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[PMID]: 25698272
[Au] Autor:Karakan T; Cengiz M; Ibis M; Akyürek N; Ünal S
[Ad] Address:Department of Gastroenterology, Gazi University Faculty of Medicine, Ankara, Turkey. drmustafacen@gmail.com.
[Ti] Title:Pancreatic metastasis in a case of small cell lung carcinoma diagnosed by EUS.
[So] Source:Turk J Gastroenterol;26(1):53-5, 2015 Jan.
[Is] ISSN:1300-4948
[Cp] Country of publication:Turkey
[La] Language:eng
[Ab] Abstract:Small-cell lung carcinoma represents a group of highly malignant tumors characterized by early and widespread metastais even at the time of diagnosis. However, the pancreas is a relatively infrequent site of metastasis by this neoplasm. A 57-year-old patient was admitted with an intense cough and complaints of abdominal discomfort. A chest X-Ray showed no evidence of lung mass but did show signs of lymphadenopathy. In addition, there was little evidence for malignancy based on a transbronchial needle aspiration. In contrast, there was a mass in the head portion of the pancreas. We diagnosed a case of small-cell lung carcinoma metastasis in the pancreas by using an endoscopic ultrasound-guided fine-needle aspiration biopsy. This case demonstrates that endoscopic ultrasound-guided fine-needle aspiration biopsy is an important tool in the diagnosis of metastatic pancreatic neoplasms.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1502
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.5152/tjg.2015.3687

  2 / 1947833 MEDLINE  
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[PMID]: 25588746
[Au] Autor:Fuchs J
[Ad] Address:Department of Pediatric Surgery and Pediatric Urology, University Children's Hospital Tuebingen, Hoppe-Seyler-Str. 3, 72076, Tübingen, Germany, joerg.fuchs@med.uni-tuebingen.de.
[Ti] Title:The role of minimally invasive surgery in pediatric solid tumors.
[So] Source:Pediatr Surg Int;31(3):213-28, 2015 Mar.
[Is] ISSN:1437-9813
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:During recent years, minimally invasive surgery (MIS) has become the standard approach for various operations in infants and children. MIS in pediatric thoracic and abdominal tumors is a controversial approach in the surgical management of childhood cancer. Meanwhile, more and more oncological biopsies and resections are being performed laparoscopically or thoracoscopically. Despite its increasing role in pediatric tumor surgery, the different national and international multicenter trial groups have not yet implemented MIS within guidelines and recommendations in most of the current treatment protocols. An increasing number of retrospective reports describes a potential role of MIS in the management of different pediatric oncological entities. Over the time, there has been a diverse development of this approach with regard to the different neoplasms. Nevertheless, there is a lack of prospective randomized trails assessing MIS. This still represents a requirement for evidence-based medicine and judging the advantages and disadvantages of this approach. The purpose of this state-of-the-art article is to review the current literature to describe the application of MIS in pediatric solid tumors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1502
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00383-015-3660-9

  3 / 1947833 MEDLINE  
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[PMID]: 25216652
[Au] Autor:Del Corso G; Tardio ML; Gissi DB; Marchetti C; Montebugnoli L; Tarsitano A
[Ad] Address:Department of Biomedical and Neuromotor Sciences, Section of Oral Science, University of Bologna, via S Vitale 59, Bologna, Italy, giacomo.delcorso@unibo.it.
[Ti] Title:Ki-67 and p53 expression in ghost cell odontogenic carcinoma: a case report and literature review.
[So] Source:Oral Maxillofac Surg;19(1):85-9, 2015 Mar.
[Is] ISSN:1865-1569
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Ghost cell odontogenic carcinomas are rare neoplasms that arise in the maxillary bones either from a calcifying odontogenic cyst or de novo. They are aggressive locally and can metastasize. We report herein a case of a ghost cell odontogenic carcinoma arising in the mandible of a Caucasian male 86 years of age. We have described the clinical and radiographic features, histological characteristics, immunohistochemistry findings, and surgical treatment. We especially focused on how Ki-67 expression guides the treatment choice. Finally, we reviewed 32 cases described in the literature and compared them with the cases described up until 2014 to help clinicians identify the diagnostic characteristics of and select appropriate treatment modalities for ghost cell odontogenic carcinomas.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1502
[Js] Journal subset:D; IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s10006-014-0465-2

