3% of patients with MC and AC respectively, had distant metastasis (p=0.07). MAC vs MC, p=0.01, MAC vs AC, p=0.03). Tumor size, tumor volume, and the rate of microsatellite instability were found significantly higher in the MC group (p<0.05). The 5-year overall (OS) and disease-free survival (DFS) were better in the MAC group compared with MC and AC groups, but these differences did not reach statistical significance (OS 92.8% vs 72.7% and 68.7%, p=0.16 and DFS 87.3% vs 58.2% and 64%, p=0.10, respectively). MC is associated with more advanced tumor size and T stages, and therefore entails reduced rate of minimally invasive procedures. In our series, the absence of distant metastasis in the patients of MAC also had a positive effect on survival.MC is associated with more advanced tumor size and T stages, and therefore entails reduced rate of minimally invasive procedures. check details In our series, the absence of distant metastasis in the patients of MAC also had a positive effect on survival.Type 2 diabetes mellitus (T2DM) is a pandemic metabolic disease worldwide. Multiple types of cancer, particularly liver cancer, are closely associated with T2DM. As a result, there is growing interest in investigating whether anti-diabetic medications could lower cancer risks in the population and even prolong patient survival among those with concurrent cancer. There are many types of anti-diabetic medications available in the clinic. The present study reviewed how different anti-diabetic drugs affect cancer risk and patient survival. On the one hand, multiple retrospective studies have shown that the different anti-diabetic medications have distinct effects on cancer risks. Insulin-raising drugs, including exogenous insulin, increased cancer risks, while drugs potentiating insulin sensitivity like metformin reduced cancer risks. On the other hand, the effects of anti-diabetic medications on patient survival are relatively less studied, except limited reports in liver cancer and pancreatic cancer. It seems that metformin could extend overall survival in patients of early-stage cancer. In contrast in the advanced cancer with metastasis, metformin has no effect or even worsens cancer mortality. It is yet unknown whether these distinct effects of metformin are attributable to the severity of the cancer staging or to the drug interactions between metformin and other medications. This question warrants reconsideration of the current clinical practice in the control of T2DM. Future large-scale prospective studies are needed to resolve this.Among biomarkers that should be useful for a molecular discrimination of patients regarding treatment strategies and prognosis in solid malignancies, novel micro-RNAs (miRs) are under investigation. Quite recently, miRs are considered very promising and significant genetic markers for categorizing patients by their molecular characteristics, as well as extending their complicated genetic signatures. miRs are short, non-coding RNAs consisting of 20-25 nucleotides located at intra- or inter-gene regions. Functional miRs mediate a positive regulation of posttranscriptional gene silencing. Their deregulation in cancer cells due to genetic (e.g., mutations, translocations), epigenetic (e.g., DNA hyper-methylation of tumor suppressor genes, extensive genomic DNA hypo-methylation, aberrant histone modification patterns) and transcriptional alterations lead to a loss of miRs-mediated repression of target mRNA. Interestingly, a biphasic role of miRs in cancers of different histogenetic origin has been confirmed. In some of them, their upregulation is correlated with an increased oncogenic activity, whereas in others, the same miR type acts as a suppressor agent. Thyroid carcinoma comprises different histological subtypes, such as papillary thyroid carcinoma (PTC), follicular thyroid carcinoma (FTC), anaplastic thyroid cancer (ATC), and medullary thyroid carcinoma. In the current molecular review, we explored the role of a specific fraction of miRs in PTC subtype by categorizing them according to their up- or down-regulation status.During lung carcinoma development, progression and metastasis, a variety of gross (chromosome) and specific (gene) genomic alterations are detected in dysplastic, neoplastic, and progressively malignant transformed epithelia as early or late genetic events. Oncogenes' overactivation combined with suppressor genes silence are crucial genetic events in malignant and pre-malignant epithelia. Especially, deregulation of crucial signalling transduction pathways that interact with strong transcription factors - such as c-Fos and c-Jun - leads to an aberrant expression of other critical genes responsible for cell homeostasis. Upregulation of c-Fos and c-Jun leading to other oncogenes overactivation seems to be correlated with aggressive biological behaviour in non-small cell lung carcinomas (NSCLCs). In the current special molecular article we explored the role of c-Fos/c-Jun complex deregulation in NSCLC based on their interactions with other genes that demonstrate modified expression profiles.In medical science, publication record is considered to be a fundamental criterion to evaluate the cost-effectiveness and the reputation of institutions and individual scientists. In current academia, thousands of scientists demonstrate a hyperprolific academic behavior that is the resultant of multiple individual characteristics that can vary from extraordinary ability and teamwork to unjustified and unethical co-authorship. Editors, reviewers and readers should have high expectations from these authors in terms of research quality and ethos.Research about heart failure (HF) has made major progress in the last years. We give here an update on the most recent findings. Landmark trials have established new treatments for HF with reduced ejection fraction. Sacubitril/valsartan was superior to enalapril in PARADIGM-HF trial, and its initiation during hospitalization for acute HF or early after discharge can now be considered. More recently, new therapeutic pathways have been developed. In the DAPA-HF and EMPEROR-Reduced trials, dapagliflozin and empagliflozin reduced the risk of the primary composite endpoint, compared with placebo [hazard ratio (HR) 0.74; 95% confidence interval (CI) 0.65-0.85; P less then 0.001 and HR 0.75; 95% CI 0.65-0.86; P less then 0.001, respectively]. Second, vericiguat, an oral soluble guanylate cyclase stimulator, reduced the composite endpoint of cardiovascular death or HF hospitalization vs. placebo (HR 0.90; 95% CI 0.82-0.98; P = 0.02). On the other hand, both the diagnosis and treatment of HF with preserved ejection fraction, as well as management of advanced HF and acute HF, remain challenging.

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