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Pancreatic Neoplasms: HELP
Articles by Aravind Sugumar
Based on 4 articles published since 2010
(Why 4 articles?)
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Between 2010 and 2020, Aravind Sugumar wrote the following 4 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Distinguishing pancreatic cancer from autoimmune pancreatitis. 2010

Sugumar, Aravind / Takahashi, Naoki / Chari, Suresh T. ·Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA. sugumar.aravind@mayo.edu ·Curr Gastroenterol Rep · Pubmed #20424980.

ABSTRACT: Both autoimmune pancreatitis (AIP) and pancreatic cancer frequently present with obstructive jaundice. However, AIP is a rare disease and its diagnosis carries vastly different therapeutic and prognostic implications compared with that of pancreatic cancer. The clinical challenge is to distinguish AIP from pancreatic cancer, because the price of misdiagnosis can be heavy. Recently, two strategies for differentiating AIP from pancreatic cancer were published, one from Japan and the other from the United States. The Japanese strategy relies on cross-sectional imaging, endoscopic retrograde pancreatogram, and serum IgG4. The American strategy uses imaging (CT scan), serology (serum IgG4), and evidence of other organ involvement (on CT scan) as the first tier of tests. If the differentiation cannot be made by these methods, a core biopsy of the pancreas, steroid trial, or surgical resection is recommended. The two strategies reflect differences in clinical practice and local preferences in the use of certain diagnostic tests. However, both strategies require thorough familiarity with the diseases and the tests being used.

2 Clinical Trial Endoscopic retrograde pancreatography criteria to diagnose autoimmune pancreatitis: an international multicentre study. 2011

Sugumar, Aravind / Levy, Michael J / Kamisawa, Terumi / Webster, G J / Kim, Myung-Hwan / Enders, Felicity / Amin, Zahir / Baron, Todd H / Chapman, Mike H / Church, Nicholas I / Clain, Jonathan E / Egawa, Naoto / Johnson, Gavin J / Okazaki, Kazuichi / Pearson, Randall K / Pereira, Stephen P / Petersen, Bret T / Read, Samantha / Sah, Raghuwansh P / Sandanayake, Neomal S / Takahashi, Naoki / Topazian, Mark D / Uchida, Kazushige / Vege, Santhi Swaroop / Chari, Suresh T. ·Division of Gastroenterology and Hepatology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. ·Gut · Pubmed #21131631.

ABSTRACT: BACKGROUND: Characteristic pancreatic duct changes on endoscopic retrograde pancreatography (ERP) have been described in autoimmune pancreatitis (AIP). The performance characteristics of ERP to diagnose AIP were determined. METHODS: The study was done in two phases. In phase I, 21 physicians from four centres in Asia, Europe and the USA, unaware of the clinical data or diagnoses, reviewed 40 preselected ERPs of patients with AIP (n=20), chronic pancreatitis (n=10) and pancreatic cancer (n=10). Physicians noted the presence or absence of key pancreatographic features and ranked the diagnostic possibilities. For phase II, a teaching module was created based on features found most useful in the diagnosis of AIP by the four best performing physicians in phase I. After a washout period of 3 months, all physicians reviewed the teaching module and reanalysed the same set of ERPs, unaware of their performance in phase I. RESULTS: In phase I the sensitivity, specificity and interobserver agreement of ERP alone to diagnose AIP were 44, 92 and 0.23, respectively. The four key features of AIP identified in phase I were (i) long (>1/3 the length of the pancreatic duct) stricture; (ii) lack of upstream dilatation from the stricture (<5 mm); (iii) multiple strictures; and (iv) side branches arising from a strictured segment. In phase II the sensitivity (71%) of ERP significantly improved (p<0.05) without a significant decline in specificity (83%) (p>0.05); the interobserver agreement was fair (0.40). CONCLUSIONS: The ability to diagnose AIP based on ERP features alone is limited but can be improved with knowledge of some key features.

