprogram and modify the cellular status whilst EID has the ability to evade the natural killer (NK) cells and the macrophages. Cancer cells get benefited by these features in terms of acquisition of nutrition, uptake of glucose, metabolic interactions with the micro environment, thereby resulting in increased nitrogen demand. In this paper, we have discussed the benefits of these emerging hallmarks for cancer cells to sustain and proliferate inside the body and the role of p53 a tumours suppressor gene and c-Myc an oncogene in the regulation of metastasis. Recognition of the broad applicability of these abstractions will progressively aid in the development of new means to treat human cancer.

The term "retractable sarcoma" (RPS) refers to a diverse group of mesenchymal-based cancers that originate in retroperitoneal tissues and vessels. Separated/dedifferentiated lip sarcomas and leiomyosarcomas are the most common RPS, but there are also interesting histological subtypes of neurotic elements. The obsessive and atomic depiction of sarcomas has made significant progress over the past ten years. In light of growth science and the microenvironment, these advancements have prompted significant modifications to their demonstration administration and the development of new remedial methods. The most prevalent RPS subtypes are represented in this survey, along with recent and ongoing pathological and atomic science discoveries.

Background: Gestational diabetes mellitus (GDM) is a complication of pregnancy that is characterized by impaired carbohydrate tolerance as a result of insulin resistance. Objective was to find association between leptin gene with leptin levels, insulin resistance as well as lipid profile in GDM patients as compared to normal glucose tolerant pregnant women.

Method: In this cross-sectional study, 100 GDM patients and 100 gestational age and BMI-matched healthy pregnant women were included. Genotyping of leptin gene LEPG2548A (rs7799039) was performed by PCR-RFLP. Biochemical parameters were estimated. Various insulin resistance models were constructed using suitable homeostasis model assessment formulae. Chi-square test was used to investigate the associations, Mann Whitney U test to compare biochemical parameters, Spearman’s test for correlation studies was used s. Odd’s ratio was computed to study the extent of risk of leptin gene polymorphism in causing GDM. ‘p’ value <0.05 was regarded as statistically significant.

Results: No significant association was observed between leptin gene polymorphism and GDM, leptin levels and insulin resistance. Comparison of IR models among cases and controls showed a significantly low (p<0.0001) HOMA B cell and HOMA 1% B cell (insulin based) as well as significantly high (p<0.0001) HOMA B cell, HOMA 1% B cell (C peptide-based) in cases. It was also observed that C-peptide based insulin resistance models were significantly high (p<0.0001) in cases as compared to controls.

Conclusion: There is no significant association between LEPG2548A alleles with GDM, leptin levels and insulin resistance C–peptide based insulin resistance models were elevated in GDM patients.