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Measures of patient radiation exposure during endoscopic retrograde cholangiography:Beyond fluoroscopy time

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World Journal of Gastroenterology 2015年第6期21卷 1900-1906页

作者： Toufic Kachaamy Edwyn Harrison Rahul Pannala William Pavlicek Michael D Crowell Douglas O Faigel cancer Treatment Centers of America Goodyear Mayo clinic Arizona

AIM:to determine whether fluoroscope time is a good predictor of patient radiation exposure during endoscopic retrograde ***:this is a prospective observational study of consecutive patients undergoing endoscopic retrograde cholangiopancreatography in a tertiary care *** related to radiation exposure were *** following measures were obtained:Fluoroscopy time(FT),dose area product(DAP)and dose at reference point(DOSERP).Coefficients of determination were calculated to analyze the correlation between FT,DAP and *** between FT and DAP/DOSRP was assessed using Bland Altman ***:Four hundred sixty-three data sets were *** time average was 7.3 *** related radiation accounted for 86%of the total DAP while acquisition films related radiation accounted for 14%of the *** any given FT there are wide ranges of DAP and DOSERP and the variability in both increases as fluoroscopy time *** coefficient of determination(R2)on the non transformed data for DAP and DOSERP versus FT were respectively 0.416 *** fluoroscopy use was the largest contributor to patient radiation exposure during endoscopic retrograde cholangiography(ERCP),there is a wide variability in DAP and DOSERP that is not accounted for by *** and DOSERP increase in variability as FT *** translates into poor accuracy of FT in predicting DAP and DOSERP at higher radiation ***:DAP and DOSERP in addition to FT should be adopted as new ERCP quality measures to estimate patient radiation exposure.

关键词： Cholangiopancreatography Endoscopic retrograde Flu

Complex role for the immune system in initiation and progression of pancreatic cancer

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World Journal of Gastroenterology 2014年第32期20卷 11160-11181页

作者： Kristin S Inman Amanda A Francis Nicole R Murray Department of cancer Biology Mayo Clinic Jacksonville FL 32224United States

The immune system plays a complex role in the development and progression of pancreatic cancer. Inflammation can promote the formation of premalignant lesions and accelerate pancreatic cancer development. Conversely, pancreatic cancer is characterized by an immunosuppressive environment, which is thought to promote tumor progression and invasion. Here we review the current literature describing the role of the immune response in the progressive development of pancreatic cancer, with a focus on the mechanisms that drive recruitment and activation of immune cells at the tumor site, and our current understanding of the function of the immune cell types at the tumor. Recent clinical and preclinical data are reviewed, detailing the involvement of the immune response in pancreatitis and pancreatic cancer, including the role of specific cytokines and implications for disease outcome. Acute pancreatitis is characterized by a predominantly innate immune response, while chronic pancreatitis elicits an immune response that involves both innate and adaptive immune cells, and often results in profound sys-temic immune-suppression. Pancreatic adenocarcinoma is characterized by marked immune dysfunction driven by immunosuppressive cell types, tumor-promoting immune cells, and defective or absent inflammatory cells. Recent studies reveal that immune cells interact with cancer stem cells and tumor stromal cells, and these interactions have an impact on development and progression of pancreatic ductal adenocarcinoma(PDAC). Finally, current PDAC therapies are reviewed and the potential for harnessing the actions of the immune response to assist in targeting pancreatic cancer using immunotherapy is discussed.

关键词： Immune system Pancreatitis Pancreatic ductal adenocarcinoma Immunosuppression Immunotherapy Inflammation

PRSS3/mesotrypsin in prostate cancer progression： mplications for translational medicine

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Asian Journal of Andrology 2013年第4期15卷 439-440页