  4 / 1947833 MEDLINE  
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[PMID]: 25518811
[Au] Autor:Qin M; Ma LQ; Tan J; Chen YR; Zhu LR; Lin R; Hu WL; Li JN; Zhang KH; Wang Y; Li JS; Xiao B; Chen HY; Chen YX; Fang JY
[Ad] Address:State Key Laboratory of Oncogene and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Department of Gastroenterology and Hepatology, Ren Ji Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
[Ti] Title:Risk factors for colorectal neoplasms based on colonoscopy and pathological diagnoses of Chinese citizens: a multicenter, case-control study.
[So] Source:Int J Colorectal Dis;30(3):353-61, 2015 Mar.
[Is] ISSN:1432-1262
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:PURPOSE: Since observational data in the urban residents are required to better assess the risk factors of colorectal neoplasm occurrence and the effectiveness of colonoscopy screening and surveillance, we conducted a case-control study at multicenters in China to identify patient characteristics and neoplasm features of colorectal adenoma (CRA) and colorectal carcinoma (CRC). METHODS: A total of 4089 patients who had undergone a colonoscopy from 19 hospitals were enrolled, of which 1106 had CRA and 466 had CRC. They were compared with controls. The analysis provides features and risk factors of colorectal neoplasm using multivariate logistic regression. RESULTS: Increasing age, a family history of colorectal cancer or previous cases of colorectal adenoma or hypertension disease, gastrointestinal surgery, regular intake of pickled food (adjusted odds ratio [aOR] 1.42, 95 % confidence interval [CI], 1.048-1.924), consumption of alcohol, and a positive result of fecal occult blood testing (FOBT; aOR 2.509, 95 % CI 1.485-4.237) were associated with an increased risk of CRA. In the CRC group, increasing age, regular intake of pickled foods, and a positive FOBT result were risk factors. In addition, a positive abdominal computed tomography (CT) before a colonoscopy and physical signs of emaciation were also significantly associated with an increasing risk of colorectal carcinoma. Regular intake of vegetables decreased the risk of both CRA and CRC. CONCLUSIONS: Age, pickled foods, and a positive FOBT are risk factors for colorectal neoplasm. Vegetable intake was associated with a decreased risk of CRA and CRC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1502
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00384-014-2090-9

  5 / 1947833 MEDLINE  
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[PMID]: 25696878
[Au] Autor:Harrison CN; Garcia NC
[Ad] Address:Department of Haematology, Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom.
[Ti] Title:Management of MPN beyond JAK2.
[So] Source:Hematology Am Soc Hematol Educ Program;2014(1):348-54, 2014 Dec 5.
[Is] ISSN:1520-4383
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Thrombocytosis has a large number of potential underlying causes, but the dominant group of hematological conditions for consideration in this setting are the myeloproliferative neoplasms (MPNs). In this chapter, we consider several key linked questions relating to the management of thrombocytosis in MPNs and discuss several issues. First, we discuss the differential diagnosis of thrombocytosis, which myeloid disorders to consider, and practical approaches to the discrimination of each individual MPN from other causes. Second, there have been several major advances in our understanding of the molecular biology of these conditions and we discuss how these findings are likely to be practically applied in the future. Third, we consider whether there is evidence that thrombocytosis contributes to the complications known to be associated with MPN: thrombosis, hemorrhage and transformation to leukemia and myelofibrosis. Last, we review current ideas for risk stratification and management of essential thrombocythemia and polycythemia vera as the 2 entities within the MPN family that are most frequently associated with thrombocytosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1502
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1182/asheducation-2014.1.348

