Ralph H Hruban

Johns Hopkins University, Baltimore, Maryland, United States

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Publications (865)5026.19 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: OBJECTIVE. Pancreatic adenocarcinoma is a rapidly progressive malignancy characterized by its tendency for early metastatic spread. MDCT is the primary diagnostic modality for the preoperative staging of patients with pancreatic cancer, with an accuracy established in multiple studies. However, for a variety of reasons, there is often a prolonged interval between staging MDCT and the surgical intervention. This study examines the relationship between the interval between imaging and surgery and the accuracy of MDCT in determining the presence or absence of metastatic disease at surgery in patients with pancreatic cancer. MATERIALS AND METHODS. Patients were identified who had undergone surgery for pancreatic cancer at our institution with a dedicated preoperative pancreas-protocol MDCT performed in our department. Findings from the preoperative MDCT report were correlated with the operative findings, as well as the time between imaging and surgery. RESULTS. Two hundred ninety-two MDCT scans were performed on 256 patients who underwent exploration for pancreatic adenocarcinoma. The patients had a median age of 67 years (range, 30-95 years), and 51.6% (132/256) were male. The median time between MDCT and surgical exploration was 15.5 days (range, 1-198 days). MDCT correctly predicted the absence of metastatic disease at surgery in 233 of 274 (85.0%) studies. MDCT was more accurate in predicting the absence of metastatic disease if the study was performed within 25 days of surgery than it was if the study was performed within more than 25 days of surgery (89.3% vs 77.0%; p = 0.0097). Furthermore, regression models showed that the negative predictive value of a given MDCT significantly decreased after approximately 4 weeks. CONCLUSION. MDCT is an accurate method to stage patients with pancreatic cancer, but its accuracy in excluding distant metastatic disease depreciates over time. Patients should undergo a repeat MDCT within 25 days of any planned definitive operative intervention for pancreatic cancer to avoid unexpectedly finding metastatic disease at surgery.
    AJR. American journal of roentgenology. 01/2015; 204(1):W37-42.
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    ABSTRACT: Purpose The purpose of the study is to evaluate the CT appearance and pattern of metastatic disease of patients with surgically resected well-differentiated duodenal neuroendocrine tumors who underwent pre-operative dual-phase CT. Methods Clinical and pathologic records and CT images of 28 patients (average age 58.0 years) following Whipple procedure were retrospectively reviewed. The size, morphology (polypoid, intraluminal mass or wall thickening, intramural mass), location, CT attenuation in the arterial and venous phases, and the presence of lymph node or liver metastases were recorded. Results On CT, 19 patients (67.8%) had neuroendocrine tumors manifested as polypoid or intraluminal masses (38 lesions, multiple tumors in 3 patients), 4 patients (14.3%) had tumors manifested as wall thickening or intramural masses, and in 5 patients (17.9%), the primary tumor was not visualized. Lesions not seen at CT were less than 0.8 cm on pathologic diagnosis. The mean size of polypoid tumors on CT was 1.2 cm (range 0.3–3.8 cm); 24 tumors were 1.0 cm or smaller, and 14 tumors were larger than 1.0 cm. Most lesions were hypervascular in the arterial phase (19/23 patients) with an increase in tumor enhancement in the venous phase in 14 patients (60.9%), decrease in enhancement in 7 patients (30.4%), and no change in enhancement in 2 patients (8.7%). Thirteen patients (46.4%) had metastatic disease from carcinoid tumor, most commonly regional enhancing lymphadenopathy. Conclusion Duodenal carcinoid tumors commonly appear as an enhancing mass in either the arterial or venous phases. If a primary tumor is not seen in the duodenum, adjacent enhancing lymphadenopathy can be a clue to the presence of a duodenal carcinoid tumor.