3 Article Quinomycin A targets Notch signaling pathway in pancreatic cancer stem cells. 2016

Ponnurangam, Sivapriya / Dandawate, Prasad R / Dhar, Animesh / Tawfik, Ossama W / Parab, Rajashri R / Mishra, Prabhu Dutt / Ranadive, Prafull / Sharma, Rajiv / Mahajan, Girish / Umar, Shahid / Weir, Scott J / Sugumar, Aravind / Jensen, Roy A / Padhye, Subhash B / Balakrishnan, Arun / Anant, Shrikant / Subramaniam, Dharmalingam. ·Department of Molecular and Integrative Physiology, The University of Kansas Medical Center, Kansas City, KS 66160, USA. · Department of Surgery, The University of Kansas Medical Center, Kansas City, KS 66160, USA. · Department of Cancer Biology, The University of Kansas Medical Center, Kansas City, KS 66160, USA. · The University of Kansas Cancer Center, Kansas City, KS 66160, USA. · Department of Pathology and Laboratory Medicine, The University of Kansas Medical Center, Kansas City, KS 66160, USA. · Piramal Life Sciences Inc, Goregaon East, Mumbai 400063, India. · Department of Pharmacology, Toxicology and Therapeutics, The University of Kansas Medical Center, Kansas City, KS 66160, USA. · Department of Internal Medicine, The University of Kansas Medical Center, Kansas City, KS 66160, USA. · Interdisciplinary Science and Technology Research Academy, Abeda Inamdar Senior College, Azam Campus, Pune, 411001, India. ·Oncotarget · Pubmed #26673007.

ABSTRACT: Cancer stem cells (CSCs) appear to explain many aspects of the neoplastic evolution of tumors and likely account for enhanced therapeutic resistance following treatment. Dysregulated Notch signaling, which affects CSCs plays an important role in pancreatic cancer progression. We have determined the ability of Quinomycin to inhibit CSCs and the Notch signaling pathway. Quinomycin treatment resulted in significant inhibition of proliferation and colony formation in pancreatic cancer cell lines, but not in normal pancreatic epithelial cells. Moreover, Quinomycin affected pancreatosphere formation. The compound also decreased the expression of CSC marker proteins DCLK1, CD44, CD24 and EPCAM. In addition, flow cytometry studies demonstrated that Quinomycin reduced the number of DCLK1+ cells. Furthermore, levels of Notch 1-4 receptors, their ligands Jagged1, Jagged2, DLL1, DLL3, DLL4 and the downstream target protein Hes-1 were reduced. The γ-secretase complex proteins, Presenilin 1, Nicastrin, Pen2, and APH-1, required for Notch activation also exhibited decreased expression. Ectopic expression of the Notch Intracellular Domain (NICD) partially rescued the cells from Quinomycin mediated growth suppression. To determine the effect of Quinomycin on tumor growth in vivo, nude mice carrying tumor xenografts were administered Quinomycin intraperitoneally every day for 21 days. Treatment with the compound significantly inhibited tumor xenograft growth, coupled with significant reduction in the expression of CSC markers and Notch signaling proteins. Together, these data suggest that Quinomycin is a potent inhibitor of pancreatic cancer that targets the stem cells by inhibiting Notch signaling proteins.

4 Article CDK-4 inhibitor P276 sensitizes pancreatic cancer cells to gemcitabine-induced apoptosis. 2012

Subramaniam, Dharmalingam / Periyasamy, Giridharan / Ponnurangam, Sivapriya / Chakrabarti, Debarshi / Sugumar, Aravind / Padigaru, Muralidhara / Weir, Scott J / Balakrishnan, Arun / Sharma, Somesh / Anant, Shrikant. ·Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas 66160, USA. ·Mol Cancer Ther · Pubmed #22532602.

ABSTRACT: Despite advances in molecular pathogenesis, pancreatic cancer remains a major unsolved health problem. It is a rapidly invasive, metastatic tumor that is resistant to standard therapies. The phosphatidylinositol-3-kinase/Akt and mTOR signaling pathways are frequently dysregulated in pancreatic cancer. Gemcitabine is the mainstay treatment for metastatic pancreatic cancer. P276 is a novel CDK inhibitor that induces G(2)/M arrest and inhibits tumor growth in vivo models. Here, we determined that P276 sensitizes pancreatic cancer cells to gemcitabine-induced apoptosis, a mechanism-mediated through inhibition of Akt-mTOR signaling. In vitro, the combination of P276 and gemcitabine resulted in a dose- and time-dependent inhibition of proliferation and colony formation of pancreatic cancer cells but not with normal pancreatic ductal cells. This combination also induced apoptosis, as seen by activated caspase-3 and increased Bax/Bcl2 ratio. Gene profiling studies showed that this combination downregulated Akt-mTOR signaling pathway, which was confirmed by Western blot analyses. There was also a downregulation of VEGF and interleukin-8 expression suggesting effects on angiogenesis pathway. In vivo, intraperitoneal administration of the P276-Gem combination significantly suppressed the growth of pancreatic cancer tumor xenografts. There was a reduction in CD31-positive blood vessels and reduced VEGF expression, again suggesting an effect on angiogenesis. Taken together, these data suggest that P276-Gem combination is a novel potent therapeutic agent that can target the Akt-mTOR signaling pathway to inhibit both tumor growth and angiogenesis.