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[PMID]: 25007146
[Au] Autor:Bishop JA; Antonescu CR; Westra WH
[Ad] Address:Departments of *Pathology †Otolaryngology/Head and Neck Surgery §Oncology, The Johns Hopkins Medical Institutions, Baltimore, MD ‡Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY.
[Ti] Title:SMARCB1 (INI-1)-deficient Carcinomas of the Sinonasal Tract.
[So] Source:Am J Surg Pathol;38(9):1282-9, 2014 Sep.
[Is] ISSN:1532-0979
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:SMARCB1 (INI-1) is a tumor-suppressor gene located on chromosome 22q11.2. Its gene product is ubiquitously expressed in nuclei of all normal tissues. SMARCB1 gene inactivation has been implicated in the pathogenesis of a diverse group of malignant neoplasms that tend to share "rhabdoid" cytomorphology. This group of SMARCB1-deficient tumors is now further expanded by a subset of carcinomas arising in the sinonasal tract. SMARCB1 immunostaining was performed on 142 sinonasal carcinomas. Tumors that showed loss of expression were further characterized for SMARCB1 deletions by fluorescence in situ hybridization. Nine of 142 (6%) primary sinonasal carcinomas showed loss of SMARCB1 expression by immunohistochemistry. Five patients were women, and patients ranged in age from 33 to 78 years (mean 59 y). The SMARCB1-deficient tumors were characterized by nests, sheets, and cords of cells without any histologic evidence of specific (eg, squamous or glandular) differentiation. The tumors comprised varying proportions of basaloid and rhabdoid cells. The SMARCB1-deficient carcinomas had been diagnosed as nonkeratinizing squamous cell carcinomas (n=3), sinonasal undifferentiated carcinomas (n=2), myoepithelial carcinoma (n=2), nonintestinal adenocarcinoma (n=1), and carcinoma, not otherwise specified (n=1). Fluorescence in situ hybridization analysis revealed SMARCB1 deletions in 6 of 8 (75%) carcinomas. The SMARCB1-deficient carcinomas did not harbor human papillomavirus or NUT-1 alterations. Six patients presented with T4 disease, 5 patients developed local recurrences and/or distant metastases, and 4 died of their disease. Inactivation of the SMARCB1 tumor-suppressor gene appears to be involved in the pathogenesis of a subset of sinonasal carcinomas, further expanding the family of SMARCB1-deficient neoplasms and further delineating a bewildering group of poorly/undifferentiated, aggressive carcinomas arising at this site. The ability to detect SMARCB1 loss by immunohistochemistry, particularly when dealing with poorly differentiated carcinomas with basaloid or rhabdoid features, should facilitate a more comprehensive understanding of these sinonasal carcinomas including clinical behavior and response to targeted therapies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/PAS.0000000000000285

  2 / 1900162 MEDLINE  
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[PMID]: 24832165
[Au] Autor:Agaimy A; Koch M; Lell M; Semrau S; Dudek W; Wachter DL; Knöll A; Iro H; Haller F; Hartmann A
[Ad] Address:*Institute of Pathology †Department of Otorhinolaryngology Head and Neck Surgery ‡Institute of Diagnostic and Interventional Radiology Departments of §Radiation Therapy ∥Thoracic Surgery ¶Institute of Virology, University Hospital of Erlangen, Erlangen, Germany.
[Ti] Title:SMARCB1(INI1)-deficient Sinonasal Basaloid Carcinoma: A Novel Member of the Expanding Family of SMARCB1-deficient Neoplasms.
[So] Source:Am J Surg Pathol;38(9):1274-81, 2014 Sep.
[Is] ISSN:1532-0979
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Poorly differentiated sinonasal carcinomas are a heterogenous group of aggressive neoplasms that encompasses squamous cell carcinoma including basaloid variant, lymphoepithelial carcinoma, sinonasal undifferentiated carcinoma, and neuroendocrine-type small cell carcinoma. We herein describe 3 cases of a hitherto unreported variant combining features of basaloid carcinoma with variable intermingled rhabdoid cells. Patients were 2 women (aged 28 and 35) and a man (52 y) who presented with sinonasal masses. All had advanced local disease with bone involvement (pT4). None had a history of irradiation or a family history of rhabdoid tumors. Treatment was surgery and adjuvant chemoradiation. One patient developed liver, lung, pleural, and pericardial metastases (63 mo) and is currently (70 mo) alive under palliative treatment. Another developed recurrent cervical lymph node metastases and died of disease 8.5 years later. The youngest patient was disease-free at last follow-up 7 years later. Histologic features were very similar in all 3 cases and showed intimate admixture of compact basaloid cell nests with peripheral palisading, perivascular pseudorosettes, and a few scattered rhabdoid cells. Rhabdoid cells were more extensive in the metastasis in 1 case but formed a minor inconspicuous component in the primary tumors in all cases. Striking features common to all cases were (1) basaloid "blue" appearance at low power, (2) papilloma-like exophytic component, (3) extensive pagetoid surface growth with prominent denuding features, and (4) replacement of underlying mucous glands mimicking an inverted papilloma. Clear-cut origin from benign papilloma and overt squamous differentiation were lacking. Diffuse (2) or partial (1) p16 expression was noted, but all cases lacked human papillomavirus DNA by molecular tests. In situ hybridization was negative for Epstein-Barr virus. Immunohistochemistry showed diffuse expression of pancytokeratin. CK5 and vimentin showed intermingling of CK5/vimentin basaloid and CK5/vimentin rhabdoid cells. Complete loss of nuclear SMARCB1 expression was seen in all cases including also the denuding carcinoma in situ-like surface lesions. To our knowledge, this variant of sinonasal carcinoma has not been reported before. The identical features in all 3 cases suggest a specific disease rather than a nonspecific dedifferentiated phenotype. Awareness of this rare variant and thus reporting of additional cases is necessary for defining its full morphologic and biological spectrum.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/PAS.0000000000000236