    Abdominal Imaging 12/2014; · 1.91 Impact Factor
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    ABSTRACT: Intraductal papillary mucinous neoplasms (IPMNs) of the pancreas are precursor lesions that progress to invasive cancer through progressively worsening dysplasia. Although smoking is an established risk factor for pancreatic adenocarcinoma, potential associations with IPMN grade of dysplasia remain unclear. Pancreatic resections for IPMN from 1995 to 2013 were retrospectively reviewed. A total of 446 patients in which the smoking status was documented were identified. Smoking history was positive in 47 % of patients. Of smokers, 50 % had branch-duct, 14 % had main-duct, and 36 % had mixed-type IPMN. Patients with main-duct IPMN were more commonly smokers (65 %), compared to smoking history in 46 % with mixed and 44 % with branch-duct IPMN (p = 0.03). High-grade dysplasia occurred in 25 % of smokers and 21 % of nonsmokers (p = 0.32), and invasive carcinoma in 25 % of smokers and 25 % nonsmokers (p = 0.95). On multivariate analysis, duct size was independently associated with high-grade dysplasia (OR = 3.17, 95 %CI = 1.79-5.64, p < 0.001). Presence of mural nodules (OR = 3.34, 95 %CI = 1.82-6.12, p < 0.001), duct size (OR = 3.87, 95 %CI = 2.21-6.75, p < 0.001), and symptoms (OR = 7.10, 95 %CI = 3.80-13.08, p < 0.001), but not smoking history (OR = 1.10, 95 %CI = 0.64-1.88, p = 0.73), were independent predictors of invasive carcinoma. Median overall survival was 70 months for smokers and 88 months for nonsmokers (p = 0.68). Positive smoking history correlated with duct type classification but does not appear to be a risk factor for harboring high-grade dysplasia or invasive carcinoma in IPMNs.
    Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract. 12/2014;
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    ABSTRACT: & Aims: Pancreatic imaging can identify neoplastic cysts but not microscopic neoplasms. Mutation analysis of pancreatic fluid following secretin stimulation might identify microscopic neoplasias in the pancreatic duct system. We determined the prevalence of mutations in KRAS and GNAS genes in pancreatic juice from subjects undergoing endoscopic ultrasound for suspected pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasms, or pancreatic adenocarcinoma. Secretin-stimulated juice samples were collected from the duodenum of 272 subjects enrolled in Cancer of the Pancreas Screening studies; 194 subjects were screened because of a family history of, or genetic predisposition to, pancreatic cancer and 78 were evaluated for pancreatic cancer (n=30) or other disorders (controls: pancreatic cysts, pancreatitis, or normal pancreata, n=48 ). Mutations were detected by digital high-resolution melt-curve analysis and pyrosequencing. The number of replicates containing a mutation determined the mutation score. KRAS mutations were detected in pancreatic juice from larger percentages of subjects with pancreatic cancer (73%) or undergoing cancer screening (50%) than controls (19%) (P=.0005). A greater proportion of patients with pancreatic cancer had at least 1 KRAS mutation detected 3 or more times (47%) than screened subjects (21%) or controls (6%, P=.002). Among screened subjects, mutations in KRAS (but not GNAS) were found in similar percentages of patients with or without pancreatic cysts. However, a greater proportion of patients over 50 ys old had KRAS mutations (54.6%) than younger patients (36.3%) (P=.032); the older subjects also more mutations in KRAS (P=.02). Mutations in KRAS are detected in pancreatic juice from the duodenum of 73% of patients with pancreatic cancer, and 50% of asymptomatic individuals with a high risk for pancreatic cancer. However, KRAS mutations are detected in pancreatic juice from 19% of controls. Mutations detected in individuals without pancreatic abnormalities, based on imaging analyses, likely arise from small PanIN lesions. ClinicalTrials.gov no: NCT00438906 and NCT00714701. Copyright © 2014 AGA Institute. Published by Elsevier Inc. All rights reserved.
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    ABSTRACT: A 3 day old infant with persistent severe hypoglycemia was found to have a cystic pancreatic tumor. Cessation of glucose infusion led to severe hypoglycemia. Pancreaticoduodenectomy was performed and revealed an intraductal papillary mucinous neoplasm (IPMN) with high-grade dysplasia. Sequencing of the IPMN revealed a KRAS gene mutation not present in surrounding normal tissues. Deep sequencing of the patient’s blood for KRAS mutations showed no evidence of mosaicism. Whole exome sequencing of the blood of the patient and both parents revealed a de novo germline SKIL mutation in the child that was not present in either parent. This suggests a possible role for SKIL in the pathogenesis of pancreatic tumors.
    Pancreatology 10/2014; · 2.04 Impact Factor
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    ABSTRACT: Neurofibromatosis 1 is a hereditary syndrome characterized by the development of numerous benign neurofibromas, a small subset of which progress to malignant peripheral nerve sheath tumors (MPNSTs). To better understand the genetic basis for MPNSTs, we performed genome-wide or targeted sequencing on 50 cases. Sixteen MPNSTs but none of the neurofibromas tested were found to have somatic mutations in SUZ12, implicating it as having a central role in malignant transformation.
