Database : MEDLINE
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[PMID]: 29521101
[Au] Autor:Wyzewski Z; Gregorczyk KP; Szczepanowska J; Szulc-Dabrowska L
[Ti] Title:Functional role of Hsp60 as a positive regulator of human viral infection progression.
[So] Source:Acta Virol;62(1):33-40, 2018.
[Is] ISSN:0001-723X
[Cp] Country of publication:Slovakia
[La] Language:eng
[Ab] Abstract:Heat shock proteins (Hsps) are a family of proteins highly conserved in evolution. Members of the Hsp family are mainly responsible for proper protein folding, however they perform many other functions in living organisms. Hsp60 is a molecular chaperone that is present in mitochondria and cytosol of eukaryotic cells, as well as on their surface. It is also found in the extracellular space and in the peripheral blood. Apart from its role in assisting protein folding in cooperation with Hsp10, Hsp60 contributes to regulation of apoptosis, as well as participates in modulation of the immune system activity. Hsp60 may favor oncogenesis by promoting survival or growth of some tumor cell types. Hsp60 is a subject of medical research due to its role in pathogenesis of certain tumors and infectious diseases. In this review we discuss mechanisms by which Hsp60 promotes development and progression of infections caused by three human viruses: hepatitis B virus (HBV), human immunodeficiency virus (HIV) and influenza A virus.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.4149/av_2018_104

  2 / 37222 MEDLINE  
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[PMID]: 29181576
[Au] Autor:Araújo R; Santos JMO; Fernandes M; Dias F; Sousa H; Ribeiro J; Bastos MMSM; Oliveira PA; Carmo D; Casaca F; Silva S; Medeiros R; Gil da Costa RM
[Ad] Address:Molecular Oncology and Viral Pathology Group, IPO Porto Research Center (CI-IPOP), Portuguese Oncology Institute of Porto (IPO Porto), Rua Dr. António Bernardino de Almeida, 4200-072, Porto, Portugal.
[Ti] Title:Expression profile of microRNA-146a along HPV-induced multistep carcinogenesis: a study in HPV16 transgenic mice.
[So] Source:J Cancer Res Clin Oncol;144(2):241-248, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:PURPOSE: Persistent human papillomavirus (HPV) infection is associated with the development of certain types of cancer and the dysregulation of microRNAs has been implicated in HPV-associated carcinogenesis. This is the case of microRNA-146a (miR-146a), which is thought to regulate tumor-associated inflammation. We sought to investigate the expression levels of miR-146a during HPV16-mediated carcinogenesis using skin samples from K14-HPV16 transgenic mice which develop the consecutive phases of the carcinogenesis process. METHODS: Female transgenic (HPV ) and wild-type (HPV ) mice were sacrificed at 24-26 weeks-old or 28-30 weeks-old. Chest and ear skin samples from HPV and HPV mice were histologically classified and used for microRNA extraction and quantification by qPCR. RESULTS: Chest skin samples from 24 to 26 weeks-old HPV mice presented diffuse epidermal hyperplasia and only 22.5% showed multifocal dysplasia, while at 28-30 weeks-old all (100.0%) HPV animals showed epidermal dysplasia. All HPV ear skin samples showed carcinoma in situ (CIS). MiR-146a expression levels were higher in HPV compared to HPV mice (p = 0.006). There was also an increase in miR-146a expression in dysplastic skin lesions compared with hyperplasic lesions (p = 0.011). Samples showing CIS had a significant decrease in miR-146a expression when compared to samples showing epidermal hyperplasia (p = 0.018) and epidermal dysplasia (p = 0.009). CONCLUSIONS: These results suggest that HPV16 induces the overexpression of miR-146a in the initial stages of carcinogenesis (hyperplasia and dysplasia), whereas decreases its expression at later stages (CIS). Taken together, these data implicate and suggest different roles of miR-146a in HPV-mediated carcinogenesis.
