Journal of Cancer Research Updates 

About: Journal of Cancer Research Updates is an academic journal. The journal publishes majorly in the area(s): Cancer & Internal medicine. It has an ISSN identifier of 1929-2260. Over the lifetime, 146 publications have been published receiving 538 citations.

Drug Resistance Mechanisms in Non-Small Cell Lung Carcinoma.

Abstract: Lung cancer is the most commonly diagnosed cancer in the world. "Driver" and "passenger" mutations identified in lung cancer indicate that genetics play a major role in the development of the disease, progression, metastasis and response to therapy. Survival rates for lung cancer treatment have remained stagnant at ~15% over the past 40 years in patients with disseminated disease despite advances in surgical techniques, radiotherapy and chemotherapy. Resistance to therapy; either intrinsic or acquired has been a major hindrance to treatment leading to great interest in studies seeking to understand and overcome resistance. Genetic information gained from molecular analyses has been critical in identifying druggable targets and tumor profiles that may be predictors of therapeutic response and mediators of resistance. Mutated or overexpressed epidermal growth factor receptor (EGFR) and translocations in the echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) genes (EML4-ALK) are examples of genetic aberrations resulting in targeted therapies for both localized and metastatic disease. Positive clinical responses have been noted in patients harboring these genetic mutations when treated with targeted therapies compared to patients lacking these mutations. Resistance is nonetheless a major factor contributing to the failure of targeted agents and standard cytotoxic agents. In this review, we examine molecular mechanisms that are potential drivers of resistance in non-small cell lung carcinoma, the most frequently diagnosed form of lung cancer. The mechanisms addressed include resistance to molecular targeted therapies as well as conventional chemotherapeutics through the activity of multidrug resistance proteins.

The Dual Role Played by p21 May Influence the Apoptotic or Anti-Apoptotic Fate in Cancer

Abstract: p21 is a cyclin-dependent kinase inhibitor that is activated in response to different stress stimuli and could act as cell cycle suppressor. p21 can bind and inhibit cyclin-dependent kinase/cyclin complexes to mediate growth arrest in G1 and G2 phases. This condition enables DNA repair and suggests that p21 could have a role of tumour suppressor. p21 is one of the transcriptional targets of p53, a protein up-regulated after cellular stress stimuli. Besides the classical p53-dependent activation, p21 transcription can be achieved by other regulators as Sp1, STAT and AP2 in a p53-independent manner. Depending on cell type and cellular conditions p21 can have anti-apoptotic or pro-apoptotic functions being involved either in tumourigenesis or in tumour suppression. The function exerted is based on subcellular localization. In the nucleus p21 inhibits proliferation by blocking the cyclin dependent kinases while in the cytoplasm it acts inhibiting pro-apoptotic protein determining cell death inhibition. The different subcellular localization is related to different prognostic role of p21 in cancer and the cellular context in which it is expressed determines if it can be considered as a specific therapeutic target or as a marker of poor prognosis. This review focuses on the recent understanding of the functions of p21 with particular attention to the dual role detected in cancer where p21 can act as tumour suppressor promoting apoptosis or as oncogene preventing it.

Tea and Cancer Prevention

Abstract: Cancer remains one of the biggest challenges in the 21 st century, therefore anti-cancer drugs and their delivery systems are under developing for better treatment. Tea is the amazing gift nature offered to us with great health benefits. Tea polyphenols especially EGCG and Theoflavins have widely been studied and expected to be a very promising nature polyphenol for the prevention of cancer, cardiology disease, aging, weight control etc. Here “Dr. Tea” summarized the past studies about tea and cancer prevention, through the chemical composition, structure, epidemiologic study and mechanism analysis. And based on the epidemiologic study results, a layer-by-layer multi-functional drug delivery system and synergy studies based on our past scientific working experience had been proposed for future tea and cancer research. A “Healthy, Harmony, Pure & Nature” tea-style of living is proposed for all human-beings towards a better living “self” and a better society.

Strategies of Targeting Tumors and Cancers

Abstract: Targeted cancer therapies use drugs that specially reach at the affected site block the growth and spread of cancer. They interfere with specific molecules involved in carcinogenesis (the process by which normal cells become cancer cells) and tumor growth. By focusing on molecular and cellular changes that are specific to cancer, targeted cancer therapies may be more effective than current treatments and less harmful to normal cells. Targeted cancer therapies interfere with cancer cell growth and division in different ways and at various points during the development, growth, and spread of cancer. The present article provides an overview of various aspects of cancers and tumors that include causes of the diseases and their underlying biology, existing methods of treatment, major strategies of cancer and tumor targeting and mechanisms of their mode of actions. The review article also presents a current state-of –the art of the cancer targeting approaches and discusses various types of advanced targeting techniques like pH, temperature and magnetic targeting. A brief account of recent literature pertaining to cancer targeting is also discussed.

Targeting Cancer Stem Cells with Defined Compounds and Drugs

Abstract: : Cancer stem cells (CSCs) are a subpopulation of tumor cells that possess self-renewal and tumor initiation capacity and the ability to give rise to the heterogenous lineages of cancer cells that comprise the tumor. CSCs possess numerous intrinsic mechanisms of resistance to chemotherapeutic drugs, novel tumor-targeted drugs and radiation therapy, allowing them to survive current cancer therapies and to initiate tumor recurrence and metastasis. Recently, different pathways that confer resistance and survival of CSCs, but also compounds and drugs that selectively target some of these pathways in CSCs have been identified. Such compounds and drugs include antibiotics like salinomycin, phytochemicals such as parthenolide, cyclopamine, EGCG, resveratrol, curcumin, sulforaphane and oxymatrine, the small molecule inhibitors vismodegib and repertaxin, monoclonal antibodies and antibody constructs raised against cell surface proteins expressed by CSCs, and, surprisingly, some classical drugs such as metformin, tranilast and thioridazine. These agents exhibit significant anti-CSC activity, alone or in combination with cytostatic drugs or tumor-targeted drugs, as recently shown in vitro and in human xenograft mice. Since current cancer therapies fail to eliminate CSCs, leading to cancer recurrence and progression, selective targeting of CSCs with compounds and drugs introduced herein may represent a novel therapeutic strategy to eradicate cancer.