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Comparable results of surgical versus non-surgical management for patients with malignant bowel obstruction-a lesson from S1316 study

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Hepatobiliary Surgery and Nutrition 2024年第2期13卷 304-306页

作者： Abdallah Al Farai Mansour Al Moundhri gi program Sultan Comprehensive Cancer Care and Research CenterMuscatOman

We had the pleasure to read the paper published online by Krouse et *** August 2023 in the Lancet Gastroenterology and Hepatology(1).The study labeled as S1316 was a prospective pragmatic comparative effectiveness trial evaluating the surgical versus non-surgical management for patients with malignant small intestinal bowel obstruction(MIO)and having an intra-abdominal or retroperitoneal primary cancer and were aged 18 years or older with a Zubrod performance status 0-2 within 1 week before admission;had a surgical indication;and treatment *** patients were divided in two *** who accepted the randomization were randomly assigned to surgical and non-surgical treatment *** who declined consent for random assignment were offered a prospective observational patient choice pathway where the patients with their caring team decide upon the treatment option.

关键词： Malignant bowel obstruction surgery non-surgical

Characterization of genetically engineered mouse models carrying Col2a1-cre-induced deletions of Lrp5 and/or Lrp6

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Bone Research 2015年第4期3卷 235-245页

作者： Cassie A Schumacher Danese M Joiner Kennen D Less Melissa Oosterhouse Drewry Bart O Williams Center for Cancer and Cell Biology Program in Skeletal Disease and Tumor MicroenvironmentVan Andel Research Institute

Mice carrying Collagen2a1-cre-mediated deletions of Lrp5 and/or Lrp6 were created and *** lacking either gene alone were viable and fertile with normal knee *** in which both Lrp5 and Lrp6 were conditionally ablated via Collagen2al-cre-mediated deletion displayed severe defects in skeletal development during *** addition,adult mice carrying Collagen2al-cre-mediated deletions of Lrp5 and/or Lrp6 displayed low bone mass suggesting that the Collagen2a1-cre transgene was active in cells that subsequently differentiated into *** both embryonic skeletal development and establishment of adult bone mass,Lrp5 and Lrp6 carry out redundant functions.

关键词： carrying Collagen displayed deletion engineered transgene viable embryogenesis redundant embryonic

CDX2 protein expression compared to alcian blue staining in the evaluation of esophageal intestinal metaplasia

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World Journal of Gastroenterology 2015年第9期21卷 2770-2776页

作者： Dennis R Johnson Maisoun Abdelbaqui Maryam Tahmasbi Zoltan Mayer Hung-Wei Lee Mokenge P Malafa Domenico Coppola Department of Anatomic Pathology Moffitt Cancer Center and Research InstituteTampaFL 33612United States Florida Digestive Health Specialists Lakewood RanchFL 34202United States Department of Oncological Sciences University of South FloridaTampaFL 33612United States gi tumor program Moffitt Cancer Center and Research InstituteTampaFL 33612United States tumor Biology program Moffitt Cancer Center and Research InstituteTampaFL 33612United States

AIM:To compare the sensitivity and specificity of CDX2 and alcian blue(AB) p H 2.5 staining in identifying esophageal intestinal ***:One hundred and ninty-nine biopsies from 186 patients were retrospectively reviewed and categorized as Barrett's esophagus(BE)(n =108); non-Barrett's esophagus(NBE)(n =48); columnar blue cells(CB) and esophageal glands(EG)(n =43).The biopsies were stained with AB and immunostained for CDX2 using a mouse monoclonal antibody from Biogenex(clone CDX2-88) and the Ventana Discovery X automated *** positive and negative predictive value of each group was used to determine the predictive power of CDX2 and AB in diagnosing intestinal ***:All of the 108 BE biopsies(100%) were positive for AB and 102 of them(94.4%) were positive for *** six BE patients(5.6%) who failed to stain with CDX2 were found to have lost the focus of intestinal metaplasia upon deeper sectioning for *** AB and CDX2 were negative in 43 out of 48(89.6%) NBE *** NBE patients(10.4%) were falsely positive for AB due to the presence of EG and CB in these *** cases were all CDX2 *** addition,5 AB negative NBE were found to be CDX2 *** on these results the CDX2 immunostain had similar sensitivity but higher specificity(100% vs about 91%) than AB in detecting intestinal type metaplasia in these *** data shows that CDX2 has a better PPV in detecting intestinal metaplasia as compared to AB(95.6% vs 71.5%,respectively).CONCLUSION:CDX2 has a better positive predictive value than AB in detecting intestinal ***2may be useful when challenged by gastro-esophageal biopsies containing mimikers of BE.

