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[PMID]: 25118636
[Au] Autor:Stewart DR; Messinger Y; Williams GM; Yang J; Field A; Schultz KA; Harney LA; Doros LA; Dehner LP; Hill DA
[Ad] Address:Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Rockville, MD, USA, drstewart@mail.nih.gov.
[Ti] Title:Nasal chondromesenchymal hamartomas arise secondary to germline and somatic mutations of DICER1 in the pleuropulmonary blastoma tumor predisposition disorder.
[So] Source:Hum Genet;133(11):1443-50, 2014 Nov.
[Is] ISSN:1432-1203
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Nasal chondromesenchymal hamartoma (NCMH) is a rare nasal tumor that typically presents in young children. We previously reported on NCMH occurrence in children with pleuropulmonary blastoma (PPB), a rare pulmonary dysembryonic sarcoma that is the hallmark neoplasm in the PPB-associated DICER1 tumor predisposition disorder. Original pathologic materials from individuals with a PPB, PPB-associated tumor and/or a DICER1 mutation were centrally reviewed by the International PPB Registry. Paraffin-embedded NCMH tumor tissue was available in three cases. Laser-capture microdissection was used to isolate mesenchymal spindle cells and cartilage in one case for Sanger sequencing of DICER1. Nine patients (5F/4M) had PPB and NCMH. NCMH was diagnosed at a median age of 10 years (range 6-21 years). NCMH developed 4.5-13 years after PPB. Presenting NCMH symptoms included chronic sinusitis and nasal congestion. Five patients had bilateral tumors. Local NCMH recurrences required several surgical resections in two patients, but all nine patients were alive at 0-16 years of follow-up. Pathogenic germline DICER1 mutations were found in 6/8 NCMH patients tested. In 2 of the patients with germline DICER1 mutations, somatic DICER1 missense mutations were also identified in their NCMH (E1813D; n = 2). Three additional PPB patients developed other nasal lesions seen in the general population (a Schneiderian papilloma, chronic sinusitis with cysts, and allergic nasal polyps with eosinophils). Two of these patients had germline DICER1 mutations. Pathogenic germline and somatic mutations of DICER1 in NCMH establishes that the genetic etiology of NCMH is similar to PPB, despite the disparate biological potential of these neoplasms.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00439-014-1474-9

  2 / 1913615 MEDLINE  
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[PMID]: 25276122
[Au] Autor:Paini M; Crippa S; Scopelliti F; Baldoni A; Manzoni A; Belfiori G; Partelli S; Falconi M
[Ad] Address:Division of Pancreatic Surgery, Ospedali Riuniti, Università Politecnica delle Marche, Via Conca 71, 60126 Ancona, Italy....
[Ti] Title:Extent of Surgery and Implications of Transection Margin Status after Resection of IPMNs.
[So] Source:Gastroenterol Res Pract;2014:269803, 2014.
[Is] ISSN:1687-6121
[Cp] Country of publication:Egypt
[La] Language:eng
[Ab] Abstract:Appropriate surgical strategies for management of intraductal papillary mucinous neoplasms (IPMNs) of the pancreas are a matter of debate. Preoperative and intraoperative evaluation of malignant potential of IPMN and of patient's comorbidities is of paramount importance to balance potential complications of surgery with tumors' risk of being or becoming malignant; the decision about the extent of pancreatic resection and the eventual total pancreatectomy needs to be determined on individual basis. The analysis of frozen-section margin of pancreas during operation is mandatory. The goal should be the complete resection of IPMN reaching negative margin, although there is still no agreed definition of "negative margin." Of note, the presence of deepithelization is often wrongly interpreted as absence of neoplasia. Management of resection margin status and stratification of surveillance of the remnant pancreas, based on characteristics of primary tumour, are of crucial importance in the management of IPMNs in order to decrease the risk of tumor recurrence after resection. Although risk of local and distant recurrence for invasive IPMNs is increased even in case of total pancreatectomy, also local recurrence after complete resection of noninvasive IPMNs is not negligible. Therefore, a long-term/life-time follow-up monitoring is of paramount importance to detect eventual recurrences.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1410
[Cu] Class update date: 141004
[Lr] Last revision date:141004
[Da] Date of entry for processing:141003
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1155/2014/269803