    Nature genetics. 10/2014;
  • Ralph H Hruban, David S Klimstra
    Seminars in Diagnostic Pathology 09/2014; · 1.62 Impact Factor
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    ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is nearly uniformly lethal, with a median overall survival in 2014 of only 6 months. The genetic progression of sporadic PDAC (SPC) is well established, with common somatic alterations in KRAS, p16/CDKN2A, TP53, and SMAD4/DPC4. Up to 10 % of all PDAC cases occur in families with two or more affected first-degree relatives (familial pancreatic cancer, FPC), but these cases do not appear to present at an obviously earlier age of onset. This is unusual because most familial cancer syndrome patients present at a substantially younger age than that of corresponding sporadic cases. Here we collated the reported age of onset for FPC and SPC from the literature. We then used an integrated approach including whole exomic sequencing, whole genome sequencing, RNA sequencing, and high density SNP microarrays to study a cohort of FPC cell lines and corresponding germline samples. We show that the four major SPC driver genes are also consistently altered in FPC and that each of the four detection strategies was able to detect the mutations in these genes, with one exception. We conclude that FPC undergoes a similar somatic molecular pathogenesis as SPC, and that the same gene targets can be used for early detection and minimal residual disease testing in FPC patients.
    Familial Cancer 09/2014; · 1.94 Impact Factor
  • Ralph H. Hruban, David S. Klimstra
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    ABSTRACT: Infiltrating ductal adenocarcinoma of the pancreas is a real enigma. On one hand it is one of the most deadly of all of the solid malignancies. On the other, the neoplastic glands can be remarkably well-differentiated and it can be difficult to distinguish between a reactive non-neoplastic gland and a gland of invasive adenocarcinoma. In this review we will present diagnostic criteria that one can “hang your hat on” when establishing the diagnosis of infiltrating ductal adenocarcinoma of the pancreas. We will also review clinically important features of the disease, and, with the impending incorporation of molecular genetics into everyday practice, we will emphasize clinical applications of cancer genetics.
    Seminars in Diagnostic Pathology 09/2014; · 1.62 Impact Factor
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    ABSTRACT: Background: Intraductal papillary mucinous neoplasms (IPMNs) have malignant potential, and can progress from low- to high-grade dysplasia to invasive adenocarcinoma. The management of patients with IPMNs is dependent on their risk of malignant progression, with surgical resection recommended for patients with branch duct-IPMN (BD-IPMN) who develop high-risk features.There is increasing evidence that liver transplant patients are at increased risk of extra-hepatic malignancy. However there are few data regarding the risk of progression of BD-IPMNs in liver transplant recipients. The aim of this study was to determine if liver transplant recipients with BD-IPMNs are at higher risk of developing high-risk features than patients with BD-IPMNs who did not receive a transplant.Methods: Consecutive patients who underwent a liver transplant with BD-IPMNs were included. Patients with BD-IPMNs with no history of immunosuppression were used as controls. Progression of the BD-IPMNs was defined as development of a high-risk feature (jaundice, dilated main pancreatic duct, mural nodule, cytology suspicious or diagnostic for malignancy, cyst diameter ≥3cm).Results: Twenty three liver transplant patients with BD-IPMN were compared with 274 control patients. The median length of follow-up was 53.7 and 24 months in liver transplant and control groups respectively. Four (17.4%) liver transplant patients and 45 (16.4%) controls developed high-risk features (p=0.99). In multivariate analysis, progression of BD-IPMNs was associated with age at diagnosis but not with liver transplantation.Conclusion: There was no statistically significant difference in the risk of developing high-risk features between the liver transplant and control groups. Liver Transpl , 2014. © 2014 AASLD.
