Browsing by Author "Laxmi Kant Pandey"

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Acute kidney injury in late pregnancy in developing countries
(2010) Jai Prakash; Shashidhar Shree Niwas; Aashish Parekh; Laxmi Kant Pandey; Loukrakpam Sharatchandra; Puneet Arora; Amit Kumar Mahapatra
Introduction: The data directly evaluating acute renal failure (ARF) in third trimester of pregnancy from Indian subcontinent are scanty. This study analyzes the clinical spectrum of ARF with respect to total birth in third trimester of pregnancy. Material: All pregnant women after the 28th week of pregnancy or in early postpartum period (up to 7 days) admitted to our hospital between August 2006 and August 2008 were screened for clinical evidence of ARF. Pregnant women with clinical diagnosis of ARF in third trimester were included in this study. Results: Of the 4758 pregnant women in third trimester, ARF developed in 85 cases (1 in 56 births). Preeclampsia, puerperal sepsis, and intrauterine death were responsible for ARF in 35.29, 24.7, and 16.67 of cases, respectively. Postpartum hemorrhage and antepartum hemorrhage were the causes of ARF in 10.59 and 8.29 of patients, respectively. Acute fatty liver of pregnancy was noted in one patient. Complicated preeclampsia (hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome, eclampsia, and uterine hemorrhage) was associated and higher incidence of ARF. Live birth occurred in 61.2 of patients with vaginal delivery in 70 cases. Renal cortical necrosis was diagnosed in two cases. Overall, mortality was 20. The puerperal sepsis contributed 41 of total death. Conclusion: ARF complicated 1.78 of total delivery in third trimester of pregnancy. Preeclampsia was the most common cause of ARF followed by puerperal sepsis. In contrast to the developed countries, incidence of ARF is still very high in late pregnancy in the developing countries. Overall mortality was 20 with highest (33) mortality in puerperal sepsis group. © 2010 Informa UK, Ltd.
Nested multiplex PCR detection of human papillomavirus 16 and 18 in pre-invasive lesions and its implication in screening of carcinoma cervix
(2014) Pradyot Prakash; Shivesh Singh; Charul Dhakad; Sulekha Pandey; Mohan Kumar; Laxmi Kant Pandey; Amrita Ghosh Kar; Gopal Nath; Anil Kumar Gulati
Introduction: Carcinoma cervix is a preventable disease and is caused by certain high risk Papillomaviruses. In the present study, our aim was to investigate the utility of nested multiplex Polymerase Chain Reaction in detecting HPV 16 and 18 in cervical scrapes/biopsy samples and to correlate with cervical cytology/ histopathology findngs. Methods: A total of 119 females were subjected for Papanicolaou smear examination of cervical scrapes and/ or histopathological examination of cervical tissues. These samples were also subjected to nested multiplex Polymerase Chain Reaction targeting HPV 16/ 18 specific E6/7 gene sequences. Results: HPV 16/18 were detected in 33.6% (40/119) cases included in the study. The overall HPV 16/ 18 positivity among cases with Negative for Intraepithelial Lesion or Malignancy, Low grade Squamous Intraepithelial Lesion, and High grade Squamous Intraepithelial Lesion was observed to be 20.8%, 44%, and 66.7% respectively. Positivity for HPV 16 in cases with SCC was found to be 80%. HPV positivity among subjects reported with reactive cellular changes, a sub category of Negative for Intraepithelial Lesion or Malignancy, was observed to be 26.6%. Conclusion: HPV 16 and 18 positivity in cases reported with different stages of pre invasive lesions of carcinoma cervix, particularly in the subcategory reactive cellular changes of Negative for Intraepithelial Lesion or Malignancy, indicates that NMPCR detection of HPV 16/ 18 may be used as a screening tool for carcinoma cervix in conjunction with Papanicolaou smear examination.
Olaparib modulates DNA repair efficiency, sensitizes cervical cancer cells to cisplatin and exhibits anti-metastatic property
(Nature Publishing Group, 2017) Chandra Bhushan Prasad; Shyam Babu Prasad; Suresh Singh Yadav; Laxmi Kant Pandey; Sunita Singh; Satyajit Pradhan; Gopeshwar Narayan
PARP1 trapping at DNA lesion by pharmacological inhibitors has been exploited in several cancers exhibiting defects in DNA repair mechanisms. PARP1 hyperactivation is involved in therapeutic resistance in multiple cancers. The role of PARP1 in cervical cancer (CC) resistance and implication of PARP inhibitor is yet to be elucidated. Our data demonstrates significantly higher expression of PARP1 in primary cervical tumors and CC cell lines SiHa and ME180. Upon cisplatin treatment CC cells display significant overexpression of PARP1 and its hyperactivation. PARP inhibitor olaparib shows significant anti-proliferative effect on CC cells and drive loss of clonogenic survival and enhanced cell death in combination with cisplatin. PARP inhibited cells show delay in resolution of γH2A.X foci and prolonged late S and G2-M phase arrest resulting in apoptosis. Further, PARP inhibition disrupts the localization of base excision repair (BER) effector XRCC1 and non-homologous end joining (NHEJ) proteins Ku80 and XRCC4. Due to disrupted relocation of repair factors, cisplatin induced stalled replication forks collapse and convert into double strand breaks (DSBs). Interestingly, PARP inhibition also shows anti-migratory and anti-invasive properties in CC cells, increases anchorage independent cell death and induces anoikis. Collectively, our data demonstrates therapeutic potential of PARP inhibitor in cervical cancer. © 2017 The Author(s).
VEGFa/VEGFR2 autocrine and paracrine signaling promotes cervical carcinogenesis via β-catenin and snail
(Elsevier Ltd, 2022) Chandra Bhushan Prasad; Deepika Singh; Laxmi Kant Pandey; Satyajit Pradhan; Sunita Singh; Gopeshwar Narayan
VEGF secretion into the tumor microenvironment by cancer cells regulates several oncogenic signaling pathways and cancer-regulated angiogenesis. VEGFR receptors are exclusively present on endothelial cells to maintain their biological homeostasis. The acquisition of unique VEGFR2 receptor and VEGFa in cervical cancer (CC) cells reflects VEGFa/VEGFR2 autocrine machinery. Given the critical role of VEGFR2 in endothelial cell proliferation, migration, and angiogenesis, we explored its function in CC epithelial-mesenchymal transition (EMT) and stemness. Here we report that VEGFR2 regulates cancer-induced angiogenesis and EMT-linked stemness in CC cells via AKT/GSK3β/β-catenin and Snail pathway. Receptor tyrosine kinase inhibitor (RTKi) of VEGFR, Pazopanib (PAZ), shows potential anti-VEGFR2 activity and inhibits VEGFa induced metastatic events such as migration, invasion, and anoikis resistance in CC cells. Similarly, PAZ also attenuates cancer-regulated angiogenesis by inhibiting VE-cadherin internalization in endothelial cells followed by inhibition of endothelial cell migration. Selective depletion of VEGFR2 ligand VEGFa in CC cells also attenuates EMT, metastatic events, and inhibition of cancer-induced angiogenesis. In addition, blocking of VEGFR2 signaling in CC cells via PAZ or shRNA alters the formation of cervical tumorspheres (TS) and their successive generation. Collectively, inhibition of functional VEGFa/VEGFR2 autocrine and paracrine axis ceases the cancer-promoting events in cervical cancer cells. Based on the finding in this study, this oncogenic pathways could be used as a potential therapeutic target in a clinical setting with conventional radio-chemotherapy to achieve synergistic killing of CC cells. © 2021 Elsevier Ltd