Exceptions to and Deviations From the INN Common Stem System.

Exceptions to and deviations from the INN common stem system.

Prescrire Int. 2013 May; 22(138): 138-9

For various reasons, mainly related to the history of the drug and of drug nomenclature, some INNs lack a common stem. As INN nomenclature has evolved, some stems have been abandoned or their definition has been modified. Some common stems are difficult to interpret or fail to achieve their objective of designating coherent therapeutic groups. This problem tends to arise particularly when: several stems are used for the same therapeutic use; stems used to designate a particular structure or origin are shared by drugs with different properties; or several stems are used to represent drugs with the same properties but different structures. HubMed – drug


2012 drug packaging review: many dangerous, reportable flaws.

Prescrire Int. 2013 May; 22(138): 134-7

Drug packaging plays an important role in protecting and providing information to patients. The packaging examined by Prescrire in 2012, on the whole, still fails to perform all of these functions effectively. Two issues are especially worrisome. First, packaging too often poses a danger to children. In addition, too many patient leaflets provide incomplete information about adverse effects, thus failing to properly protect the most vulnerable patients. Yet, the method Prescrire used to analyse drug packaging shows that it is not difficult to detect and anticipate risks. It is up to healthcare professionals to take advantage of the method, to protect patients from, and report, dangerous packaging. HubMed – drug


Lower urinary tract dysfunction: From basic science to clinical management. Foreword.

Int J Urol. 2013 Jan; 20(1): 3
de Groat WC

HubMed – drug


Antibody-based antiangiogenic and antilymphangiogenic therapies to prevent tumor growth and progression.

Acta Biochim Pol. 2013 Jul 1;
Bzowska M, M??yk-Kope? R, Próchnicki T, Kulesza M, Klaus T, Bereta J

Blood and lymphatic vessel formation is an indispensable factor for cancer progression and metastasis. Therefore, various strategies designed to block angiogenesis and lymphangiogenesis are being investigated in the hope to arrest and reverse tumor development. Monoclonal antibodies, owing to their unequalled diversity and specificity, might be applied to selectively inhibit the pathways that cancer cells utilize to build up a network of blood vessels and lymphatics. Among the possible targets of antibody-based therapies are proangiogenic and prolymphangiogenic growth factors from the VEGF family and the receptors to which they bind (VEGFRs). Here, we present molecular mechanisms of angiogenesis and lymphangiogenesis exploited by tumors to progress and metastasise, with examples of antibody-based therapeutic agents directed at interfering with these processes. The expanding knowledge of vascular biology helps to explain some of the problems encountered in such therapies, that arise due to the redundancy in signaling networks controlling the formation of blood and lymphatic vessels, and lead to tumor drug resistance. Nonetheless, combined treatments and treatments focused on newly discovered proangiogenic and prolymphangiogenic factors give hope that more prominent therapeutic effects might be achieved in the future. Cancer is the leading cause of death in developed countries. Although localized tumors are successfully treated by surgery, radiotherapy and other more selective methods, medicine is often helpless in the face of metastatic disease – the most lethal form of cancer. Therefore, enormous efforts are being made to create specific agents with a potential to suppress tumor growth and prevent the processes that cause benign tumors to gain metastatic competence and begin to spread to distant organs. Progression from benign to malignant tumor involves an increase in tumor cell proliferation rate and in the ability to migrate and invade other tissues. Metastatic tumor cells utilize blood and lymph vessels as routes for dissemination. Tumor-derived factors stimulate formation of new blood vessels (angiogenesis) and lymph vessels (lymphangiogenesis), which actively support tumor growth and spreading. Different approaches are applied to inhibit tumor progression. This review will particularly focus on antibody-based therapies inhibiting proangiogenic and prolymphangiogenic signals mediated by endothelial cell growth factors and their receptors. An overview of potential targets for therapeutic monoclonal antibodies in these processes is shown in Table 1. In the future, strategies utilizing such antibodies, alone or combined with other antitumor therapies, may become a method of choice in the treatment of metastatic cancers. HubMed – drug


Emerging Therapeutic Biomarkers in Endometrial Cancer.

Biomed Res Int. 2013; 2013: 130362
Dong P, Kaneuchi M, Konno Y, Watari H, Sudo S, Sakuragi N

Although clinical trials of molecular therapies targeting critical biomarkers (mTOR, epidermal growth factor receptor/epidermal growth factor receptor 2, and vascular endothelial growth factor) in endometrial cancer show modest effects, there are still challenges that might remain regarding primary/acquired drug resistance and unexpected side effects on normal tissues. New studies that aim to target both genetic and epigenetic alterations (noncoding microRNA) underlying malignant properties of tumor cells and to specifically attack tumor cells using cell surface markers overexpressed in tumor tissue are emerging. More importantly, strategies that disrupt the cancer stem cell/epithelial-mesenchymal transition-dependent signals and reactivate antitumor immune responses would bring new hope for complete elimination of all cell compartments in endometrial cancer. We briefly review the current status of molecular therapies tested in clinical trials and mainly discuss the potential therapeutic candidates that are possibly used to develop more effective and specific therapies against endometrial cancer progression and metastasis. HubMed – drug