作者： Evette S Radisky Department of cancer Biology Mayo Clinic ComprehensiveCancer Center Jacksonville FL 32224 USA

prostate cancer morbidity and morta lity are caused by metastasis to othervital organs and tissues. Metastatic prostate cancer is a terminal disease in need of improved therapies. Hoclda et al. have iden tified prostate cancer cell upregulation of the digestive protease PRSS3/mesotrypsin in association with metastasis and recur rence. Gene silencing of PRSS3 led to pronounced reductions in invasion and metastasis in cell culture and in an orthoto pic mouse model of prostate cancer. Importantly, a recently developed inhibitor of mesotrypsin was equally effective in sup pressing invasion. These results identify mesotrypsin as a potential therapeutic tar get in metastatic prostate cancer. Prostate cancer is a disease that can lie latent for decades or can progress rapidly to systemic metastasis and deathand the molecular pathways that distinguish between indolent and aggressive cancers are not well defined. Assessment of patient prognosis is therefore a critical challengewho is likely to benefit from further interventions, and who should be spared further treatment？ Prostatespecific antigen assays provide a valuable surveillance tool, but prostatespe cific antigen is not a specific marker for aggressive prostate cancers, and only a frac tion of the many men who experience pro statespecific antigen relapse after initial treatment will ever develop overt meta stasis.1＇2 Thus, there is an unmet clinical need for additional and more specific biomarkers that define subsets of patients at greatest risk of metastatic progression. An additional unmet need is encountered by patients with advanced diseasecurrent therapies are inadequate, since metastatic prostate cancerinevitably develops resistance to androgen deprivation therapy, at which time sub sequent treatment of castrationresistant pro state cancer with standard chemotherapy agent docetaxel, and even with newer regi mens incorporating agents that block andro gen signaling via alternative mechanisms, can provide only mod

关键词： PRSS3/mesotrypsin progression implications

Checkpoint Inhibition in the Treatment of Unresectable,Advanced Lymphoepithelioma-like Hepatocellular Carcinoma

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Journal of clinical and Translational Hepatology 2021年第2期9卷 265-268页

作者： David J.Hermel Emma Z.Du Ray Lin Catherine T.Frenette Darren S.Sigal Division of Hematology and Oncology Scripps Clinic and Scripps MD Anderson Cancer CenterLa JollaCAUSA Division of Pathology Scripps Clinic and Scripps MD Anderson Cancer CenterLa JollaCAUSA Division of Radiation Oncology Scripps Clinic and Scripps MD Anderson Cancer CenterLa JollaCAUSA Division of Gastroenterology Scripps Clinic and Scripps MD Anderson Cancer CenterLa JollaCAUSA

Lymphoepithelioma-like hepatocellular carcinoma(LELHCC)is a very rare neoplasm,with distinct epidemiologic,morphologic and clinical *** mechanistic insight into the pathogenesis of this carcinoma suggests a pivotal role for the host immune system in the proliferation and progression of this ***,while detailed genomic profiling of these hepatic tumors have revealed an intra-tumoral inflammatory mutational signature that may predispose to immune checkpoint inhibitor efficacy,no published report has described their use in this tumor ***,with near 100 cases of LEL-HCC reported in the literature to date and the majority of cases confined to localized and resectable disease,current evidencebased practices in the unresectable setting are lacking,with unknown benefit of chemotherapy or *** report on the case of a 68 year-old man with unresectable,advanced LEL-HCC who had evidence of disease stability after starting on the immune checkpoint inhibitor *** disease response persisted off therapy for over a year and was potentially augmented by radiotherapy at the site of local *** this extremely rare tumor subtype,this case highlights the potential efficacy and safety of immune checkpoint blockade in LEL-HCC and reinforces the need for more robust,large-scale analysis of patients with these rare tumors to better evaluate treatment strategies and outcomes.