关键词： Barrett’s esophagus Alcian blue pH 2.5 CDX2 Intest

Dissecting the multifactorial nature of demyelinating disease

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Neural Regeneration Research 2018年第4期13卷 628-632页

作者： Karolina Kucharova William B.Stallcup Sanford Burnham Prebys Medical Discovery Institute Cancer Center Tumor Microenvironment and Cancer Immunology ProgramLa Jolla CA USA

Chondroitin sulfate proteoglycan-4（CSPG4） is a surface component of two key cell types（oligodendrocyte progenitor cells（OPCs） and myeloid cells） present in lysolecithin-induced lesions in mouse spinal *** types of CSPG4 manipulations have been used to study the roles of these cells in myelin damage and repair：（1） OPC and myeloid-specific ablation of CSPG4,and（2） transplantation of enhanced green fluorescent protein（EGFP）-labeled progenitors to distinguish between bone marrow-derived macrophages and resident *** of CSPG4 in OPCs does not affect myelin damage,but decreases myelin repair,due to reduced proliferation of CSPG4-null OPCs that diminishes generation of mature oligodendrocytes for *** of CSPG4 in myeloid cells greatly decreases recruitment of macrophages to spinal cord lesions,resulting in smaller initial lesions,but also in significantly diminished myelin *** the absence of macrophage recruitment,OPC proliferation is greatly impaired,again leading to decreased generation of myelinating *** may promote OPC proliferation via phagocytosis of myelin debris and/or secretion of factors that stimulate OPC *** are not able to substitute for macrophages in promoting OPC *** additional feature of lesions in myeloid-specific CSPG4 null mice is the persistence of poorly-differentiated platelet-derived growth factor receptor α（PDGFRα）＋ macrophages that may prolong damage.

关键词： myelin damage myelin repair chondroitin sulfate proteoglycan 4 oligodendrocyte progenitors macrophages microglia Cre-Lox technology bone marrow transplantation

Bone loss from Wnt inhibition mitigated by concurrent alendronate therapy

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Bone Research 2018年第2期6卷 167-176页

作者： Babita Madan Mitchell J.McDonald Gabrielle E.Foxa Cassandra R.Diegel Bart O.Williams David M.Virshup program in Cancer and Stem Cell Biology Duke-NUS Medical School Center for Cancer and Cell Biology and program for Skeletal Disease and tumor Microenvironment Van Andel Research Institute Department of Pediatrics Duke University

Dysregulated Wnt signaling is associated with the pathogenesis of cancers, fibrosis, and vascular diseases. Inhibition of Wnt signaling has shown efficacy in various pre-clinical models of these disorders. One of the key challenges in developing targeted anti-cancer drugs is to balance efficacy with on-target toxicity. given the crucial role Wnts play in the differentiation of osteoblasts and osteoclasts, acute inhibition of Wnt signaling is likely to affect bone homeostasis. In this study, we evaluated the skeletal effect of small molecule inhibitor of an o-acyl transferase porcupine（PORCN） that prevents Wnt signaling by blocking the secretion of all Wnts. Micro-computed tomography and histomorphometric evaluation revealed that the bones of mice treated with two structurally distinct PORCN inhibitors LGK974 and ETC-1922159（ETC-159） had loss-of-bone volume and density within 4 weeks of exposure. This decreased bone mass was associated with a significant increase in adipocytes within the bone marrow. Notably,simultaneous administration of a clinically approved anti-resorptive, alendronate, a member of the bisphosphonate family,mitigated loss-of-bone mass seen upon ETC-159 treatment by regulating activity of osteoclasts and blocking accumulation of bone marrow adipocytes. Our results support the addition of bone protective agents when treating patients with PORCN *** of bone toxicity can extend the therapeutic utility of Wnt pathway inhibitors.

