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Pancreatic Neoplasms: HELP
Articles by S. Khan
Based on 4 articles published since 2010
(Why 4 articles?)
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Between 2010 and 2020, S. Khan wrote the following 4 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Functional assessment in the multimodality imaging of pancreatic neuro-endocrine tumours. 2010

Bhate, K / Mok, W Y / Tran, K / Khan, S / Al-Nahhas, A. ·Department of Nuclear Medicine, Imperial Healthcare Trust, Hammersmith Hospital, London, UK. ·Minerva Endocrinol · Pubmed #20386524.

ABSTRACT: Pancreatic neuroendocrine tumours comprise a heterogeneous group that are rare but could result in serious manifestations. Surgical excision provides the best approach to treatment but many patients may have small lesions that are difficult to detect, or present with wide spread disease by the time of diagnosis. In addition to clinical assessment and biochemical tests, imaging is a major factor in establishing the diagnosis. Cross-sectional imaging such as US, CT and MR, play a major role in the initial assessment. However, they may miss small lesions or metastatic spread. Functional Imaging became possible with the development of somatostatin receptor imaging using 111In-octreotide, which when combined with anatomical imaging could provide enhanced detection. A major improvement has been achieved by combining receptor and PET inaging through the use of 68Ga-DOTA complexes that have been shown to have a much better sensitivity than other imaging modalities and can provide the basis for radionuclide treatment with 90Y or 177Lu labelled with DOTA complexes.

2 Article MUC13 interaction with receptor tyrosine kinase HER2 drives pancreatic ductal adenocarcinoma progression. 2017

Khan, S / Sikander, M / Ebeling, M C / Ganju, A / Kumari, S / Yallapu, M M / Hafeez, B B / Ise, T / Nagata, S / Zafar, N / Behrman, S W / Wan, J Y / Ghimire, H M / Sahay, P / Pradhan, P / Chauhan, S C / Jaggi, M. ·Department of Pharmaceutical Sciences and Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA. · Cancer Biology Research Center, Sanford Research, Sioux Falls, SD, USA. · Center for Drug Design Research, National Institutes of Biomedical Innovation, Health and Nutrition (NIBIOHN), Ibaraki City, Osaka, Japan. · Department of Pathology, University of Tennessee Health Science Center, Memphis, TN, USA. · Department of Surgery, University of Tennessee Health Science Center, Memphis, TN, USA. · Department of Biostatistics & Epidemiology, University of Tennessee Health Science Center, Memphis, TN, USA. · Department of Physics, University of Memphis, Memphis, TN, USA. ·Oncogene · Pubmed #27321183.

ABSTRACT: Although MUC13, a transmembrane mucin, is aberrantly expressed in pancreatic ductal adenocarcinoma (PDAC) and generally correlates with increased expression of HER2, the underlying mechanism remains poorly understood. Herein, we found that MUC13 co-localizes and interacts with HER2 in PDAC cells (reciprocal co-immunoprecipitation, immunofluorescence, proximity ligation, co-capping assays) and tissues (immunohistofluorescence). The results from this study demonstrate that MUC13 functionally interacts and activates HER2 at p1248 in PDAC cells, leading to stimulation of HER2 signaling cascade, including ERK1/2, FAK, AKT and PAK1 as well as regulation of the growth, cytoskeleton remodeling and motility, invasion of PDAC cells-all collectively contributing to PDAC progression. Interestingly, all of these phenotypic effects of MUC13-HER2 co-localization could be effectively compromised by depleting MUC13 and mediated by the first and second EGF-like domains of MUC13. Further, MUC13-HER2 co-localization also holds true in PDAC tissues with a strong functional correlation with events contributing to increased degree of disorder and cancer aggressiveness. In brief, findings presented here provide compelling evidence of a functional ramification of MUC13-HER2: this interaction could be potentially exploited for targeted therapeutics in a subset of patients harboring an aggressive form of PDAC.

3 Article Risk of cancer other than breast or ovarian in individuals with BRCA1 and BRCA2 mutations. 2012

Moran, A / O'Hara, C / Khan, S / Shack, L / Woodward, E / Maher, E R / Lalloo, F / Evans, D G R. ·North West Cancer Intelligence Service, The Christie NHS Foundation Trust, Manchester, M20 3LJ, UK. ·Fam Cancer · Pubmed #22187320.

ABSTRACT: The risks of cancers other than breast and ovarian amongst BRCA1 and BRCA2 mutation carriers are based on relatively few family based studies with the risk of specific cancers tested in population based samples of cancers from founder populations. We assessed risks of "other cancers" in 268 BRCA1 families and 222 BRCA2 families using a person years at risk analysis from 1975 to 2005. Cancer confirmations were overall higher than in previous family based studies at 64%. There was no overall increase in risk for BRCA1 carriers although oesophagus had a significant increased RR of 2.9 (95% CI 1.1-6.0) and stomach at 2.4 (95% CI 1.2-4.3), these were based mainly on unconfirmed cases. For BRCA2 increased risks for cancers of the pancreas (RR 4.1, 95% CI 1.9-7.8) and prostate (RR 6.3, 95% CI 4.3-9.0) and uveal melanoma (RR 99.4, 95% CI 11.1-359.8) were confirmed. Possible new associations with oesophagus (RR 4.1, 95% CI 1.9-7.8) and stomach (RR 2.7, 95% CI 1.3-4.8) were detected but these findings should be treated with caution due to lower confirmation rates. In contrast to previous research a higher risk of prostate cancer was found in males with mutations in the BRCA2 OCCR region. The present study strengthens the known links between BRCA2 and pancreatic and prostate cancer, but throws further doubt onto any association with BRCA1. New associations with upper gastro-intestinal malignancy need to be treated with caution and confirmed by large prospective studies.

4 Article Improved control of severe hypoglycemia in patients with malignant insulinomas by peptide receptor radionuclide therapy. 2011

van Schaik, E / van Vliet, E I / Feelders, R A / Krenning, E P / Khan, S / Kamp, K / Valkema, R / van Nederveen, F H / Teunissen, J J M / Kwekkeboom, D J / de Herder, W W. ·Department of Internal Medicine, Section of Endocrinology, Erasmus Medical Center, 's Gravendijkwal 230, 3015 CE Rotterdam, The Netherlands. ·J Clin Endocrinol Metab · Pubmed #21917872.

ABSTRACT: CONTEXT: Insulinomas are relatively rare neuroendocrine tumors of the pancreas. Only 10% are considered malignant. Control of insulin hypersecretion and hypoglycemia in patients with malignant insulinomas may be extremely difficult. Different medications and chemotherapy schedules have been used. PATIENTS: Five patients with metastatic insulinomas and severe, poorly controllable, hypoglycemia are described. These patients required continuous glucose infusion to control severe hypoglycemia, which were induced by the high levels of insulin secretion. Conventional medications, such as diazoxide, or streptozotocin-based chemotherapies had been used to control hypoglycemia but were ineffective and/or produced adverse effects. All patients were treated with sc octreotide. INTERVENTION: Peptide receptor radionuclide therapy with radiolabeled-somatostatin analogs was used. RESULTS: After the start of radiolabeled somatostatin analog therapy, the five patients with metastatic insulinomas had stable disease for a mean period of 27 months. During these months, the patients were without any hypoglycemic episodes. Finally, three of five patients died because of progressive disease. CONCLUSIONS: Radiolabeled somatostatin analog therapy can stabilize tumor growth and can be very successful in further controlling severe hypoglycemia in malignant insulinomas. In our series, this eventually resulted in improved survival outside the hospital setting.