Publish in OALib Journal

ISSN: 2333-9721

APC: Only $99


Search Results: 1 - 10 of 1719 matches for " Pinku Mukherjee "
All listed articles are free for downloading (OA Articles)
Page 1 /1719
Display every page Item
Physiological Role of Plasmacytoid Dendritic Cells and Their Potential Use in Cancer Immunity
Jorge Schettini,Pinku Mukherjee
Clinical and Developmental Immunology , 2008, DOI: 10.1155/2008/106321
Abstract: Dendritic cells (DCs) play a pivotal role in the control of innate and adaptive immune responses. They are a heterogeneous cell population, where plasmacytoid dendritic cells (pDCs) are a unique subset capable of secreting high levels of type I IFNs. It has been demonstrated that pDCs can coordinate events during the course of viral infection, atopy, autoimmune diseases, and cancer. Therefore, pDC, as a main source of type I IFN, is an attractive target for therapeutic manipulations of the immune system to elicit a powerful immune response against tumor antigens in combination with other therapies. The therapeutic vaccination with antigen-pulsed DCs has shown a limited efficacy to generate an effective long-lasting immune response against tumor cells. A rational manipulation and design of vaccines which could include DC subsets outside “Langerhans cell paradigm” might allow us to improve the therapeutic approaches for cancer patients.
Pancreatic Cancer Cells Isolated from Muc1-Null Tumors Favor the Generation of a Mature Less Suppressive MDSC Population
Amritha Kidiyoor,Stephen Lee Rego,Pinku Mukherjee
Frontiers in Immunology , 2014, DOI: 10.3389/fimmu.2014.00067
Abstract: Mucin 1 (MUC1) is a transmembrane mucin glycoprotein that is over-expressed and aberrantly glycosylated in >80% of human pancreatic ductal adenocarcinoma (PDA) and is associated with poor prognosis. To understand the role of MUC1 in PDA, we have recently developed two mouse models of spontaneous PDA, one that expresses full-length human MUC1 transgene (KCM mice) and one that is null for MUC1 (KCKO mice). We have previously reported that KCM mice express high levels of myeloid derived suppressor cells (MDSCs) in their tumors and develop highly aggressive PDA. To further understand the underlying mechanism for high MDSC levels in KCM-tumors, we generated primary cell lines from KCM and KCKO-tumors. In this study, we report that MDSCs derived using KCM cells express significantly higher levels of arginase 1 and inducible nitric oxide synthase (markers associated with immune suppression) and lower levels of CD115 (a marker associated with maturation of myeloid cells) as compared to KCKO-derived MDSCs. Functionally, KCM-derived MDSCs secrete significantly higher levels of urea and nitric oxide (NO) when co-cultured with normal splenic cells as compared to KCKO-derived MDSCs. Data indicates that KCM-derived MDSCs remain immature and are more suppressive as compared to KCKO-derived MDSCs. This was further corroborated in vivo where MDSCs isolated from KCM-tumor-bearing mice retained their immature state and were highly suppressive as compared to MDSCs derived from KCKO-tumor-bearing mice. Finally, we show that KCM cells secrete significantly higher levels of prostaglandin E2 (PGE2), a COX-2 metabolite and a known driver of suppressive MDSCs as compared to KCKO cells. Thus, inhibiting PGE2 with a specific COX-2 inhibitor reverses the immunosuppressive and immature phenotype of KCM-derived MDSCs. This is the first report that clearly suggests a functional role of pancreatic tumor-associated MUC1 in the development of functional MDSCs.