  3 / 1900162 MEDLINE  
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[PMID]: 24705316
[Au] Autor:Carter JM; Sukov WR; Montgomery E; Goldblum JR; Billings SD; Fritchie KJ; Folpe AL
[Ad] Address:*Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN †Department of Pathology, The Johns Hopkins Hospital, Baltimore, MD ‡Department of Anatomic Pathology, Cleveland Clinic, Cleveland, OH.
[Ti] Title:TGFBR3 and MGEA5 Rearrangements in Pleomorphic Hyalinizing Angiectatic Tumors and the Spectrum of Related Neoplasms.
[So] Source:Am J Surg Pathol;38(9):1182-992, 2014 Sep.
[Is] ISSN:1532-0979
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pleomorphic hyalinizing angiectatic tumor (PHAT) is a rare, locally aggressive tumor of the distal extremities with a proclivity for local recurrence. PHATs contain characteristic ectatic, thin-walled vessels, lined by fibrin, and are surrounded by groups of variably pleomorphic spindled to epithelioid neoplastic cells. The putative precursor lesion of PHAT, originally termed "early PHAT" shares many clinicopathologic features with hemosiderotic fibrolipomatous tumor (HFLT). HFLT, myxoinflammatory fibroblastic sarcoma (MIFS), and tumors showing hybrid features of HFLT and MIFS often show TGFBR3 and MGEA5 gene rearrangements. To date, only a small number of PHATs has been tested for either rearrangement; all have been negative. We hypothesized that PHATs contain TGFBR3 and/or MGEA5 rearrangements. Cases of PHAT (all containing areas of HFLT) (N=10), HFLT (N=7), MIFS (N=6), hybrid HFLT/MIFS (N=3), and PHAT-like undifferentiated pleomorphic sarcomas (N=7) were retrieved from our institutional and consultation archives and analyzed for TGFBR3 and MGEA5 rearrangements using a break-apart probe strategy for FISH. Six of 10 PHATs harbored TGFBR3 and/or MGEA5 gene rearrangements: 4 cases had both TGFBR3 and MGEA5 rearrangements, and 2 cases contained MGEA5 rearrangements. Two of 7 HFLTs were positive: 1 case had a TGFBR3 rearrangement, and 1 case had an MGEA5 rearrangement. One of 6 MIFSs had an MGEA5 rearrangement. All 3 hybrid HFLT/MIFS cases were positive: 2 cases had both TGFBR3 and MGEA5 rearrangements, and 1 case had a TGFBR3 rearrangement. All PHAT-like undifferentiated pleomorphic sarcomas were negative. We report, for the first time, the presence of TGFBR3 and/or MGEA5 rearrangements in tumors showing mixed features of HFLT and PHAT. The presence of such rearrangements strongly suggests that HFLT is related to both PHAT and MIFS and that the latter 2 tumors may represent morphologic variants of a single, genetically defined entity in which only MIFS has acquired the capacity to metastasize.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/PAS.0000000000000212