[Mh] MeSH terms primary: Carcinogenesis/genetics
Human papillomavirus 16/genetics
MicroRNAs/biosynthesis
[Mh] MeSH terms secundary: Animals
Carcinogenesis/metabolism
Carcinogenesis/pathology
Female
Hyperplasia/virology
Mice
Mice, Transgenic
MicroRNAs/genetics
Papillomavirus Infections/genetics
Papillomavirus Infections/metabolism
Papillomavirus Infections/virology
Skin/pathology
Skin/virology
Skin Neoplasms/genetics
Skin Neoplasms/metabolism
Skin Neoplasms/pathology
Skin Neoplasms/virology
Transcriptome
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (MicroRNAs); 0 (Mirn146 microRNA, mouse)
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:171129
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2549-5

  3 / 37222 MEDLINE  
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[PMID]: 29157613
[Au] Autor:Fajgenbaum DC; Shilling D
[Ad] Address:Division of Translational Medicine and Human Genetics, Hospital of the University of Pennsylvania, 3400 Spruce Street, Silverstein 5, Suite S05094, Philadelphia, PA 19104, USA. Electronic address: davidfa@pennmedicine.upenn.edu.
[Ti] Title:Castleman Disease Pathogenesis.
[So] Source:Hematol Oncol Clin North Am;32(1):11-21, 2018 02.
[Is] ISSN:1558-1977
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Castleman disease (CD) describes a group of heterogeneous disorders with common lymph node histopathologic features, including atrophic or hyperplastic germinal centers, prominent follicular dendritic cells, hypervascularization, polyclonal lymphoproliferation, and/or polytypic plasmacytosis. The cause and pathogenesis of the four subtypes of CD (unicentric CD; human herpesvirus-8-associated multicentric CD; polyradiculoneuropathy, organomegaly, endocrinopathy, monoclonal plasma cell disorder, and skin changes [POEMS]-associated multicentric CD; and idiopathic multicentric CD) vary considerably. This article provides a summary of our current understanding of the cause, cell types, signaling pathways, and effector cytokines implicated in the pathogenesis of each subtype.
[Mh] MeSH terms primary: Castleman Disease
Cytokines/blood
Herpesviridae Infections
Herpesvirus 8, Human/metabolism
Lymph Nodes
Neoplasm Proteins/blood
Signal Transduction
[Mh] MeSH terms secundary: Castleman Disease/blood
Castleman Disease/physiopathology
Castleman Disease/virology
Herpesviridae Infections/blood
Herpesviridae Infections/physiopathology
Humans
Lymph Nodes/metabolism
Lymph Nodes/physiopathology
Lymph Nodes/virology
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Cytokines); 0 (Neoplasm Proteins)
[Em] Entry month:1801
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[Js] Journal subset:IM
[Da] Date of entry for processing:171122
[St] Status:MEDLINE

  4 / 37222 MEDLINE  
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[PMID]: 29157611
[Au] Autor:Simpson D
[Ad] Address:North Shore Hospital, Private Bag 93-503, Takapuna, Auckland 0740, New Zealand. Electronic address: david.simpson@waitematadhb.govt.nz.
[Ti] Title:Epidemiology of Castleman Disease.
[So] Source:Hematol Oncol Clin North Am;32(1):1-10, 2018 02.
[Is] ISSN:1558-1977
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Castleman disease is a rare entity, including unicentric Castleman disease (UCD), human herpesvirus-8 plus Castleman disease (HHV-8+MCD), and idiopathic multicentric Castleman disease (iMCD). UCD is the most common at 16 per million person years and occurs at every age. HHV-8+MCD incidence varies widely, mostly affecting human immunodeficiency virus-positive men. iMCD is likely a more heterogeneous disease with an estimated incidence of 5 per million person years. Improved definitions should improve understanding of the epidemiology of Castleman disease and its subtypes.
[Mh] MeSH terms primary: Castleman Disease/classification
Castleman Disease/epidemiology
[Mh] MeSH terms secundary: Female
HIV Seropositivity/complications
HIV Seropositivity/epidemiology
Herpesviridae Infections/classification
Herpesviridae Infections/epidemiology
Herpesvirus 8, Human
Humans
Incidence
Male
Sex Factors
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1801
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[Js] Journal subset:IM
[Da] Date of entry for processing:171122
[St] Status:MEDLINE

  5 / 37222 MEDLINE  
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[PMID]: 28453696
[Au] Autor:Böger C; Krüger S; Behrens HM; Bock S; Haag J; Kalthoff H; Röcken C
[Ad] Address:Department of Pathology, Christian-Albrechts-University, Kiel, Germany
[Ti] Title:Epstein-Barr virus-associated gastric cancer reveals intratumoral heterogeneity of PIK3CA mutations.