Collagen induced arthritis increases secondary metastasis in MMTV-PyV MT mouse model of mammary cancer
Lopamudra Roy, Sriparna Ghosh, Latha B Pathangey, Teresa L Tinder, Helen E Gruber, Pinku Mukherjee
BMC Cancer , 2011, DOI: 10.1186/1471-2407-11-365
Abstract: To establish the novel link between arthritis induced inflammation and secondary metastasis associated with breast cancer, PyV MT mice that spontaneously develop mammary gland carcinoma were injected with Type II collagen (CII) to induce arthritis at 9 and 18 weeks of age for pre-metastatic and metastatic condition. The sites of secondary metastasis and the associated inflammatory microenvironment were evaluated.A significant increase in breast cancer-associated secondary metastasis to the lungs and bones was observed in the arthritic versus the non-arthritic PyV MT mice along with an increase in primary tumor burden. We report significant increases in the levels of interstitial cellular infiltrates and pro-inflammatory cytokines such as interleukin-17 (IL-17), interleukin-6 (IL-6), Pro- Matrix metallopeptidase 9 (Pro-MMP9), insulin like growth factor-II (GF-II) and macrophage colony stimulating factor (M-CSF) in the arthritic lung and bone milieu as well as in the circulation. These pro-inflammatory cytokines along with the inflammatory microenvironment may be the underlying factors facilitating tumor progression and metastasis in arthritic PyV MT mice. This was further substantiated by treatment with celecoxib, an anti-inflammatory drug + αIL-17 antibody that significantly reduced the secondary metastasis to lung and bone.The data generated not only reveal the underlying mechanism of high susceptibility to bone and lung metastasis in an arthritic condition but our combination therapies may lead to treatment modalities that will be capable of reducing tumor burden, and preventing relapse and metastasis in arthritic patients with breast cancer.While advances have been made in breast cancer therapies, metastatic breast cancer remains an incurable disease, and thus the prevention of metastases must be a priority. The preference of breast cancer cells to grow in the bone and lung is underscored by the fact that 65-75% of patients with advanced disease develop metastasi
Mechanisms underlying the growth inhibitory effects of the cyclo-oxygenase-2 inhibitor celecoxib in human breast cancer cells
Gargi D Basu, Latha B Pathangey, Teresa L Tinder, Sandra J Gendler, Pinku Mukherjee
Breast Cancer Research , 2005, DOI: 10.1186/bcr1019
Abstract: MDA-MB-231 (highly invasive) and MDA-MB-468 (moderately invasive) cell lines were treated with varying concentrations of celecoxib in vitro, and the effects of this agent on cell growth and angiogenesis were monitored by evaluating cell proliferation, apoptosis, cell cycle arrest, and vasculogenic mimicry. The in vitro results of MDA-MB-231 cell line were further confirmed in vivo in a mouse xenograft model.The highly invasive MDA-MB-231 cells express higher levels of COX-2 than do the less invasive MDA-MB-468 cells. Celecoxib treatment inhibited COX-2 activity, indicated by prostaglandin E2 secretion, and caused significant growth arrest in both breast cancer cell lines. In the highly invasive MDA-MB-231 cells, the mechanism of celecoxib-induced growth arrest was by induction of apoptosis, associated with reduced activation of protein kinase B/Akt, and subsequent activation of caspases 3 and 7. In the less invasive MDA-MB-468 cells, growth arrest was a consequence of cell cycle arrest at the G0/G1 checkpoint. Celecoxib-induced growth inhibition was reversed by addition of exogenous prostaglandin E2 in MDA-MB-468 cells but not in MDA-MB-231 cells. Furthermore, MDA-MB-468 cells formed significantly fewer extracellular matrix associated microvascular channels in vitro than did the high COX-2 expressing MDA-MB-231 cells. Celecoxib treatment not only inhibited cell growth and vascular channel formation but also reduced vascular endothelial growth factor levels. The in vitro findings corroborated in vivo data from a mouse xenograft model in which daily administration of celecoxib significantly reduced tumor growth of MDA-MB-231 cells, which was associated with reduced vascularization and increased necrosis in the tumor mass.The disparate molecular mechanisms of celecoxib-induced growth inhibition in human breast cancer cells depends upon the level of COX-2 expression and the invasive potential of the cell lines examined. Data suggest a role for COX-2 not only in the grow
Exacerbated metastatic disease in a mouse mammary tumor model following latent gammaherpesvirus infection
Vinita S Chauhan, Daniel A Nelson, Lopamudra Das Roy, Pinku Mukherjee, Kenneth L Bost
Infectious Agents and Cancer , 2012, DOI: 10.1186/1750-9378-7-11
Abstract: Mice latently infected with HV-68 had a similar primary tumor burden, but much greater metastatic disease, when compared to mock treated mice given the transplantable tumor, 4?T1. This was true for lung lesions, as well as secondary tumor masses. Increased expression of pan-cytokeratin and VEGF-A in tumors from HV-68 infected mice was consistent with increased metastatic disease in these animals. Surprisingly, no viral particles could be cultured from tumor tissues, and the presence of viral DNA or RNA transcripts could not be detected in primary or secondary tumor tissues.Latent HV-68 infection had no significant effect on the size of primary 4?T1 mammary tumors, but exacerbated the number of metastatic lung lesions and secondary tumors when compared to mock treated mice. Increased expression of the tumor marker, pan-cytokeratin, and VEGF-A in tumors of mice harboring latent virus was consistent with an exacerbated metastatic disease. Mechanisms responsible for this exacerbation are indirect, since no virus could be detected in cancerous tissues.