  4 / 1900162 MEDLINE  
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[PMID]: 25030833
[Au] Autor:Zhang L; Liao Q; Hu Y; Zhao Y
[Ti] Title:Paraganglioma of the pancreas: a potentially functional and malignant tumor.
[So] Source:World J Surg Oncol;12(1):218, 2014.
[Is] ISSN:1477-7819
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Paragangliomas are neoplasms that arise from extra-adrenal chromaffin cells. Pancreatic paragangliomas are rare, and few are malignant. To the best of our knowledge, no cases of functional pancreatic paragangliomas have been reported in the literature to date. We present two cases of pancreatic paragangliomas with pathological confirmation. In the case 1, clinical testing and pathological analysis revealed functional and malignant characteristics of the tumor, which carried a poor prognosis. In case 2, functional paraganglioma was suspected. The clinical presentations and outcomes of these two patients are summarized, and the relevant literature is reviewed. Because of the small number of cases reported previously, few characteristics of these tumors are known. The best methods of predicting the malignant and functional potential of these tumors remain unknown. We propose careful preoperative treatment and close postoperative follow-up of paraganglioma patients because of the functional and malignant potential of these tumors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1186/1477-7819-12-218

  5 / 1900162 MEDLINE  
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[PMID]: 24816032
[Au] Autor:Cottingham MD; Kalbaugh CA; Fisher JA
[Ad] Address:Department of Social Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
[Ti] Title:Tracking the pharmaceutical pipeline: clinical trials and global disease burden.
[So] Source:Clin Transl Sci;7(4):297-9, 2014 Aug.
[Is] ISSN:1752-8062
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Aggregate data about pharmaceutical research and development (R&D) tend to examine Phase III trials. Hence, there are few published data about investigational drugs in earlier phases of clinical development that might fail. It is also unclear how well R&D corresponds to disease burden. We track the pharmaceutical pipeline using data from industry publications that provide otherwise unreported information about industry-sponsored clinical trials. The sample includes 2,477 unique drug entities in 4,182 clinical trials. The majority of drugs targeted neoplasms (26.20%), neurological diseases/diseases of the sense organs (13.48%), infectious and parasitic diseases (10.5%), and endocrine, metabolic, nutrition, and immunity disorders (9.45%). Less than 6% of drugs targeted diseases of the circulatory system, which represent the most prevalent causes of global mortality. Detailing the pharmaceutical pipeline, our findings suggest that pharmaceutical development does not adequately address global disease burden. Future research on the under-reported details of Phase I and II clinical trials is needed to understand how the industry operates and how its resource-allocation matches global health concerns.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/cts.12163

  6 / 1900162 MEDLINE  
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[PMID]: 25114854
[Au] Autor:Mustonen MV; Pyrhönen S; Kellokumpu-Lehtinen PL
[Ad] Address:Mika VJ Mustonen, Orion Corporation, Orion Pharma, FIN-02101, Espoo, Finland.
[Ti] Title:Toremifene in the treatment of breast cancer.
[So] Source:World J Clin Oncol;5(3):393-405, 2014 Aug 10.
[Is] ISSN:2218-4333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Although more widespread screening and routine adjuvant therapy has improved the outcome for breast cancer patients in recent years, there remains considerable scope for improving the efficacy, safety and tolerability of adjuvant therapy in the early stage disease and the treatment of advanced disease. Toremifene is a selective estrogen receptor modifier (SERM) that has been widely used for decades in hormone receptor positive breast cancer both in early and late stage disease. Its efficacy has been well established in nine prospective randomized phase III trials compared to tamoxifen involving more than 5500 patients, as well as in several large uncontrolled and non-randomized studies. Although most studies show therapeutic equivalence between the two SERMs, some show an advantage for toremifene. Several meta-analyses have also confirmed that the efficacy of toremifene is at least as good as that of tamoxifen. In terms of safety and tolerability toremifene is broadly similar to tamoxifen although there is some evidence that toremifene is less likely to cause uterine neoplasms, serious vascular events and it has a more positive effect on serum lipids than does tamoxifen. Toremifene is therefore effective and safe in the treatment of breast cancer. It provides not only a useful therapeutic alternative to tamoxifen, but may bring specific benefits.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1408
[Cu] Class update date: 140815
[Lr] Last revision date:140815
[Da] Date of entry for processing:140812
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.5306/wjco.v5.i3.393