关键词： Wnt ETC Bone loss Wnt inhibition mitigated concurrent alendronate therapy

Perspectives in the treatment of pancreatic adenocarcinoma

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World Journal of Gastroenterology 2015年第31期21卷 9297-9316页

作者： Angel Cid-Arregui Victoria Juarez German Cancer Research Center Trans- lational ImmunologyTumor Immunology Program Asteria Pharma GmbH 68723 OftersheimGermany

Pancreatic ductal adenocarcinoma(PDAC) is an incurable lethal disease whose incidence rate is growing. There is no effective screening for detection of early stage tumors and,in most cases,PDAC is diagnosed at advanced disease stages,when radical pancreatic resection is not possible. The aggressive nature of pancreatic tumor cells lies in the complex genetic mechanisms behind their uncontrolled capability to grow and metastasize,which involve essential adaptive changes in cellular metabolism,signaling,adhesion and immunoediting. In addition,PDAC cells promote a dense functional stroma that facilitates tumor resistance to chemotherapy and radiation. During the last two decades,gemcitabine has been the reference for the systemic treatment of PDAC. However,recently,a regimen combining fluorouracil,irinotecan,oxaliplatin,and leucovorin(FOLFIRINOX) and another combining albumin-bound paclitaxel with gemcitabine have shown clear therapeutic advantage in advanced PDAC,with survival outcomes of 11.3 and 8.5 mo on phase Ⅲ trials,respectively,over singleagent gemcitabine. With the pending issue of their higher toxicities,these regimens set the reference for ongoing and future clinical studies in advanced PDAC. In addition,the efficacy of oral fluoropyrimidine(S-1) has been well documented in Asiatic PDAC patients. The development of therapeutic approaches other than cytotoxic drugs has proven difficult in the past,with only one drug(erlotinib) approved to date. Besides,a number of agents targeting signaling pathways in tumor or stroma cells are being investigated. Likewise,immunotherapies that target PDAC in various ways are the subject of a number of clinical trials. The search for reliable biomarkers with diagnostic and prognostic value using genomics and mass spectrometry methods may facilitate monitoring and refinement of therapies. This review focuses on current understanding of the pathogenesis of PDAC and the latest developments in the treatment of advanced PDAC.

关键词： Pancreatic adenocarcinoma tumor sur-veillance Biom

ICC density predicts bacterial overgrowth in a rat model of post-infectious IBS

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World Journal of Gastroenterology 2010年第29期16卷 3680-3686页

作者： Sam-Ryong Jee Walter Morales Kimberly Low Christopher Chang Amy Zhu Venkata Pokkunuri Soumya Chatterjee Edy Soffer Jeffrey L Conklin Mark Pimentel gi Motility program Division of GastroenterologyCedars-Sinai Medical Center

AIM:To investigate the interstitial cells of Cajal(ICC) number using a new rat ***:Sprague-Dawley rats were assigned to two *** first group received gavage with Campylobacter jejuni(***) *** second group was gavaged with *** months after clearance of Campylobacter from the stool,precise segments of duodenum,jejunum,and ileum were ligated in self-contained loops of bowel that were preserved in anaerobic *** muscular plexus ICC(DMP-ICC) were quantified by two blinded readers assessing the tissue in a random,coded *** number of ICC per villus was compared among controls,Campylobacter recovered rats without small intestinal bacterial overgrowth(SIBO),and Campylobacter recovered rats with ***:Three months after recovery,27% of rats gavaged with *** had *** rats with SIBO had a lower number of DMP-ICC than controls in the jejunum and *** there appeared to be a density threshold of 0.12 DMP-ICC/villus that was associated with *** ileal density of DMP-ICC was 0.12(P<0.05).If the density of ICC was < 0.12 DMP-ICC/villus in more than one location of the bowel,88% of these had SIBO compared to 6% in those who did not(P<0.001).CONCLUSION:In this post-infectious rat model,the development of SIBO appears to be associated with a reduction in *** study of this rat model might help understand the pathophysiology of postinfectious irritable bowel syndrome.