  6 / 1947833 MEDLINE  
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[PMID]: 25696868
[Au] Autor:Nangalia J; Green TR
[Ad] Address:Cambridge Institute for Medical Research and Wellcome Trust/MRC Stem Cell Institute, Department of Haematology, University of Cambridge, Cambridge, United Kingdom; and Department of Haematology, Addenbrooke's Hospital, Cambridge, United Kingdom.
[Ti] Title:The evolving genomic landscape of myeloproliferative neoplasms.
[So] Source:Hematology Am Soc Hematol Educ Program;2014(1):287-96, 2014 Dec 5.
[Is] ISSN:1520-4383
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Our understanding of the genetic basis of the Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) has moved forward at a staggering pace over the last decade. With the discoveries of underlying mutations in JAK2, MPL, and, most recently, calreticulin (CALR), that together account for ∼90% of patients with MPNs, these conditions are now among the best characterized of hematological malignancies. While JAK-STAT pathway activation has been shown to be central to the pathogenesis of the MPN phenotype, the mechanism by which mutant CALR alters cellular function to result in myeloid proliferation remains unclear. Other mutations in several epigenetic modifiers, such as ASXL1, DNMT3a, TET2, EZH2, IDH1, and IDH2, as well as in genes involved in mRNA splicing, such as SF3B1 and U2AF2, have also been described in recent years in patients with MPNs, and evidence is emerging as to how these may be contributing to disease biology. From a therapeutic perspective, the discovery of aberrations in JAK2 has rapidly translated into the successful clinical use of JAK inhibitors in MPNs. Mutant calreticulin has the potential to be a tumor-specific therapeutic target because the mutations generate a novel protein C-terminus. In this chapter, we detail the genomic alterations that underlie MPNs, with a focus on the recent discovery of mutations in CALR, and explore the clinical and biological relevance of the altered genomic landscape in MPNs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1502
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1182/asheducation-2014.1.287

  7 / 1947833 MEDLINE  
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[PMID]: 25696867
[Au] Autor:Geyer HL; Mesa RA
[Ad] Address:Division of Hospital Internal Medicine and.
[Ti] Title:Therapy for myeloproliferative neoplasms: when, which agent, and how?
[So] Source:Hematology Am Soc Hematol Educ Program;2014(1):277-86, 2014 Dec 5.
[Is] ISSN:1520-4383
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Myeloproliferative neoplasms, including polycythemia vera (PV), essential thrombocythemia, and myelofibrosis (MF) (both primary and secondary), are recognized for their burdensome symptom profiles, life-threatening complications, and risk of progression to acute leukemia. Recent advancements in our ability to diagnose and prognosticate these clonal malignancies have paralleled the development of MPN-targeted therapies that have had a significant impact on disease burden and quality of life. Ruxolitinib has shown success in alleviating the symptomatic burden, reducing splenomegaly and improving quality of life in patients with MF. The role and clinical expectations of JAK2 inhibition continues to expand to a variety of investigational arenas. Clinical trials for patients with MF focus on new JAK inhibitors with potentially less myelosuppression (pacritinib) or even activity for anemia (momelotinib). Further efforts focus on combination trials (including a JAK inhibitor base) or targeting new pathways (ie, telomerase). Similarly, therapy for PV continues to evolve with phase 3 trials investigating optimal frontline therapy (hydroxyurea or IFN) and second-line therapy for hydroxyurea-refractory or intolerant PV with JAK inhibitors. In this chapter, we review the evolving data and role of JAK inhibition (alone or in combination) in the management of patients with MPNs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1502
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1182/asheducation-2014.1.277

