Lucknow Cancer Institute

Lucknow, India

Lucknow Cancer Institute

Lucknow, India
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Mitra A.K.,CSIR - Central Electrochemical Research Institute | Singh S.V.,CSIR - Central Electrochemical Research Institute | Garg V.K.,Lucknow Cancer Institute | Sharma M.,Lucknow Cancer Institute | And 2 more authors.
Indian Journal of Medical Research | Year: 2011

Background & objectives: Imbalances in compactly regulated DNA repair pathways in the form of single nucleotide polymorphisms (SNPs) within vital DNA repair genes may result in insufficient DNA repair and increase in DNA breaks thus rendering the human system vulnerable to the debilitatory effects of grave diseases like cancers. The present study involves investigation of association of the non-synonymous SNP rs1052133 (C8069G/Ser326Cys) located in the exonic region of the gene human 8-oxoguanine DNA glycosylase (hOGG1) with the risk of squamous cell carcinomas of the head and neck (SCCHN). Methods: Case-control based genetic association study was performed among 575 (250 SCCHN cases and 325 normal healthy controls) sub-population cluster-matched (Indo-Europeans linguistic subgroup + Caucasoid morphological subtype) samples from the north Indian States of Uttar Pradesh and Uttarakhand using polymerase chain reaction followed by restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing analysis. Results: Our results demonstrated statistically significant protective association for the heterozygous CG [Odds Ratio (OR) 0.6587, 95% Confidence Interval (CI) 0.4615 to 0.9402, P=0.0238], homozygous mutant GG (OR 0.2570, 95% CI 0.1070 to 0.6175, P=0.0013) and combined mutant CG + GG (OR 0.6057, 95% CI 0.4272 to 0.8586, P=0.0059) genotypes. Interpretation & conclusions: The results indicate that the polymorphism rs1052133 is strongly associated with SCCHN susceptibility and the mutant (G) allele might be a protective factor for SCCHN among north Indian subpopulations.

Singh N.,CSIR - Central Electrochemical Research Institute | Nigam M.,CSIR - Central Electrochemical Research Institute | Nigam M.,Allahabad University | Ranjan V.,CSIR - Central Electrochemical Research Institute | And 11 more authors.
Cancer Science | Year: 2011

Cyclophosphamide (CPA) has efficacy as a breast cancer therapy. However, toxicity to CPA limits its clinical applications. Hence there is a need to develop compounds that may be combined with it to improve the efficacy and overcome toxicity. We showed previously that Resveratrol (RES), a chemopreventive agent, increased the growth inhibitory effect of CPA-treated MCF-7 cells. Here we have explored the molecular basis of 5mM CPA and 50μM RES as a combination on cell-cycle progression, apoptosis and oxidative stress in MCF-7 breast cancer cells. Efficacy of the combination was also evaluated in a serum-free tumor explant culture model. The combination elicited enhanced anti-proliferative action coupled with differential expression of cell-cycle, apoptosis and stress factors. Furthermore, co-treatment superiority in histologically validated ER positive breast cancer explants suggests that this combination may be a worthy future clinical anti-neoplastic regimen. © 2011 Japanese Cancer Association.

Ratnagiri R.,Lucknow Cancer Institute | Garg V.,Lucknow Cancer Institute | Chaturvedi R.,Lucknow Cancer Institute
Journal of Cancer Research and Therapeutics | Year: 2012

Extra-osseous osteosarcomas constitute about 1-1.2% of all osteosarcomas. The most common sites are the extremities, thorax, and the abdomen. Retroperitoneal osteosarcomas are rare and very few cases have been reported. They are similar in their biology to high grade soft tissue sarcomas. R0 resection appears to be the best possible treatment for these tumors. All three variants of conventional osteosarcoma-osteoblastic, chondroblastic, and fibroblastic have been described in these tumors. Chemotherapy has been attempted with adriamycin-based regimens with poor results. Unlike extremity osteosarcomas, these tumors have been found to be chemoresistant. The 5 year survival has ranged from a dismal 12% to about 25%. We report a 46-year-old male who presented with a kidney tumor infiltrating the descending colon, but turned out to be an extra osseous osteosarcoma. An R0 resection was done and adjuvant chemotherapy given.

Kumari Kanchan R.,CSIR - Central Electrochemical Research Institute | Tripathi C.,CSIR - Central Electrochemical Research Institute | Singh Baghel K.,CSIR - Central Electrochemical Research Institute | Kumar Dwivedi S.,CSIR - Central Electrochemical Research Institute | And 10 more authors.
Free Radical Biology and Medicine | Year: 2012

The estrogen receptor (ER) plays a cardinal role in estrogen-responsive breast carcinogenesis. It is, however, unclear as to how estrogen-ER interaction potentiates breast cancer progression. Compelling evidence supports estrogen-induced redox alterations, such as augmented reactive oxygen species (ROS) levels, as having a crucial role in breast carcinogenesis. Despite ER being a biological mediator of the majority of estrogen-induced cellular responses; its role in estrogen-induced tissue-specific ROS generation remains largely debatable. We examined a panel of human breast cancer specimens and found that ER-positive breast cancer specimens exhibited a higher incidence of augmented O2 •- levels compared to matched normal tissue. ROS are known to function as signal transducers and ROS-mediated signaling remains a key complementary mechanism that drives carcinogenesis by activating redox-sensitive oncogenic pathways. Additional studies revealed that augmented O2 •- levels in breast cancer specimens coincided with mammalian target of rapamycin complex 2 (mTORC2) hyperactivation. Detailed investigations using in vitro experiments established that 17β-estradiol (E2)-stimulated breast cancer cells exhibited transiently upregulated O2 •- levels, with the presence of ER being a crucial determinant for the phenomenon to take place. Gene expression, ER transactivation, and confocal studies revealed that the E2-induced transient O2 •- upregulation was effected by ER through a nongenomic pathway possibly involving mitochondria. Furthermore, E2 treatment activated mTORC2 in breast cancer cells in a characteristically ER-dependent manner. Interestingly, altering O2 •- anion levels through chemical/genetic methods caused significant modulation of the mTORC2 signaling cascade. Taken together, our findings unravel a novel nongenomic pathway unique to estrogen-responsive breast cancer cells wherein, upon stimulation by E2, ER may regulate mTORC2 activity in a redox-dependent manner by transiently modulating O2 •- levels particularly within mitochondria. The findings suggest that therapies aimed at counteracting these redox alterations and/or resultant signaling cascades may complement conventional treatments for estrogen-responsive breast cancer. © 2012 Elsevier Inc. All rights reserved.

PubMed | KGMU, CSIR - Central Electrochemical Research Institute and Lucknow Cancer Institute
Type: | Journal: Oncogene | Year: 2016

Augmented reactive oxygen species levels consequential to functional alteration of key mitochondrial attributes contribute to carcinogenesis, either directly via oxidative DNA damage infliction or indirectly via activation of oncogenic signaling cascades. We previously reported activation of a key oncogenic signaling cascade via mammalian target of rapamycin (mTOR) signaling complex-2 (mTORC2) owing to estrogen receptor (ER-)-dependent augmentation of O

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