  7 / 1900162 MEDLINE  
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[PMID]: 25114385
[Au] Autor:Mhuircheartaigh JN; Lin YC; Wu JS
[Ad] Address:Department of Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States.
[Ti] Title:Bone tumor mimickers: A pictorial essay.
[So] Source:Indian J Radiol Imaging;24(3):225-36, 2014 Jul.
[Is] ISSN:0971-3026
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:Focal lesions in bone are very common and many of these lesions are not bone tumors. These bone tumor mimickers can include numerous normal anatomic variants and non-neoplastic processes. Many of these tumor mimickers can be left alone, while others can be due to a significant disease process. It is important for the radiologist and clinician to be aware of these bone tumor mimickers and understand the characteristic features which allow discrimination between them and true neoplasms in order to avoid unnecessary additional workup. Knowing which lesions to leave alone or which ones require workup can prevent misdiagnosis and reduce patient anxiety.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Cu] Class update date: 140815
[Lr] Last revision date:140815
[Da] Date of entry for processing:140812
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.4103/0971-3026.137026

  8 / 1900162 MEDLINE  
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[PMID]: 25049393
[Au] Autor:Kroczynska B; Mehrotra S; Majchrzak-Kita B; Arslan AD; Altman JK; Stein BL; McMahon B; Kozlowski P; Kahle PJ; Eklund EA; Fish EN; Platanias LC
[Ad] Address:Robert H. Lurie Comprehensive Cancer Center andDivision of Hematology/Oncology, Northwestern University Medical School, Chicago, IL 60611;...
[Ti] Title:Regulatory effects of SKAR in interferon α signaling and its role in the generation of type I IFN responses.
[So] Source:Proc Natl Acad Sci U S A;111(31):11377-82, 2014 Aug 5.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:We provide evidence that S6 kinase 1 (S6K1) Aly/REF-like target (SKAR) is engaged in IFN-α signaling and plays a key role in the generation of IFN responses. Our data demonstrate that IFN-α induces phosphorylation of SKAR, which is mediated by either the p90 ribosomal protein S6 kinase (RSK) or p70 S6 kinase (S6K1), in a cell type-specific manner. This type I IFN-inducible phosphorylation of SKAR results in enhanced interaction with the eukaryotic initiation factor (eIF)4G and recruitment of activated RSK1 to 5' cap mRNA. Our studies also establish that SKAR is present in cap-binding CBP80 immune complexes and that this interaction is mediated by eIF4G. We demonstrate that inducible protein expression of key IFN-α-regulated protein products such as ISG15 and p21(WAF1/CIP1) requires SKAR activity. Importantly, our studies define a requirement for SKAR in the generation of IFN-α-dependent inhibitory effects on malignant hematopoietic progenitors from patients with chronic myeloid leukemia or myeloproliferative neoplasms. Taken altogether, these findings establish critical and essential roles for SKAR in the regulation of mRNA translation of IFN-sensitive genes and induction of IFN-α biological responses.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1408
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1405250111