[So] Source:Ann Oncol;28(5):1005-1014, 2017 05 01.
[Is] ISSN:1569-8041
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background: Recent whole-genome sequencing identified four molecular subtypes of gastric cancer (GC), of which the subgroup of Epstein-Barr virus-associated GC (EBVaGC) showed a significant enrichment of PIK3CA mutations. We here aimed to validate independently the enrichment of PIK3CA mutations in EBVaGC of a Central European GC cohort, to correlate EBV status with clinico-pathological patient characteristics and to test for a major issue of GC, intratumoral heterogeneity. Patients and methods: In a first step, 484 GCs were screened for EBV and PIK3CA hot spot mutations of exon 9/20 using EBER in situ hybridization and pyrosequencing, respectively. Secondly, an extended sequencing of PIK3CA also utilizing next generation sequencing was carried out in all EBVaGCs and 96 corresponding lymph node metastases. Results: Twenty-two GCs were EBER-positive, all being of latency type I. Intratumoral heterogeneity of EBER-positivity was found in 18% of EBVaGCs. Twenty-three GCs held PIK3CA mutations in hot spot regions of exon 9 or 20, being significantly more common in EBVaGCs (P < 0.001). Subsequent extended sequencing of PIK3CA of EBVaGCs showed that 14% harvested three to five different PIK3CA genotypes (including wildtype) in the same primary tumor, albeit in histologically and spatially distinct tumor areas, and that intratumoral heterogeneity of PIK3CA was also present in the corresponding lymph node metastases. Conclusions: Our findings unravel issues of tumor heterogeneity and illustrate that the assessment of the EBV status in tissue biopsies might carry the risk of sampling errors, which may significantly hamper adequate molecular tumor classification in a more clinical setting. Moreover, this is the first report of intratumoral heterogeneity of PIK3CA mutations in GC, and our findings lead to the conclusion that PIK3CA mutant and -wildtype tumor subclones are skilled to metastasize independently to different regional lymph nodes.
[Mh] MeSH terms primary: Adenocarcinoma/genetics
Class I Phosphatidylinositol 3-Kinases/genetics
Epstein-Barr Virus Infections/genetics
Stomach Neoplasms/genetics
[Mh] MeSH terms secundary: Adenocarcinoma/mortality
Adenocarcinoma/secondary
Adenocarcinoma/virology
Aged
Epstein-Barr Virus Infections/mortality
Epstein-Barr Virus Infections/pathology
Epstein-Barr Virus Infections/virology
Female
Gene Frequency
Genetic Association Studies
Genetic Heterogeneity
Genetic Predisposition to Disease
High-Throughput Nucleotide Sequencing
Humans
Kaplan-Meier Estimate
Lymphatic Metastasis
Male
Molecular Diagnostic Techniques
Mutation
Stomach Neoplasms/mortality
Stomach Neoplasms/pathology
Stomach Neoplasms/virology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:EC 2.7.1.137 (Class I Phosphatidylinositol 3-Kinases); EC 2.7.1.137 (PIK3CA protein, human)
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:170429
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdx047

  6 / 37222 MEDLINE  
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[PMID]: 27771623
[Au] Autor:Suri D; Bhattad S; Gupta A; Trehan A; Bansal D; Rajwanshi A; Das A; Rawat A; Singh S
[Ad] Address:Pediatric Allergy and Immunology Unit, Advanced Pediatrics Centre, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
[Ti] Title:Malignancies in Children with Human Immunodeficiency Virus Infection - Our Experience at Chandigarh, North India.
[So] Source:J Trop Pediatr;63(3):210-216, 2017 06 01.