关键词： Immune checkpoint inhibitor Lymphoepithelioma-like hepatocellular carcinoma Stereotactic body radiation therapy Immunotherapy LEL-HCC

Immunohistochemical evaluation of vitamin D receptor(VDR) expression in cutaneous melanoma tissues and four VDR gene polymorphisms

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cancer Biology & Medicine 2017年第2期14卷 162-175页

作者： Francesco La Marra Giuseppe Stinco Cinzia Buligan Giovanni Chiriacò Diego Serraino Carla Di Loreto Sabina Cauci Department of Medical Area School of MedicineUniversity of Udine Dermatology clinic Udine University-HospitalUniversity of Udine Unit of cancer Epidemiology CRO Aviano National Cancer Institute

Objective:Vitamin D receptor(VDR)mediates vitamin D *** examined whether VDR expression in excised melanoma tissues is associated with VDR gene(VDR)***:We evaluated VDR protein expression(by monoclonal antibody immunostaining),melanoma characteristics,and carriage of VDR-Fok I-rs2228570(C>T),VDR-Bsm I-rs1544410(G>A),VDR-ApaI-rs7975232(T>G),and VDR-TaqI-rs731236(T>C)polymorphisms(by restriction fragment length polymorphism).Absence or presence of restriction site was denoted by a capital or lower letter,respectively:"F"and"f"for Fok I,"B"and"b"for Bsm I,"A"and"a"for ApaI,and "T"and"t"for TaqI ***-four Italian cutaneous primary melanomas(52.1±12.7 years old)were studied;51.4% were stage Ⅰ,21.6% stage Ⅱ ,13.5% stage Ⅲ,and 13.5% stage Ⅳ *** expression was categorized as follows:100% positive vs.1,regression,tumor-infiltrating lymphocytes,tumoral infiltration of vascular tissues,additional skin and non-skin cancers,and melanoma ***:We highlighted that VDR polymorphisms can affect VDR expression in excised melanoma *** VDR expression in AATT carriers is a new finding that merits further *** expression possibly poses implications for vitamin D supplementation against *** expression and VDR genotype may become precise medicinal tools for melanoma in the future.

关键词： Vitamin D receptor VDR protein expression VDR polymorphism cutaneous melanoma metastatic melanoma skin cancer predictive biomarkers FokI polymorphism

Bsm I(rs1544410) and Fok I(rs2228570) vitamin D receptor polymorphisms, smoking, and body mass index as risk factors of cutaneous malignant melanoma in northeast Italy

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cancer Biology & Medicine 2017年第3期14卷 302-318页

作者： Sabina Cauci Vincenzo Maione Cinzia Buligan Martina Linussio Diego Serraino Giuseppe Stinco Department of Medicine University of UdineUdine 33100Italy Dermatology clinic University Hospital of Brescia Brescia 25123Italy Dermatology clinic University Hospital of UdineUdine 33100Italy Unit of cancer Epidemiology CRO Aviano National Cancer InstituteAviano 33081Italy

Objective:To investigate whether vitamin D receptor gene(VDR)Bsm I-rs1544410 and Fok I-rs2228570 polymorphisms,smoking duration,and body mass index(BMI)are risk factors for cutaneous melanoma,especially metastatic ***:We studied 120 cutaneous melanoma cases[68 stage I and II non-metastatic melanoma(NMet M)patients,plus 52Stage III and IV metastatic melanoma(Met M)patients],and 120 matching healthy controls from northeast *** polymorphisms were measured by restriction fragment length polymorphism *** or presence of Bsm I and Fok I restriction sites was denoted by"B"and"F"or by"b"and"f,"***:VDR-Bsm I bb genotype was more frequent among Met M(32.7%)than among NMet M cases(13.2%),with odds ratio(OR)=*** of all melanoma patients vs healthy controls showed that the following biomarkers were at risk:≥20 years of smoking(OR=2.43);≥20 years of smoking combined with bb(OR=4.78),Bb+bb(OR=2.30),Ff(OR=3.04),and Ff+ff(OR=3.08);obesity(BMI>30Conclusions:Risk factors for cutaneous Met M include two VDR polymorphisms combined with smoking duration and *** suggest gene-environment implications in melanoma susceptibility and *** studies in larger cohorts and in subjects with different genetic background are warranted to extend our findings.