  3 / 1913615 MEDLINE  
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[PMID]: 25276167
[Au] Autor:Kornasiewicz O; Debski M; Grat M; Lenartowicz B; Stepnowska M; Szalas A; Bar-Andziak E; Krawczyk M
[Ad] Address:Department of General, Transplant and Liver Surgery, Medical University of Warsaw, Poland....
[Ti] Title:Enzymatic activity of type 1 iodothyronine deiodinase in selected liver tumors.
[So] Source:Arch Med Sci;10(4):801-5, 2014 Aug 29.
[Is] ISSN:1734-1922
[Cp] Country of publication:Poland
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Type 1 iodothyronine deiodinase (D1) converts thyroxin (T4) into tri-iodothyronine (T3). Strong evidence indicates that thyroid hormone metabolism is disturbed in neoplasms such as thyroid and breast cancer. However, there is limited data concerning the function of the D1 enzyme in liver tumors. We aimed to estimate the enzymatic activity of D1 in two different common liver tumors. MATERIAL AND METHODS: We obtained 20 tumor samples from patients who had undergone a liver resection. Of the tissue samples, there were 13 benign lesions of focal nodular hyperplasia (FNH) and 7 malignant lesions of hepatocellular carcinomas (HCC). The D1 activity was assessed by measuring the amount of radioactive iodine released in reaction to D1-catalysed deiodination. Groups were compared by the Mann-Whitney non-parametrical test for independent trials, and the Kruskal Wallis test. RESULTS: The enzymatic activity of D1 was not significantly altered in the FNH group (median = 536 fmol/mg of protein/min; p = 0.972) and HCC group (367 fmol/mg; p = 0.128) when compared to matched normal liver parenchyma controls (546 fmol/mg and 556 fmol/mg, respectively). CONCLUSIONS: Liver parenchyma expresses high levels of D1. The results clearly revealed that D1 activity was not significantly different between benign and malignant tumors (FNH and HCC) compared to healthy liver parenchyma cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Cu] Class update date: 141004
[Lr] Last revision date:141004
[Da] Date of entry for processing:141003
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.5114/aoms.2013.34323

  4 / 1913615 MEDLINE  
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[PMID]: 24987060
[Au] Autor:Ezponda T; Licht JD
[Ad] Address:Division of Hematology/Oncology, Robert H. Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
[Ti] Title:Molecular pathways: deregulation of histone h3 lysine 27 methylation in cancer-different paths, same destination.
[So] Source:Clin Cancer Res;20(19):5001-8, 2014 Oct 1.
[Is] ISSN:1078-0432
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Methylation of lysine 27 on histone H3 (H3K27me), a modification associated with gene repression, plays a critical role in regulating the expression of genes that determine the balance between cell differentiation and proliferation. Alteration of the level of this histone modification has emerged as a recurrent theme in many types of cancer, demonstrating that either excess or lack of H3K27 methylation can have oncogenic effects. Cancer genome sequencing has revealed the genetic basis of H3K27me deregulation, including mutations of the components of the H3K27 methyltransferase complex PRC2 and accessory proteins, and deletions and inactivating mutations of the H3K27 demethylase UTX in a wide variety of neoplasms. More recently, mutations of lysine 27 on histone H3 itself were shown to prevent H3K27me in pediatric glioblastomas. Aberrant expression or mutations in proteins that recognize H3K27me3 also occur in cancer and may result in misinterpretation of this mark. In addition, due to the cross-talk between different epigenetic modifications, alterations of chromatin modifiers controlling H3K36me, or even mutations of this residue, can ultimately regulate H3K27me levels and distribution across the genome. The significance of mutations altering H3K27me is underscored by the fact that many tumors harboring such lesions often have a poor clinical outcome. New therapeutic approaches targeting aberrant H3K27 methylation include small molecules that block the action of mutant EZH2 in germinal center-derived lymphoma. Understanding the biologic consequences and gene expression pathways affected by aberrant H3K27 methylation may also lead to other new therapeutic strategies. Clin Cancer Res; 20(19); 5001-8. ©2014 AACR.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1410
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1158/1078-0432.CCR-13-2499