[Is] ISSN:1465-3664
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Background: With improved survival in children living with human immunodeficiency virus (HIV) infection (CLHIV), malignancies are being increasingly recognized. Patients and methods: Among the CLHIV registered at our institute from January 1994 to March 2015, children with malignancy were analysed in detail. Results: In total, 734 children affected by HIV were registered. Out of these, 11 children (9 boys, 2 girls) were diagnosed to have malignancy. Malignancy was the presenting feature of HIV infection in 4 children. High-grade non-Hodgkin lymphoma (NHL) was the most common malignancy noted in 9 of 11 (81%) children, whereas the remaining 2 children had Hodgkin's lymphoma. Survival in our cohort was 80% among children in whom chemotherapy was initiated, and overall survival was 36% (4 of 11 children). Conclusion: NHL was the most common malignancy in CLHIV in our cohort. Low-conditioning chemotherapy protocols along with initiation of anti-retroviral therapy resulted in improved outcomes in CLHIV with malignancy.
[Mh] MeSH terms primary: HIV Infections/complications
Neoplasms/complications
[Mh] MeSH terms secundary: Adolescent
Age Distribution
Child
Cohort Studies
Female
HIV Infections/diagnosis
HIV Infections/epidemiology
Humans
India
Lymphoma, AIDS-Related/diagnosis
Lymphoma, AIDS-Related/epidemiology
Lymphoma, AIDS-Related/pathology
Lymphoma, Non-Hodgkin
Male
Medical Records
Neoplasms/mortality
Risk Factors
Sex Distribution
Survival Rate
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:161025
[St] Status:MEDLINE
[do] DOI:10.1093/tropej/fmw074

  7 / 37222 MEDLINE  
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[PMID]: 29510685
[Au] Autor:Ramadori G; Bosio P; Moriconi F; Malik IA
[Ad] Address:Department of Gastroenterology and Endocrinology, University Medical Center Goettingen, Robert-Koch-Street 40, D-37075, Goettingen, Germany. gramado@med.uni-goettingen.de.
[Ti] Title:Case report: 8 years after liver transplantation: de novo hepatocellular carcinoma 8 months after HCV clearance through IFN-free antiviral therapy.
[So] Source:BMC Cancer;18(1):257, 2018 Mar 06.
[Is] ISSN:1471-2407
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: After orthotopic liver transplantation (OLT) for hepatocellular carcinoma (HCC), recurrent HCC mostly develops within 2 years. All cases of de novo HCC described so far occurred later than 2 years after OLT. Prevention of post-transplantation HCC has usually been tried to achieve by curing or controlling recurrent liver disease. This has been rationale for treatment with interferon (IFN)/ribavirin of HCV-recurrence in patients after OLT, transplanted for advanced HCV-induced liver disease and/or HCC. The availability of new and more efficient drugs has improved chances also for previously difficult-to-treat HCV-positive patients. CASE PRESENTATION: A 75 year-old male patient who had undergone OLT for decompensated HCV-cirrhosis in 2009, and bilio-digestive surgery in 2011 under tracrolimus (0.5 mg/day) and prednisone (5 mg/day) immunosuppressive therapy, started to receive antiviral treatment for recurrent HCV-infection of graft with 200 mg/day ribavirin in combination with ledipasvir and sofosbuvir by the end of October 2015. Because of multiple side effects (anemia, asthenia, infections, and reduction of kidney functions - palliated by treatment with erythropoietin), treatment was stopped after 16 weeks. At the third control, a minimal increase in alpha-fetoprotein (AFP) serum level to 10 µg/L was measured 8 months after therapy, whereas both liver sonography and serum transaminases were normal. The patient's general condition; however, remained poor, and a magnetic resonance imaging (MRI) of abdomen was performed 2 months later. A nodule of 3 cm in diameter with a pseudocapsule was found centrally in the liver. The patient had to be hospitalized for recurrent infections of the lung, overt ascites and peritonitis. Rapid tumor growth (10 cm) was detected during last stay in hospital (April 2017), concomitant with a rise of AFP-serum levels to 91 µg/L. The family decided to take the patient home, and best supportive care was provided by a general practitioner, local nurses and the patient's dedicated wife until his death. CONCLUSION: Before treating OLT patients with HCV graft reinfection one should not only consider possible advantages of newly effective antiviral-therapies, but also life expectancy and possible side effects (difficult to manage at an outpatient service basis), including severe disadvantages such as the development of HCC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1186/s12885-018-4175-2

  8 / 37222 MEDLINE  
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[PMID]: 29180487
[Au] Autor:Pierog PL; Zhao Y; Singh S; Dai J; Yap GS; Fitzgerald-Bocarsly P
[Ad] Address:Department of Pathology and Laboratory Medicine, Rutgers New Jersey Medical School, Newark, NJ 07103.
