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Qadir M.I.,Bahauddin Zakariya University | Ali M.,Bahauddin Zakariya University | Muhammad S.A.,Bahauddin Zakariya University | Hanif M.,Bahauddin Zakariya University | And 2 more authors.
Reviews in Medical Microbiology | Year: 2015

AIDS is a disease, caused by the HIV belonging to the retroviral family, transmitted through blood, body fluids and unprotected sexual contact that may involve a number of complications of immune, cardiovascular and pulmonary systems. Antiretroviral drugs are usually used in treatment. Mild bone loss occurs with the start of antiretroviral treatment. Bone mass seems to be constant and improved in prolonged use of antiretrovirals. Oral and parenteral bisphosphonates are useful in patients, and they are referred to first-line treatment to prevent frailty and bone rupture. © 2015 Wolters Kluwer Health, Inc. All rights reserved. Source

Saleem M.,The University of Faisalabad | Abbas K.,The University of Faisalabad | Manan M.,The University of Faisalabad | Ijaz H.,The University of Faisalabad | And 5 more authors.
Pakistan Journal of Pharmaceutical Sciences | Year: 2015

Epigenetics means the study of alterations in the genetic material that affect the phenotype but does not affect the genotype. Epigenetics cause alterations in cell properties, which are inherited; but it does not cause alterations in DNA sequence. Epigenetic mediated silencing of gene is of four types, which are DNA methylation, histone deacetylation, RNA associated silencing and Genomic imprinting. Other factors (environmental and xenobiotics) can also cause gene silencing but DNA methytlation and changes in histones of chromatin are two important changes, which are responsible for malignant diseases. Two groups of drugs are under development, which corrects the epigenetic alterations. These are histone deacetylation (HDAC) inhibitors and DNA methytransferase (DNMT) inhibitors. These drugs may be used in cancer because in cancer, hypermethylation of cancer suppressor gene causes gene silencing. Epigenetic therapy scope is likely to increase in future. © 2015, Pakistan Journal of Pharmaceutical Sciences. All rights reserved. Source

Halim T.A.,RLMC | Farooqi A.A.,Laboratory for Translational Oncology and Personalized Medicine | Zaman F.,RLMC
Cancer Cell International | Year: 2013

HPV encoded proteins can elicit ectopic protein-protein interactions that re-wire signaling pathways, in a mode that promotes malignancy. Moreover, accumulating data related to HPV is now providing compelling substantiation of a central role played by HPV in escaping immunosurveillance and impairment of apoptotic response. What emerges is an intricate network of Wnt, TGF, Notch signaling cascades that forms higher-order ligand-receptor complexes routing downstream signaling in HPV infected cells. These HPV infected cells are regulated both extracellularly by ligand receptor axis and intracellularly by HPV encoded proteins and impair TRAIL mediated apoptosis. We divide this review into different sections addressing how linear signaling pathways integrate to facilitate carcinogenesis and compounds that directly or indirectly reverse these aberrant interactions offer new possibilities for therapy in cancer. Although HPV encoded proteins mediated misrepresentation of pathways is difficult to target, improved drug-discovery platforms and new technologies have facilitated the discovery of agents that can target dysregulated pathways in HPV infected cervical cancer cells, thus setting the stage for preclinical models and clinical trials. © 2013 Halim et al.; licensee BioMed Central Ltd. Source

Farooqi A.A.,Institute of Biomedical and Genetic Engineering IB&GE | Li K.-T.,Kaohsiung Medical University | Fayyaz S.,Laboratory for Translational Oncology and Personalized Medicine | Chang Y.-T.,National Sun Yat - sen University | And 5 more authors.
Tumor Biology | Year: 2015

Prior research has demonstrated how the endoplasmic reticulum (ER) functions as a multifunctional organelle and as a well-orchestrated protein-folding unit. It consists of sensors which detect stress-induced unfolded/misfolded proteins and it is the place where protein folding is catalyzed with chaperones. During this folding process, an immaculate disulfide bond formation requires an oxidized environment provided by the ER. Protein folding and the generation of reactive oxygen species (ROS) as a protein oxidative byproduct in ER are crosslinked. An ER stress-induced response also mediates the expression of the apoptosis-associated gene C/EBP-homologous protein (CHOP) and death receptor 5 (DR5). ER stress induces the upregulation of tumor necrosis factor-related apoptosis inducing ligand (TRAIL) receptor and opening new horizons for therapeutic research. These findings can be used to maximize TRAIL-induced apoptosis in xenografted mice. This review summarizes the current understanding of the interplay between ER stress and ROS. We also discuss how damage-associated molecular patterns (DAMPs) function as modulators of immunogenic cell death and how natural products and drugs have shown potential in regulating ER stress and ROS in different cancer cell lines. Drugs as inducers and inhibitors of ROS modulation may respectively exert inducible and inhibitory effects on ER stress and unfolded protein response (UPR). Reconceptualization of the molecular crosstalk among ROS modulating effectors, ER stress, and DAMPs will lead to advances in anticancer therapy. © 2015, The Author(s). Source

Lin X.,Capital Medical University | Farooqi A.A.,Laboratory for Translational Oncology and Personalized Medicine | Qureshi M.Z.,GCU | Romero M.A.,Autonomous University of Guerrero | And 2 more authors.
Archivum Immunologiae et Therapiae Experimentalis | Year: 2016

It is becoming characteristically more understandable that within tumor cells, there lies a sub-population of tumor cells with “stem cell” like properties and remarkable ability of self-renewal. Many features of these self-renewing cells are comparable with normal stem cells and are termed as “cancer stem cells”. Accumulating experimentally verified data has started to scratch the surface of spatio-temporally dysregulated intracellular signaling cascades in the biology of prostate cancer stem cells. We partition this multicomponent review into how different signaling cascades operate in cancer stem cells and how bioactive ingredients isolated from natural sources may modulate signaling network. © 2016, L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland. Source

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