  9 / 1900162 MEDLINE  
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[PMID]: 24691445
[Au] Autor:Rielland M; Cantor DJ; Graveline R; Hajdu C; Mara L; Diaz Bde D; Miller G; David G
[Ti] Title:Senescence-associated SIN3B promotes inflammation and pancreatic cancer progression.
[So] Source:J Clin Invest;124(5):2125-35, 2014 May 1.
[Is] ISSN:1558-8238
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pancreatic ductal adenocarcinoma (PDAC) is strikingly resistant to conventional therapeutic approaches. We previously demonstrated that the histone deacetylase-associated protein SIN3B is essential for oncogene-induced senescence in cultured cells. Here, using a mouse model of pancreatic cancer, we have demonstrated that SIN3B is required for activated KRAS-induced senescence in vivo. Surprisingly, impaired senescence as the result of genetic inactivation of Sin3B was associated with delayed PDAC progression and correlated with an impaired inflammatory response. In murine and human pancreatic cells and tissues, levels of SIN3B correlated with KRAS-induced production of IL-1α. Furthermore, evaluation of human pancreatic tissue and cancer cells revealed that Sin3B was decreased in control and PDAC samples, compared with samples from patients with pancreatic inflammation. These results indicate that senescence-associated inflammation positively correlates with PDAC progression and suggest that SIN3B has potential as a therapeutic target for inhibiting inflammation-driven tumorigenesis.
[Mh] MeSH terms primary: Carcinoma, Pancreatic Ductal/metabolism
Pancreatic Neoplasms/metabolism
Repressor Proteins/metabolism
[Mh] MeSH terms secundary: Animals
Carcinoma, Pancreatic Ductal/genetics
Carcinoma, Pancreatic Ductal/pathology
Cell Aging/genetics
Cell Line, Tumor
Humans
Inflammation/genetics
Inflammation/metabolism
Inflammation/pathology
Interleukin-1alpha/genetics
Interleukin-1alpha/metabolism
Mice
Mice, Knockout
Pancreatic Neoplasms/genetics
Pancreatic Neoplasms/pathology
Proto-Oncogene Proteins/genetics
Proto-Oncogene Proteins/metabolism
Proto-Oncogene Proteins p21(ras)/genetics
Proto-Oncogene Proteins p21(ras)/metabolism
Repressor Proteins/genetics
ras Proteins/genetics
ras Proteins/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (IL1A protein, human); 0 (Interleukin-1alpha); 0 (KRAS protein, human); 0 (Proto-Oncogene Proteins); 0 (Repressor Proteins); 0 (SIN3B protein, human); 0 (Sin3b protein, mouse); EC 3.6.5.2 (Kras2 protein, mouse); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras)); EC 3.6.5.2 (ras Proteins)
[Em] Entry month:1406
[Cu] Class update date: 140815
[Lr] Last revision date:140815
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:140606
[St] Status:MEDLINE

  10 / 1900162 MEDLINE  
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[PMID]: 24847587
[Au] Autor:Misganaw A; Mariam DH; Ali A; Araya T
[Ti] Title:Epidemiology of major non-communicable diseases in Ethiopia: a systematic review.
[So] Source:J Health Popul Nutr;32(1):1-13, 2014 Mar.
[Is] ISSN:1606-0997
[Cp] Country of publication:Bangladesh
[La] Language:eng
[Ab] Abstract:Impact of non-communicable diseases is not well-documented in Ethiopia. We aimed to document the prevalence and mortality associated with four major non-communicable diseases in Ethiopia: cardiovascular disease, cancer, diabetes, and chronic obstructive pulmonary disease. Associated risk factors: hypertension, tobacco-use, harmful use of alcohol, overweight/obesity, and khat-chewing were also studied. Systematic review of peer-reviewed and grey literature between 1960 and 2011 was done using PubMed search engines and local libraries to identify prevalence studies on the four diseases. In total, 32 studies were found, and half of these studies were from Addis Ababa. Two hospital-based studies reviewed the prevalence of cardiovascular disease and found a prevalence of 7.2% and 24%; a hospital-based study reviewed cancer prevalence and found a prevalence of 0.3%; two hospital-based studies reviewed diabetes prevalence and found a prevalence of 0.5% and 1.2%; and two hospital-based studies reviewed prevalence of asthma and found a prevalence of 1% and 3.5%. Few community-based studies were done on the prevalence of diabetes and chronic pulmonary obstructive disease among the population. Several studies reviewed the impact of these diseases on mortality: cardiovascular disease accounts for 24% of deaths in Addis Ababa, cancer causes 10% of deaths in the urban settings and 2% deaths in rural setting, and diabetes causes 5% and chronic obstructive pulmonary disease causes 3% of deaths. Several studies reviewed the impact of these diseases on hospital admissions: cardiovascular disease accounts for 3%-12.6% and found to have increased between 1970s and 2000s; cancer accounts for 1.1%-2.8%, diabetes accounts for 0.5%-1.2%, and chronic obstructive diseases account for 2.7%-4.3% of morbidity. Overall, the major non-communicable diseases and related risk factors are highly prevalent, and evidence-based interventions should be designed.
[Mh] MeSH terms primary: Cardiovascular Diseases/epidemiology
Diabetes Mellitus/epidemiology
Neoplasms/epidemiology
Pulmonary Disease, Chronic Obstructive/epidemiology
[Mh] MeSH terms secundary: Alcoholism/epidemiology
Causality
Comorbidity
Ethiopia/epidemiology
Humans
Hypertension/epidemiology
Overweight/epidemiology
Prevalence
Risk Factors
Tobacco Use/epidemiology
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1406
[Cu] Class update date: 140815
[Lr] Last revision date:140815
[Js] Journal subset:IM
[Da] Date of entry for processing:140522
[St] Status:MEDLINE


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