  5 / 1913615 MEDLINE  
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[PMID]: 25062259
[Au] Autor:Morrison AO; Gardner JM; Goldsmith SM; Parker DC
[Ad] Address:Departments of *Pathology and Laboratory Medicine, and †Dermatology, Emory University, Atlanta, GA; and ‡Department of Pathology, University of Arkansas for Medical Sciences, Little Rock, AR.
[Ti] Title:Primary cutaneous adenoid cystic carcinoma of the scalp with p16 expression: a case report and review of the literature.
[So] Source:Am J Dermatopathol;36(9):e163-6, 2014 Sep.
[Is] ISSN:1533-0311
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Adenoid cystic carcinoma (ACC) is a rare carcinoma that typically arises in salivary glands but can also occur in other sites including skin. Primary salivary ACC is a locally aggressive tumor characterized by local recurrence and late metastasis. Primary cutaneous ACC is found predominately on the scalp and is more indolent than salivary ACC; and, despite a high incidence of local recurrence, metastases are exceedingly rare. METHODS: A 62-year-old white male presented with a 6-mm mobile, blue-tinted nodule on the left mid scalp unchanged for several years. RESULTS: The histopathological findings of an excisional biopsy were diagnostic for a primary cutaneous ACC. Immunohistochemistry demonstrated focal positivity for p16. CONCLUSIONS: Primary cutaneous ACC is a rare malignancy that should be considered in the differential diagnosis of adnexal neoplasms and, when occurring on the head and neck, must be distinguished from cutaneous involvement by salivary ACC. The majority of reported salivary ACC with p16 protein expression were not positive for high-risk human papilloma virus by in situ hybridization. Immunostaining for p16 has previously been reported in salivary gland ACC. This is the first report in the English literature of p16 immunoexpression in primary cutaneous ACC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1097/DAD.0000000000000094

  6 / 1913615 MEDLINE  
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[PMID]: 25148182
[Au] Autor:Feng ST; Luo Y; Chan T; Peng Z; Chen J; Chen M; Li ZP
[Ad] Address:1 Department of Radiology, The First Affiliated Hospital, Sun Yat-Sen University, 58th, The Second Zhongshan Rd, Guangzhou, Guangdong 510080, China.
[Ti] Title:CT evaluation of gastroenteric neuroendocrine tumors: relationship between ct features and the pathologic classification.
[So] Source:AJR Am J Roentgenol;203(3):W260-6, 2014 Sep.
[Is] ISSN:1546-3141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: The objective of our study was to compare the CT features of gastroenteric neuroendocrine neoplasms (GE-NENs) with the pathologic classification and to analyze the correlation between the CT features and classification of GE-NENs. MATERIALS AND METHODS: Fifty-six cases of pathologically and immunohisto-chemically proven GE-NENs, including 25 cases of neuroendocrine tumors (NETs) (i.e., G1 and G2 tumors) and 31 cases of neuroendocrine carcinomas (NECs) (i.e., G3 tumors and mixed adenoneuroendocrine carcinomas) were studied. We analyzed various CT features of the primary tumor, nodal status, and metastasis and compared these features with pathologic grading. RESULTS: The CT features that favor NEC over NET include larger tumor size (> 4.0 cm), transmural invasion, circumscribed tumor with both intra- and extraluminal involvement, circumferential growth, areas of cystic change or necrosis, ulceration, mesenteric fat infiltration, and lymphadenopathy, with p values of 0.044, 0.002, 0.024, 0.008, 0.002, 0.007, 0.002, and < 0.001, respectively. The CT features that do not distinguish between the two types of GE-NENs include tumor boundary, growth pattern, degree of enhancement, adjacent organ invasion, distant organ metastasis, and peritoneal seeding, with p values of 0.277, 0.153, 0.672, 1.000, 0.159, and 0.877, respectively. CONCLUSION: CT can be useful in the classification of GE-NENs.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1408
[Js] Journal subset:AIM; IM
[St] Status:In-Process
[do] DOI:10.2214/AJR.13.11310