[Ti] Title: Inactivates Human Plasmacytoid Dendritic Cells by Functional Mimicry of IL-10.
[So] Source:J Immunol;200(1):186-195, 2018 01 01.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Plasmacytoid dendritic cells (pDCs) are the major producers of IFN-α, an antiviral cytokine involved in immunomodulation and control of HIV type 1 replication, whereas is a life-threatening opportunistic infection in AIDS patients. During infection with HIV type 1, human pDCs decrease in circulation and remaining pDC produce lower amounts of IFN-α in response to viral stimulation. In this study, we investigated the impact of coinfection with on the innate virus-directed responses of human pDCs. Using intracellular flow cytometry and fluorescence microscopy, we determined that invaded but did not induce IFN-α or TNF-α in human pDC. However, inhibited IFN-α and TNF-α produced in response to HSV and HIV, thus functionally inactivating pDC. IFN-α production was inhibited only in cells infected by , which inhibited neither uptake of GFP-HSV nor localization of TLR9 in CD71 endosomes, directing us to investigate downstream events. Using imaging flow cytometry, we found that both and IL-10 inhibited virus-induced nuclear translocation, but not phosphorylation, of IFN response factor 7. Blockade of IFN response factor 7 nuclear translocation and inhibition of the IFN-α response was partially reversed by a deficiency in the -derived ROP16 kinase, known to directly phosphorylate STAT3, a critical mediator of IL-10's anti-inflammatory effects. Taken together, our results indicate that suppresses pDC activation by mimicking IL-10's regulatory effects through an ROP16 kinase-dependent mechanism. Our findings further imply a convergent mechanism of inhibition of TLR signaling by and IL-10 and suggest potential negative consequences of HIV/ coinfection.
[Mh] MeSH terms primary: Dendritic Cells/immunology
HIV Infections/immunology
HIV-1/immunology
Interleukin-10/metabolism
Opportunistic Infections/immunology
Protein-Tyrosine Kinases/metabolism
Protozoan Proteins/metabolism
Toxoplasma/immunology
Toxoplasmosis/immunology
[Mh] MeSH terms secundary: Cell Differentiation
Cells, Cultured
Coinfection
Dendritic Cells/parasitology
Humans
Immunity, Innate
Immunomodulation
Interferon Regulatory Factor-7/metabolism
Interferon-alpha/metabolism
STAT3 Transcription Factor/metabolism
Signal Transduction
Toll-Like Receptor 9/metabolism
Tumor Necrosis Factor-alpha/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (IRF7 protein, human); 0 (Interferon Regulatory Factor-7); 0 (Interferon-alpha); 0 (Protozoan Proteins); 0 (STAT3 Transcription Factor); 0 (Toll-Like Receptor 9); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Rop16 protein, Toxoplasma gondii)
[Em] Entry month:1801
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:171129
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1701045

  9 / 37222 MEDLINE  
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[PMID]: 29489654
[Au] Autor:Kroeber ES; Mathewos A; Wondemagegnehu T; Aynalem A; Gemechu T; Piszczan S; Timotewos G; Addissie A; Wienke A; Unverzagt S; Thomssen C; Jemal A; Kantelhardt EJ
[Ad] Address:Institute of Medical Epidemiology, Biostatistics and Informatics, Martin-Luther-University, Halle an der Saale, Germany.
[Ti] Title:Vulvar cancer in Ethiopia: A cohort study on the characteristics and survival of 86 patients.