  8 / 1947833 MEDLINE  
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[PMID]: 25696866
[Au] Autor:Chen E; Mullally A
[Ad] Address:Division of Hematology, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
[Ti] Title:How does JAK2V617F contribute to the pathogenesis of myeloproliferative neoplasms?
[So] Source:Hematology Am Soc Hematol Educ Program;2014(1):268-76, 2014 Dec 5.
[Is] ISSN:1520-4383
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:A decade on from the discovery of the JAK2V617F mutation in the majority of patients with myeloproliferative neoplasms (MPNs), JAK2V617F is now firmly installed in the hematology curriculum of medical students and the diagnostic-testing algorithm of clinicians. Furthermore, the oral JAK1/JAK2 inhibitor ruxolitinib, rationally designed to target activated JAK2 signaling in MPN, has been approved by the Food and Drug Administration (FDA) of the United States for the past 3 years for the treatment of intermediate- and advanced-phase myelofibrosis. Notwithstanding this, JAK2V617F continues to stimulate the MPN research community and novel insights into understanding the mechanisms by which JAK2V617F contributes to the pathogenesis of MPN are continually emerging. In this chapter, we focus on recent advances in 4 main areas: (1) the molecular processes coopted by JAK2V617F to induce MPN, (2) the role that JAK2V617F plays in phenotypic diversity in MPN, (3) the functional impact of JAK2V617F on hematopoietic stem cells, and (4) therapeutic strategies to target JAK2V617F. Although great strides have been made, significant deficits still exist in our understanding of the precise mechanisms by which JAK2V617F-mutant hematopoietic stem cells emerge and persist to engender clonal hematopoiesis in MPN and in developing strategies to preferentially target the JAK2V617F-mutant clone therapeutically. Critically, although myelofibrosis remains arguably the greatest clinical challenge in JAK2V617F-mediated MPN, the current understanding of myelofibrosis-specific disease biology remains quite rudimentary. Therefore, many important biological questions pertaining to JAK2V617F will continue to engage and challenge the MPN research community in the coming decade.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1502
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1182/asheducation-2014.1.268

  9 / 1947833 MEDLINE  
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[PMID]: 25696854
[Au] Autor:Silverman LB
[Ad] Address:Department of Pediatric Oncology, Dana-Farber Cancer Institute and Division of Pediatric Hematology-Oncology, Boston Children's Hospital, Boston, MA.
[Ti] Title:Balancing cure and long-term risks in acute lymphoblastic leukemia.
[So] Source:Hematology Am Soc Hematol Educ Program;2014(1):190-7, 2014 Dec 5.
[Is] ISSN:1520-4383
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cure rates for children and adolescents with acute lymphoblastic leukemia (ALL) have improved dramatically over the last few decades. With this success has come increasing recognition of the adverse late effects of treatment. The significant long-term sequelae in the earliest cohort of long-term survivors treated in the 1970s and 1980s are well documented. To reduce the incidence of these late effects, the majority of pediatric patients treated on more contemporary regimens receive less intensive treatment than did those treated 30-40 years ago. However, current therapies are not risk free; children treated with contemporary regimens remain at risk for developing long-term toxicities, including cardiac dysfunction, osteonecrosis, neurocognitive impairment, and second malignant neoplasms. One of the great challenges facing clinical investigators today is to identify interventions that will reduce the frequency and severity of long-term toxicities without adversely affecting cure rates. The use of dexrazoxane as a cardioprotectant (to prevent anthracycline-associated cardiotoxicity) and alternate-week dosing of dexamethasone (to reduce the risk of osteonecrosis) are examples of 2 such successful strategies. This article provides an overview of the long-term toxicities associated with current therapies and reviews results of clinical trials designed to minimize the burden of cure in long-term survivors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1502
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1182/asheducation-2014.1.190

  10 / 1947833 MEDLINE  
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[PMID]: 25696849
[Au] Autor:Harris NL
[Ad] Address:Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA.
[Ti] Title:Indolent lymphoma: follicular lymphoma and the microenvironment-insights from the microscope.
[So] Source:Hematology Am Soc Hematol Educ Program;2014(1):158-62, 2014 Dec 5.
[Is] ISSN:1520-4383
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Follicular lymphomas (FLs) are neoplasms of germinal center (GC) B cells, which retain many of the morphologic, immunophenotypic, genetic, and functional features of normal GC B cells. Both normal GCs and neoplastic follicles of FL also contain non-neoplastic cells (microenvironment) that influence and are influenced by the GC and FL B cells and are likely important for tumor cell survival. Many insights into the nature of the GC/FL microenvironment have come from morphologic and immunophenotypic analysis, both before and after the discoveries from gene expression profiling. This chapter reviews what we have learned from the microscope and highlights the pitfalls involved in trying to enumerate cells in the microenvironment for clinical prognostication.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1502
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1182/asheducation-2014.1.158


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