  7 / 1913615 MEDLINE  
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[PMID]: 24937779
[Au] Autor:Demaria S; Pilones KA; Vanpouille-Box C; Golden EB; Formenti SC
[Ad] Address:a Department of Pathology, New York University School of Medicine, and NYU Cancer Institute, New York, New York 10016.
[Ti] Title:The optimal partnership of radiation and immunotherapy: from preclinical studies to clinical translation.
[So] Source:Radiat Res;182(2):170-81, 2014 Aug.
[Is] ISSN:1938-5404
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The main role of the immune system is to restore tissue homeostasis when altered by pathogenic processes, including neoplastic transformation. Immune-mediated tumor rejection has been recognized as an extrinsic tumor suppressor mechanism that tumors need to overcome to progress. By the time a tumor becomes clinically apparent it has successfully escaped immune control by establishing an immunosuppressive microenvironment. Ionizing radiation applied locally to a tumor alters these tumor-host interactions. Accumulating evidence indicates that standard therapeutic doses of radiation have the potential to recover tumor immunogenicity and convert the tumor into an in situ personalized vaccine. Radiotherapy induces an immunogenic tumor cell death promoting cross-presentation of tumor-derived antigens by dendritic cells to T cells. In addition, radiotherapy stimulates chemokine-mediated recruitment of effector T cells to the tumor, and cellular recognition and killing by T cells that is facilitated by upregulation of major histocompatibility antigens, NKG2D ligands, adhesion molecules and death receptors. Despite these effects, radiotherapy alone is only rarely capable of generating enough proinflammatory signals to sufficiently overcome suppression, as it can also activate immunosuppressive factors. However, our group and others have shown that when combined with targeted immunotherapy agents radiotherapy significantly contributes to a therapeutically effective anti-tumor immune response. To illustrate this partnership between radiation and immunotherapy we will discuss as an example our experience in preclinical models and the molecular mechanisms identified. Additionally, the clinical translation of these combinations will be discussed.
[Mh] MeSH terms primary: Immunotherapy/methods
Neoplasms/immunology
Neoplasms/radiotherapy
Radiotherapy/methods
Translational Medical Research/methods
[Mh] MeSH terms secundary: Animals
Combined Modality Therapy
Humans
Neoplasms/metabolism
Neoplasms/pathology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; REVIEW
[Em] Entry month:1409
[Cu] Class update date: 141004
[Lr] Last revision date:141004
[Js] Journal subset:IM; S
[Da] Date of entry for processing:140809
[St] Status:MEDLINE
[do] DOI:10.1667/RR13500.1

  8 / 1913615 MEDLINE  
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[PMID]: 25029318
[Au] Autor:Anderson RR; Kulesz-Martin MF
[Ad] Address:Harvard Medical School Department of Dermatology, Massachusetts Institute of Technology and Wellman Center for Photomedicine, Boston, Massachusetts, USA.
[Ti] Title:Montagna symposium 2013-light and skin: how light sustains, damages, treats, images and modifies skin biology.
[So] Source:J Invest Dermatol;134(8):2064-7, 2014 Aug.
[Is] ISSN:1523-1747
[Cp] Country of publication:United States
[La] Language:eng
[Mh] MeSH terms primary: Light/adverse effects
Skin/radiation effects
[Mh] MeSH terms secundary: DNA Damage
Humans
Skin Aging
Skin Neoplasms/etiology
Sunlight/adverse effects
Toll-Like Receptor 3/physiology
Ultraviolet Rays/adverse effects
[Pt] Publication type:CONGRESSES; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (Toll-Like Receptor 3)
[Em] Entry month:1409
[Cu] Class update date: 141004
[Lr] Last revision date:141004
[Js] Journal subset:IM
[Da] Date of entry for processing:140717
[St] Status:MEDLINE
[do] DOI:10.1038/jid.2014.99