    Liver Transplantation 08/2014; · 3.94 Impact Factor
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    ABSTRACT: Purpose Groove pancreatitis is a rare focal form of chronic pancreatitis that occurs in the pancreaticoduodenal groove between the major and minor papillae, duodenum and pancreatic head. Radiologic appearance and clinical presentation can result in suspicion of malignancy rendering pancreaticoduodenectomy inevitable. This study reports dual phase CT findings in a series of 12 patients with pathology proven groove pancreatitis. Materials and Methods Retrospective review of preoperative CT findings in 12 patients with histologically proven groove pancreatitis after pancreaticoduodenectomy. Size, location, attenuation, presence of mass or cystic components in the pancreas, groove and duodenum, calcifications, duodenal stenosis and ductal changes were recorded. Clinical data, laboratory values, endoscopic ultrasonographic and histopathological findings were collected. Results Soft tissue thickening in the groove was seen in all patients. Pancreatic head, groove and duodenum were all involved in 75% patients. A discrete lesion in the pancreatic head was seen in half of the patients, most of which appeared hypodense on both arterial and venous phases. Cystic changes in pancreatic head were seen in 75% patients. Duodenal involvement was seen in 92% patients including wall thickening and cyst formation. The main pancreatic duct was dilated in 7 patients, with an abrupt cut off in 3 and a smooth tapering stricture in 4. Five patients had evidence of chronic pancreatitis with parenchymal calcifications. Conclusion Presence of mass or soft tissue thickening in the groove with cystic duodenal thickening is highly suggestive of groove pancreatitis. Recognizing common radiological features may help in diagnosis and reduce suspicion of malignancy.
    European Journal of Radiology 08/2014; · 2.51 Impact Factor
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    ABSTRACT: The aim of this study was to evaluate the ability of computed tomography (CT) in differentiating between intrapancreatic accessory spleen (IPAS) from pancreatic neuroendocrine tumor (PanNET).
    Journal of computer assisted tomography. 06/2014;
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    ABSTRACT: Background: Evidence suggests the incidence of oral tongue squamous cell carcinoma is increasing in young patients, many who have no history of tobacco use. Methods We clinically reviewed 89 oral tongue cancer patients. Exomic sequencing of tumor DNA from 6 non-smokers was performed and compared to previously sequenced cases. RNA from 20 tumors was evaluated by massively parallel sequencing to search for potentially oncogenic viruses. Results Non-smokers (53 of 89) were younger than smokers (36 of 89) (mean 50.4 vs. 61.9 years, P<0.001), and appeared more likely to be female, (58.5% vs. 38.9%, P=0.069). Non-smokers had fewer TP53 mutations (P=0.02) than smokers. No tumor-associated viruses were detected. Conclusions The young age of non-smoker oral tongue cancer patients, and fewer TP53 mutations suggest a viral role in this disease. Our efforts to identify such a virus were unsuccessful. Further studies are warranted to elucidate the drivers of carcinogenesis in these patients. Head Neck, 2014.
    Head & neck. 06/2014;
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    ABSTRACT: Background: Solid-pseudopapillary neoplasm (SPN) is a rare pancreatic malignancy with an excellent prognosis. It is most commonly diagnosed in young women. This article comprehensively reviews the clinical, pathological and radiological features of this neoplasm, as well as its clinical management. Methods: A literature review of SPN was performed of all articles published in the English language in PubMed prior to November 1, 2013. Cytomorphological features, histopathology, immunohistochemistry, patient general demographics, molecular studies, radiologic imaging and clinical management were reviewed. Results: SPN displays distinct cytomorphological features on fine-needle aspiration - thin, delicate, branching vessels in a 'Chinese character' pattern lined by one to several layers of loosely cohesive neoplastic cells. Nuclear features include indented or grooved nuclei with an evenly distributed chromatin pattern and small inconspicuous nucleoli. SPN is characteristically immunoreactive for CD10, β-catenin (in an abnormal nuclear pattern), CD99 in a perinuclear dot-like pattern, α1-antitrypsin, and progesterone receptor. Almost all SPNs harbor an activating point mutation in exon 3 of the β-catenin gene (CTNNB1). Clinicopathological features generally do not correlate with prognosis, and most patients experience excellent long-term survival. Conclusions: SPN can mimic other neoplasms of the pancreas, which can lead to diagnostic challenges in a limited cytologic specimen. Distinct cytomorphological features can help distinguish SPNs from other pancreatic neoplasms. Complete surgical resection as well as resection of metastatic disease is preferred given a low rate of tumor recurrence and long periods of disease-free intervals. © 2014 S. Karger AG, Basel.