Breast cancer-associated metastasis is significantly increased in a model of autoimmune arthritis
Lopamudra Das Roy, Latha B Pathangey, Teresa L Tinder, Jorge L Schettini, Helen E Gruber, Pinku Mukherjee
Breast Cancer Research , 2009, DOI: 10.1186/bcr2345
Abstract: To determine if chronic inflammation induced by autoimmune arthritis contributes to increased breast cancer-associated metastasis, we generated mammary gland tumors in SKG mice that were genetically prone to develop AA. Two breast cancer cell lines, one highly metastatic (4T1) and the other non-metastatic (TUBO) were used to generate the tumors in the mammary fat pad. Lung and bone metastasis and the associated inflammatory milieu were evaluated in the arthritic versus the non-arthritic mice.We report a three-fold increase in lung metastasis and a significant increase in the incidence of bone metastasis in the pro-arthritic and arthritic mice compared to non-arthritic control mice. We also report that the metastatic breast cancer cells augment the severity of arthritis resulting in a vicious cycle that increases both bone destruction and metastasis. Enhanced neutrophilic and granulocytic infiltration in lungs and bone of the pro-arthritic and arthritic mice and subsequent increase in circulating levels of proinflammatory cytokines, such as macrophage colony stimulating factor (M-CSF), interleukin-17 (IL-17), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF), and tumor necrosis factor-alpha (TNF-alpha) may contribute to the increased metastasis. Treatment with anti-IL17 + celecoxib, an anti-inflammatory drug completely abrogated the development of metastasis and significantly reduced the primary tumor burden.The data clearly has important clinical implications for patients diagnosed with metastatic breast cancer, especially with regards to the prognosis and treatment options.Metastasis is regulated not only by intrinsic genetic changes in malignant cells, but also by the microenvironment. Several studies have demonstrated that sites of chronic inflammation are often associated with the establishment and growth of various malignancies [1]. A common inflammatory condition in humans is autoimmune arthritis (AA) that causes inflammation and deformity of the
A novel role for cyclooxygenase-2 in regulating vascular channel formation by human breast cancer cells
Gargi D Basu, Winnie S Liang, Dietrich A Stephan, Lee T Wegener, Christopher R Conley, Barbara A Pockaj, Pinku Mukherjee
Breast Cancer Research , 2006, DOI: 10.1186/bcr1626
Abstract: To determine whether COX-2 regulates vascular channel formation, we assessed whether treatment with celecoxib (a selective COX-2 inhibitor) or silencing COX-2 synthesis by siRNA inhibits vascular channel formation by breast cancer cell lines. Cell lines were selected based on their invasive potential and COX-2 expression. Additionally, gene expression analysis was performed to identify candidate genes involved in COX-2-induced vascular channel formation. Finally, vascular channels were analyzed in surgically resected human breast cancer specimens that expressed varying levels of COX-2.We found that invasive human breast cancer cells that over-express COX-2 develop vascular channels when plated on three-dimensional matigel cultures, whereas non-invasive cell lines that express low levels of COX-2 did not develop such channels. Similarly, we identified vascular channels in high-grade invasive ductal carcinoma of the breast over-expressing COX-2, but not in low-grade breast tumors. Vascular channel formation was significantly suppressed when cells were treated with celecoxib or COX-2 siRNA. Inhibition of channel formation was abrogated by addition of exogenous prostaglandin E2. In vitro results were corroborated in vivo in tumor-bearing mice treated with celecoxib. Using gene expression profiling, we identified several genes in the angiogenic and survival pathways that are engaged in vascular channel formation.Antivascular therapies targeting tumor cell vasculogenic mimicry may be an effective approach to the treatment of patients with highly metastatic breast cancer.Tumor growth and metastasis are thought to be angiogenesis-related processes [1]. However, it has recently been reported that an angiogenesis-independent pathway, in which tumors can feed themselves without the use of classical blood vessels, exists in very aggressive tumors of the lung and breast, as well as in melanomas [2-4]. This is known as vasculogenic mimicry (VM), a phenomenon in which epithelial t