  9 / 1913615 MEDLINE  
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[PMID]: 24754623
[Au] Autor:Howard BV; Metzger JS; Koller KR; Jolly SE; Asay ED; Wang H; Wolfe AW; Hopkins SE; Kaufmann C; Raymer TW; Trimble B; Provost EM; Ebbesson SO; Austin MA; Howard WJ; Umans JG; Boyer BB
[Ad] Address:Barbara V. Howard, Hong Wang, and Jason G. Umans are with the MedStar Health Research Institute, Hyattsville, MD. Jesse S. Metzger is with the University of Alaska, Anchorage. Kathryn R. Koller, Elvin D. Asay, Abbie W. Wolfe, and Ellen M. Provost are with the Alaska Native Tribal Health Consortium Division of Community Health Services, Anchorage. Stacey E. Jolly is with the Cleveland Clinic Medicine Institute, Cleveland, OH. Scarlett E. Hopkins, Cristiane Kaufmann, and Bert B. Boyer are with the University of Alaska Fairbanks Center for Alaska Native Health Research. Terry W. Raymer and Brian Trimble are with the Alaska Native Medical Center, Anchorage. Sven O. E. Ebbesson is with the Norton Sound Health Corporation, Nome, AK. Melissa A. Austin is with the Department of Epidemiology, University of Washington, Seattle. William James Howard is with the MedStar Washington Hospital Center, Washington, DC.
[Ti] Title:All-cause, cardiovascular, and cancer mortality in western Alaska Native people: western Alaska Tribal Collaborative for Health (WATCH).
[So] Source:Am J Public Health;104(7):1334-40, 2014 Jul.
[Is] ISSN:1541-0048
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVES: We determined all-cause, cardiovascular disease (CVD), and cancer mortality in western Alaska Native people and examined agreement between death certificate information and adjudicated cause of deaths. METHODS: Data from 4 cohort studies were consolidated. Death certificates and medical records were reviewed and adjudicated according to standard criteria. We compared adjudicated CVD and cancer deaths with death certificates by calculating sensitivity, specificity, predictive values, and κ statistics. RESULTS: Men (n = 2116) and women (n = 2453), aged 18 to 95 years, were followed an average of 6.7 years. The major cause of death in men was trauma (25%), followed by CVD (19%) and cancer (13%). The major cause of death in women was CVD (24%), followed by cancer (19%) and trauma (8%). Stroke rates in both genders were higher than those of US Whites. Only 56% of deaths classified as CVD by death certificate were classified as CVD by standard criteria; discordance was higher among men (55%) than women (32%; κs = 0.4 and 0.7). CONCLUSIONS: We found lower rates for coronary heart disease death but high rates of stroke mortality. Death certificates overestimated CVD mortality; concordance between the 2 methods is better for cancer mortality. The results point to the importance of cohort studies in this population in providing data to assist in health care planning.
[Mh] MeSH terms primary: Cardiovascular Diseases/ethnology
Cardiovascular Diseases/mortality
Mortality/ethnology
Neoplasms/ethnology
Neoplasms/mortality
[Mh] MeSH terms secundary: Adolescent
Adult
Aged
Aged, 80 and over
Alaska/epidemiology
Cause of Death
Female
Health Surveys
Humans
Male
Middle Aged
Young Adult
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1407
[Cu] Class update date: 141004
[Lr] Last revision date:141004
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:140612
[St] Status:MEDLINE
[do] DOI:10.2105/AJPH.2013.301614

  10 / 1913615 MEDLINE  
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[PMID]: 24457247
[Au] Autor:Rajan A; Kotlyar D; Giaccone G
[Ad] Address:Medical Oncology Branch, National Cancer Institute/National Institutes of Health, Bethesda, Maryland.
[Ti] Title:Acute autoimmune hepatitis, myositis, and myasthenic crisis in a patient with thymoma.
[So] Source:J Thorac Oncol;8(10):e87-8, 2013 Oct.
[Is] ISSN:1556-1380
[Cp] Country of publication:United States
[La] Language:eng
[Mh] MeSH terms primary: Hepatitis, Autoimmune/etiology
Myasthenia Gravis/etiology
Myositis/etiology
Thymoma/complications
Thymus Neoplasms/complications
[Mh] MeSH terms secundary: Acute Disease
Adult
Antineoplastic Combined Chemotherapy Protocols/therapeutic use
Hepatitis, Autoimmune/diagnosis
Hepatitis, Autoimmune/drug therapy
Humans
Male
Myasthenia Gravis/diagnosis
Myasthenia Gravis/drug therapy
Myositis/diagnosis
Myositis/drug therapy
Prognosis
Thymoma/diagnosis
Thymoma/drug therapy
Thymus Neoplasms/diagnosis
Thymus Neoplasms/drug therapy
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Em] Entry month:1409
[Cu] Class update date: 141004
[Lr] Last revision date:141004
[Js] Journal subset:IM
[Da] Date of entry for processing:140124
[St] Status:MEDLINE
[do] DOI:10.1097/JTO.0b013e318298832b


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