关键词： Vitamin D receptor VDR polymorphism cutaneous melanoma metastatic melanoma smoking body mass index obesity skin cancer

Perspectives on immunotherapy utilization for hepatobiliary cancers in the United States

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Hepatobiliary Surgery and Nutrition 2020年第4期9卷 501-504页

作者： Pedro Luiz Serrano Usón Junior Daniel Ahn Mohamad Bassam Sonbol Tanios Bekaii-Saab Mitesh J.Borad Hospital Israelita Albert Einstein São PauloBrazil Mayo clinic cancer Center Mayo ClinicPhoenixAZUSA

Strategies involving immunotherapy and targeted therapies are emerging in the last years as valuable options for patients with hepatobiliary cancer(HBC)including hepatocellular carcinoma(HCC),gallbladder cancer(GBC),i... 详细信息

关键词： immunotherapy hepato biliary

Lineage plasticity-mediated therapy resistance in prostate cancer

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Asian Journal of Andrology 2019年第3期21卷 241-248页

作者： Alexandra M Blee Haojie Huang Department of Biochemistry and Molecular Biology Mayo Clinic College of Medicine Rochester MN 55905 USA Biochemistry and Molecular Biology Graduate Program Mayo Clinic Graduate School of Biomedical Sciences Rochester MN 55905 USA Department of Urology Mayo Clinic College of Medicine Rochester MN 55905 USA Mayo clinic cancer Center Mayo Clinic College of Medicine Rochester MN 55905 USA

Therapy resistance is a significant challenge for prostate cancer treatment in clinic. Although targeted therapies such as androgen deprivation and androgen receptor (AR) inhibition are effective initially, tumor cells eventually evade these strategies through multiple mechanisms. Lineage reprogramming in response to hormone therapy represents a key mechanism that is increasingly observed. The studies in this area have revealed specific combinations of alterations present in adenocarcinomas that provide cells with the ability to transdifferentiate and perpetuate AR-independent tumor growth after androgen-based therapies. Interestingly, several master regulators have been identified that drive plasticity, some of which also play key roles during development and differentiation of the cell lineages in the normal prostate. Thus, further study of each AR-independent tumor type and understanding underlying mechanisms are warranted to develop combinational therapies that combat lineage plasticity in prostate cancer.

关键词： lineage plasticity neuroendocrine prostate cancer therapy resistance transdifferentiation

Scaffold attachment factor B 1： an intrinsic inhibitor ot androgen receptor downregulated in prostate cancer

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Asian Journal of Andrology 2013年第6期15卷 703-704页

作者： Haojie Huang Department of Biochemistry and Molecular Biology Mayo Clinic College of Medicine Rochester MN 55905 USA Department of Urology Mayo Clinic College of Medicine Rochester MN 55905 USA Mayo clinic cancer Center Mayo Clinic College of Medicine. Rochester. MN 55905. USA

The androgen receptor （AR） is a pleio-trophic transcription factor that regu-lates expression of a large number of genes involved in many diverse cellular processes. The AR activation pathways have been studied extensively. However, the molecular mechanism and biological significance of AR inhibitory signals remain poorly understoo＆ Mukhopadhyay et aL have now identified the nuclear matrix protein scaffold attachmenl factor B1 （SAFB1） as a novel AR corepressor. The authors found that SAFB1 physically associates with AR protein and inhibits AR transcriptional activity and androgen-sens- itive gene expression. SAFB1 had no effect on chromatin occupancy of AR, but silencin of SAFB1 abolished recruitment MST1, known AR repressor, at AR target loci. The also showed that SAFB1 interacts with EZH2 SUZ12 and EED, three core components o the Polycomb repressive complex 2 （PRC2）, which catalyzes the gene repression histone modification H3 lysine 27 trimethylation （H3K27me3）. The authors further showed that forced expression of SAFB1 increases H3K27me3 at AR target loci and this effec requires EZH2. Finally, the authors demon strated that expression of SAFB1 is downre-guiated in human prostate cancer （PCa） specimens and SAFB1 knockdown results in an aggressive phenotype of PCa. These find-ings identify SAFB1 as an important node for integration of multiple inhibitory signals ot AR, which represents a viable pathway fol therapeutic intervention of PCa.

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