[So] Source:Medicine (Baltimore);97(9):e0041, 2018 Mar.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Vulvar cancer (VC) is strongly associated with human papilloma virus (HPV) infections and immunosuppression (e.g., HIV). However, there is limited information on VC patient characteristics and survival in parts of sub-Saharan Africa, including Ethiopia, where chronic HPV and HIV infections are prevalent. The aim of this study is to provide a first view on VC patient characteristics in a sub-Saharan African setting.We present a retrospective analysis of records of 86 VC patients diagnosed between January 2010 and October 2015 at Addis Ababa University Hospital and other major health facilities in Ethiopia. Follow-up for vital status was obtained by telephone contact with patients or relatives. The primary endpoint was all-cause mortality.The median age of the patients was 39 (range: 20-85) years, 83% with known HIV status were positive and 81% presented with FIGO stages 2 or 3. The median follow-up time for surviving patients was 17 months (range: 0.1-65.0 months). The 1- and 2-year survival rates were 80% and 51%, respectively. Approximately 37% of patients received surgery, 38% received radiotherapy, and 33% received chemotherapy. Patients who received therapy had better survival than those who did not [adjusted hazard ratios: surgery, 0.44 (95% CI, 0.19-1.03); radiotherapy, 0.36 (95% CI, 0.14-0.90); chemotherapy, 0.42 (95% CI, 0.15-1.12)].A substantial proportion of VC patients in Ethiopia present at a late stage and receive suboptimal treatment. HIV infections appear to be a common comorbid condition. These conditions result in poor outcomes.
[Mh] MeSH terms primary: Vulvar Neoplasms/epidemiology
[Mh] MeSH terms secundary: Adult
Aged
Aged, 80 and over
Comorbidity
Ethiopia/epidemiology
Female
HIV Infections/epidemiology
Humans
Middle Aged
Neoplasm Staging
Retrospective Studies
Survival Rate
Vulvar Neoplasms/mortality
Vulvar Neoplasms/pathology
Vulvar Neoplasms/therapy
[Pt] Publication type:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180301
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000010041

  10 / 37222 MEDLINE  
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[PMID]: 29480859
[Au] Autor:Hong YT; Hong KH
[Ad] Address:Department of Otolaryngology-HNS, Institute for Medical Science, Chonbuk National University, Chonbuk National University Hospital, Jeonju, South Korea.
[Ti] Title:Sequential occurrence of diffuse large B-cell lymphoma and carcinoma in the nasopharynx: A case report.
[So] Source:Medicine (Baltimore);97(2):e9595, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: The sequential occurrence of the 2 malignancies development of nasopharyngeal carcinoma (NPC) and lymphoma is extremely rare and their coexistence raises the question of a common etiologic factor. CLINICAL FINDINGS/CLINICAL CONCERNS: A 71-year-old previously healthy man presented with diffuse large B-cell lymphoma (BCL) followed by NPC almost 2 years later with Epstein-Barr virus (EBV) positive. DIAGNOSIS: Endoscopic examination characterized a fixed, hard and nontender mass in the nasopharynx and biopsies were done. INTERVENTION: A patient successfully underwent chemotherapy for lymphoma and chemoradiation for carcinoma sequentially. OUTCOMES: He was followed up every 3 months for 1 year with endoscopic and radiological examinations. The nasopharynx mass was completely resolved after chemoradiation therapy. CONCLUSION: The presentation with diffuse large B-cell lymphoma (BCL) and NPC in this patient was perhaps caused by dual EBV infection or a different oncogenic mechanism.
[Mh] MeSH terms primary: Carcinoma/drug therapy
Carcinoma/radiotherapy
Epstein-Barr Virus Infections/complications
Lymphoma, Large B-Cell, Diffuse/drug therapy
Nasopharyngeal Neoplasms/drug therapy
Nasopharyngeal Neoplasms/radiotherapy
Neoplasms, Second Primary/drug therapy
Neoplasms, Second Primary/radiotherapy
[Mh] MeSH terms secundary: Aged
Carcinoma/pathology
Carcinoma/virology
Humans
Lymphoma, Large B-Cell, Diffuse/diagnostic imaging
Lymphoma, Large B-Cell, Diffuse/pathology
Lymphoma, Large B-Cell, Diffuse/virology
Male
Nasopharyngeal Neoplasms/pathology
Nasopharyngeal Neoplasms/virology
Neoplasms, Second Primary/pathology
Neoplasms, Second Primary/virology
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180305
[Lr] Last revision date:180305
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180227
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009595


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