    Acta cytologica 06/2014; · 0.69 Impact Factor
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    ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is considered a "nonimmunogenic" neoplasm. Single-agent immunotherapies have failed to demonstrate significant clinical activity in PDAC and other "nonimmunogenic" tumors, in part due to a complex tumor microenvironment (TME) that provides a formidable barrier to immune infiltration and function. We designed a neoadjuvant and adjuvant clinical trial comparing an irradiated, granulocyte-macrophage colony-stimulating factor (GM-CSF)-secreting, allogeneic PDAC vaccine (GVAX) given as a single agent or in combination with low-dose cyclophosphamide to deplete regulatory T cells (Treg) as a means to study how the TME is altered by immunotherapy. Examination of resected PDACs revealed the formation of vaccine-induced intratumoral tertiary lymphoid aggregates in 33 of 39 patients 2 weeks after vaccine treatment. Immunohistochemical analysis showed these aggregates to be regulatory structures of adaptive immunity. Microarray analysis of microdissected aggregates identified gene-expression signatures in five signaling pathways involved in regulating immune-cell activation and trafficking that were associated with improved postvaccination responses. A suppressed Treg pathway and an enhanced Th17 pathway within these aggregates were associated with improved survival, enhanced postvaccination mesothelin-specific T-cell responses, and increased intratumoral Teff:Treg ratios. This study provides the first example of immune-based therapy converting a "nonimmunogenic" neoplasm into an "immunogenic" neoplasm by inducing infiltration of T cells and development of tertiary lymphoid structures in the TME. Post-GVAX T-cell infiltration and aggregate formation resulted in the upregulation of immunosuppressive regulatory mechanisms, including the PD-1-PD-L1 pathway, suggesting that patients with vaccine-primed PDAC may be better candidates than vaccine-naïve patients for immune checkpoint and other immunomodulatory therapies. Cancer Immunol Res; 2(7); 1-16. ©2014 AACR.
    Cancer immunology research. 06/2014;
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    ABSTRACT: Pancreatic cancer is the deadliest of all solid malignancies. Early detection offers the best hope for a cure, but characteristics of this disease, such as the lack of early clinical symptoms, make the early detection difficult. Recent genetic mapping of the molecular evolution of pancreatic cancer suggests that a large window of opportunity exists for the early detection of pancreatic neoplasia, and developments in cancer genetics offer new, potentially highly specific approaches for screening of curable pancreatic neoplasia. We review the challenges of screening for early pancreatic neoplasia, as well as opportunities presented by incorporating molecular genetics into these efforts. Cancer Res; 74(13); 1-9. ©2014 AACR.
    Cancer research. 06/2014;
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    ABSTRACT: Many patients with pancreatic cancer have metastases to distant organs at the time of initial presentation. Recent studies examining the evolution of pancreatic cancer at the genetic level have shown that clonal complexity of metastatic pancreatic cancer is already initiated within primary tumors, and organ-specific metastases are derived from different subclones. However, we do not yet understand to what extent the evolution of pancreatic cancer contributes to proteomic and signaling alterations. We hypothesized that genetic heterogeneity of metastatic pancreatic cancer results in heterogeneity at the proteome level. To address this, we employed a model system in which cells isolated from three sites of metastasis (liver, lung and peritoneum) from a single patient were compared. We used a SILAC-based accurate quantitative proteomic strategy combined with a high resolution mass spectrometry to analyze the total proteome and tyrosine phosphoproteome of each of the distal metastases. Our data reveal distinct patterns of both overall proteome expression as well as tyrosine kinase activities across the three different metastatic lesions. This heterogeneity is significant because it led to differential sensitivity of the neoplastic cells to small molecule inhibitors targeting various kinases and other pathways. For example, R428, a tyrosine kinase inhibitor that targets Axl receptor tyrosine kinase, was able to inhibit cells derived from lung and liver metastases much more effectively than cells from the peritoneal metastasis. Finally, we confirmed that administration of R428 in mice bearing xenografts of cells derived from the three different metastatic sites significantly diminished tumors formed from liver and lung metastasis-derived cell lines as compared to tumors derived from the peritoneal metastasis cell line. Overall, our data provide proof-of-principle support that personalized therapy of multiple organ metastases in a single patient should involve administration of a combination of agents with each agent targeted to the features of different subclones.