Direct Observation of Re-entrant Multiferroic CuO at High Pressures
Rajesh Jana,Pinku Saha,Vivek Pareek,Abhisek Basu,Guruprasad Mandal,Sutanu Kapri,Sayan Bhattacharya,Goutam Dev Mukherjee
Physics , 2015,
Abstract: We have carried out a detailed experimental investigation on CuO using dielectric constant, ac resistance, Raman spectroscopy and X-ray diffraction measurements at high pressures and room temperature. Both dielectric constant and dielectric loss show an anomalous peak in the pressure range 3.4-4 GPa indicating a ferroelectric transition. Raman studies show anomalous behaviour of the Ag mode with a slope change in the mode frequency and a minimum in the mode FWHM at 3.4 GPa indicating a strong spin phonon coupling along [1 0 -1] direction. A step like behaviour in the intensity of the Ag mode is observed at 3.4 GPa, indicating a change in the polarization of the mode. A maximum in the intensity of (2,0,-2)Bragg peak at 3.4 GPa points the occurrence of critical scattering due to emergence of magnetic exchange interaction. All our experimental evidences show to the presence of re-entrant type-II multiferroic behaviour in CuO at about 4 GPa.
Ex Ante Inequality and Under-Nutrition Vulnerability Dynamics: Case Study of the Sundarbans Delta Region, West Bengal, India  [PDF]
Moumita Mukherjee
Food and Nutrition Sciences (FNS) , 2014, DOI: 10.4236/fns.2014.520207
Abstract: In this paper ex ante inequality measure is used to estimate inequality in childhood chronic under-nutrition among different vulnerable subgroups. Ex ante inequality in nutritional achievement is determined by estimating Concentration Index by ranking the sample population as per different contextual absolute and predicted vulnerabilities. Such vulnerabilities include climatic shock induced asset loss, livelihood insecurity, physical accessibility and consumption sacrifice after treatment seeking of children for under-nutrition related morbidities and perception of care givers regarding quality and effectiveness of care provided by unqualified providers. Results found that vulnerability to consumption poverty aggravated chronic under-nutrition among less vulnerable groups mainly among those who perceived that unqualified providers provided quality service and were very effective during crisis. Whereas, vulnerability to investment poverty due to asset loss aggravates chronic under-nutrition among more vulnerable groups as their low economic resilience against any safety net results in no treatment seeking but rely on home remedies to cure the child. Though due to good social cohesion, traditional knowledge and beliefs for treatment are shared among each other but this is not sufficient to break the under-nutrition morbidity vicious circle, especially when the under-nutrition is chronic in nature. So the paper finally suggests several policy suggestions for different vulnerable segments.
Poverty Reduction and Pattern of Chronic Childhood Under-Nutrition in India: How Far Does the Link Exist?  [PDF]
Moumita Mukherjee
Food and Nutrition Sciences (FNS) , 2014, DOI: 10.4236/fns.2014.520208
Abstract: In spite of an established link between poverty and under-nutrition in India, fall in under-nutrition is sluggish with fall in poverty. This research paper aims to seek answer on the effect of poverty decline on child under-nutrition in India over a period of one and a half decades. After examining the extent of association between poverty reduction and reciprocal changes in child under-nutrition, the paper found that although there was a definite influence of poverty levels on child under-nutrition at the state-level, the strength of the impact was not very high. This possibly explains why improvements in nutritional status among children have failed to keep up pace with steady reduction in mass poverty across the states in the last couple of decades. The results also strongly reiterate the magnificent role of child’s healthcare utilization and higher public spending which can help to capitalize on the increase in economic capabilities at the household level, resulting from robust economic growth and alleviation of endemic poverty.
Page 1 /1719
Display every page Item

Copyright © 2008-2017 Open Access Library. All rights reserved.