    Molecular & cellular proteomics : MCP. 06/2014;
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    ABSTRACT: Pancreatic cancer is the fourth leading cause of cancer-related death in the world. The etiology of pancreatic cancer is heterogeneous with a wide range of alterations that have already been reported at the level of the genome, transcriptome, and proteome. The past decade has witnessed a large number of experimental studies using high-throughput technology platforms to identify genes whose expression at the transcript or protein levels is altered in pancreatic cancer. Based on expression studies, a number of molecules have also been proposed as potential biomarkers for diagnosis and prognosis of this deadly cancer. Currently, there are no repositories which provide an integrative view of multiple Omics data sets from published research on pancreatic cancer. Here, we describe the development of a web-based resource, Pancreatic Cancer Database (http://www.pancreaticcancerdatabase.org), as a unified platform for pancreatic cancer research. PCD contains manually curated information pertaining to quantitative alterations in miRNA, mRNA, and proteins obtained from small-scale as well as high-throughput studies of pancreatic cancer tissues and cell lines. We believe that PCD will serve as an integrative platform for scientific community involved in pancreatic cancer research.
    Cancer biology & therapy 05/2014; 15(8). · 3.29 Impact Factor
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    ABSTRACT: One-hundred-fifty-three biliary cancers, including 70 intrahepatic cholangiocarcinomas (ICC), 57 extrahepatic cholangiocarcinomas (ECC) and 26 gallbladder carcinomas (GBC) were assessed for mutations in 56 genes using multigene next-generation sequencing. Expression of EGFR and mTOR pathway genes was investigated by immunohistochemistry. At least one mutated gene was observed in 118/153 (77%) cancers. The genes most frequently involved were KRAS (28%), TP53 (18%), ARID1A (12%), IDH1/2 (9%), PBRM1 (9%), BAP1 (7%), and PIK3CA (7%). IDH1/2 (p=0.0005) and BAP1 (p=0.0097) mutations were characteristic of ICC, while KRAS (p=0.0019) and TP53 (p=0.0019) were more frequent in ECC and GBC. Multivariate analysis identified tumour stage and TP53 mutations as independent predictors of survival. Alterations in chromatin remodeling genes (ARID1A, BAP1, PBRM1, SMARCB1) were seen in 31% of cases. Potentially actionable mutations were seen in 104/153 (68%) cancers: i) KRAS/NRAS/BRAF mutations were found in 34% of cancers; ii) mTOR pathway activation was documented by immunohistochemistry in 51% of cases and by mutations in mTOR pathway genes in 19% of cancers; iii) TGF-ß/Smad signaling was altered in 10.5% cancers; iv) mutations in tyrosine kinase receptors were found in 9% cases. Our study identified molecular subgroups of cholangiocarcinomas that can be explored for specific drug targeting in clinical trials.
    Oncotarget 05/2014; 5(9):2839-52. · 6.64 Impact Factor
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    ABSTRACT: Incidental pancreatic cysts are common, a small number of which are premalignant or malignant. Multidisciplinary care has been shown to alter management and improve outcomes in many types of cancers, but its role has not been examined in patients with pancreatic cysts. We assessed the effect of a multidisciplinary pancreatic cyst clinic (MPCC) on the diagnosis and management of patients with pancreatic cysts. The referring institution and MPCC diagnosis and management plan were recorded. Patient were placed into one of five categories-no, low, intermediate, or high risk of malignancy within the cyst, and malignant cyst-on the basis of their diagnosis. Patients were assigned one of four management options: surveillance, surgical resection, further evaluation, or discharge with no further follow-up required. The MPCC was deemed to have altered patient care if the patient was assigned a different risk or management category after the MPCC review. Referring institution records were available for 262 patients (198 women; mean age 62.7 years), with data on risk category available in 138 patients and management category in 225. The most common diagnosis was branch duct intraductal papillary mucinous neoplasm. MPCC review altered the risk category in 11 (8.0%) of 138 patients. The management category was altered in 68 (30.2%) of 225 patients. Management was increased in 52 patients, including 22 patients who were recommended surgical resection. Management was decreased in 16 patients, including 10 who had their recommendation changed from surgery to surveillance. MPCC is helpful and alters the management over 30% of patients.
    Annals of Surgical Oncology 05/2014; · 4.12 Impact Factor

Publication Stats

44k Citations
5,026.19 Total Impact Points


  • 1992–2014
    • Johns Hopkins University
      • • Department of Pathology
      • • Department of Surgery
      • • Department of Medicine
      • • Department of Otolaryngology - Head and Neck Surgery
      Baltimore, Maryland, United States
    • University of Massachusetts Boston
      Boston, Massachusetts, United States
  • 1984–2014
    • Johns Hopkins Medicine
      • • Department of Surgery
      • • Department of Pathology
      • • Department of Radiology and Radiological Science
      Baltimore, Maryland, United States
  • 2013
    • University of Colorado
      • Division of GI, Tumor and Endocrine Surgery
      Denver, CO, United States
  • 2009–2013
    • Howard Hughes Medical Institute
      Ashburn, Virginia, United States
    • Cambridge Institute for Medical Research
      Cambridge, England, United Kingdom
    • Johns Hopkins Bloomberg School of Public Health
      Baltimore, Maryland, United States
  • 2012
    • Weill Cornell Medical College
      • Department of Pathology and Laboratory Medicine
      New York City, NY, United States
  • 2011–2012
    • Vanderbilt University
      Nashville, Michigan, United States
    • Cancer Research UK Cambridge Institute
      Cambridge, England, United Kingdom
    • Centro Nacional de Investigaciones Oncológicas
      Madrid, Madrid, Spain
    • University Medical Center Utrecht
      • Department of Pathology
      Utrecht, Provincie Utrecht, Netherlands
    • University of Bonn
      Bonn, North Rhine-Westphalia, Germany
  • 1995–2012
    • University of Chicago
      • Department of Radiation & Cellular Oncology
      Chicago, IL, United States
    • The Ohio State University
      • Pathology
      Columbus, OH, United States
  • 2008–2011
    • Shizuoka Cancer Center
      Sizuoka, Shizuoka, Japan
    • University College Dublin
      • School of Medicine & Medical Science
      Dublin, L, Ireland
    • Thomas Jefferson University
      • Department of Surgery
      Philadelphia, PA, United States
  • 2000–2011
    • University of Texas Southwestern Medical Center
      • Department of Pathology
      Dallas, TX, United States
  • 2010
    • University of Texas MD Anderson Cancer Center
      • Department of Pathology
      Houston, TX, United States
  • 2007–2009
    • Purdue University
      West Lafayette, Indiana, United States
    • Southern Illinois Healthcare
      Illinois, United States
    • Cold Spring Harbor Laboratory
      Cold Spring Harbor, New York, United States
  • 1990–2009
    • Memorial Sloan-Kettering Cancer Center
      • • Department of Pathology
      • • Department of Surgery
      New York City, NY, United States
  • 2005–2007
    • Louisiana State University Health Sciences Center New Orleans
      • Department of Pathology
      Baton Rouge, LA, United States
    • Eastern Virginia Medical School
      • Department of Surgery
      Norfolk, VA, United States
    • Sapienza University of Rome
      Roma, Latium, Italy
    • Roswell Park Cancer Institute
      • Department of Cancer Genetics
      Buffalo, NY, United States
    • University of Michigan
      • Department of Pathology
      Ann Arbor, MI, United States
    • Dartmouth–Hitchcock Medical Center
      Lebanon, New Hampshire, United States
  • 2003–2007
    • Mayo Clinic - Rochester
      • • Department of Laboratory Medicine & Pathology
      • • Department of Health Science Research
      Rochester, MN, United States
    • National and Kapodistrian University of Athens
      • Department of Surgery
      Athens, Attiki, Greece
    • Mayo Foundation for Medical Education and Research
      • Department of Pathology
      Scottsdale, AZ, United States
    • Wayne State University
      • Department of Pathology
      Detroit, MI, United States
  • 2006
    • Indiana University-Purdue University Indianapolis
      • Department of Surgery
      Indianapolis, IN, United States
  • 2004–2006
    • University of Pennsylvania
      • Department of Medicine
      Philadelphia, Pennsylvania, United States
    • National Human Genome Research Institute
      Maryland, United States
  • 2002–2004
    • Karmanos Cancer Institute
      • Division of Hematology and Oncology
      Detroit, Michigan, United States
  • 1997–2002
    • Academisch Medisch Centrum Universiteit van Amsterdam
      • Department of Pathology
      Amsterdam, North Holland, Netherlands
  • 1995–1999
    • University of Amsterdam
      • • Faculty of Medicine AMC
      • • Department of Pathology
      Amsterdam, North Holland, Netherlands
  • 1998
    • Stanford University
      • Department of Medicine
      Stanford, CA, United States
  • 1993
    • Greater Baltimore Medical Center
      Baltimore, Maryland, United States