关键词： Post-infectious irritable bowel syndrome Bacterial overgrowth Interstitial cells of Cajal Campylobacter

A Comprehensive Overview of Skeletal Phenotypes Associated with Alterations in Wnt/β-catenin Signaling in Humans and Mice

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Bone Research 2013年第1期1卷 27-71页

作者： Kevin A.Maupin Casey J.Droscha Bart O.Williams program for Skeletal Pathobiology and Center for tumor Metastasis Van Andel Research Institute333 Bostwick NEGrand RapidsMI 49503USA

The Wnt signaling pathway plays key roles in differentiation and development and alterations in this signaling pathway are causally associated with numerous human diseases. While several laboratories were examining roles for Wnt signaling in skeletal development during the 1990s, interest in the pathway rose exponentially when three key papers were published in 2001-2002. One report found that loss of the Wnt co-receptor, Low-density lipoprotein related protein-5 （LRPS）, was the underlying genetic cause of the syndrome Osteoporosis pseudoglioma （OPPG）. OPPG is characterized by early-onset osteoporosis causing increased susceptibility to debilitating fractures. Shortly thereafter, two groups reported that individuals carrying a specific point mutation in LRP5 （G171V） develop high-bone mass. Subsequent to this, the causative mechanisms for these observations heightened the need to understand the mechanisms by which Wnt signaling controlled bone development and homeostasis and encouraged significant investment from biotechnology and pharmaceutical companies to develop methods to activate Wnt signaling to increase bone mass to treat osteoporosis and other bone disease. In this review, we will briefly summarize the cellular mechanisms underlying Wnt signaling and discuss the observations related to OPPG and the high-bone mass disorders that heightened the appreciation of the role of Wnt signaling in normal bone development and homeostasis. We will then present a comprehensive overview of the core components of the pathway with an emphasis on the phenotypes associated with mice carrying genetically engineered mutations in these genes and clinical observations that further link alterations in the pathway to changes in human bone.

关键词： Wnt signaling mouse models Lrp5/Lrp6 -catenin skeletal phenotypes

HPV18 Utilizes Two Alternative Branch Sites for E6*I Splicing to Produce E7 Protein

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Virologica Sinica 2019年第2期34卷 211-221页

作者： Ayslan Castro Brant Vladimir Majerciak Miguel Angelo Martins Moreira Zhi-Ming Zheng tumor Virus RNA Biology Section RNA Biology Laboratory Center for Cancer Research National Cancer Institute NIH Frederick MD 21702 USA Genetics Post-Graduation program Rio de Janeiro Federal University Rio de Janeiro Brazil Genetics program Nacional Cancer Institute INCA Rio de Janeiro 20231-050 Brazil

Human papillomavirus 18(HPV18) E6 and E7 oncogenes are transcribed as a single bicistronic E6 E7 pre-mRNA. The E6 ORF region in the bicistronic E6 E7 pre-mRNA contains an intron. Splicing of this intron disrupts the E6 ORF integrity and produces a spliced E6*I RNA for efficient E7 translation. Here we report that the E6 intron has two overlapped branch point sequences(BPS) upstream of its 30 splice site, with an identical heptamer AACUAAC, for E6*I splicing. One heptamer has a branch site adenosine(underlined) at nt 384 and the other at nt 388. E6*I splicing efficiency correlates to the expression level of E6 and E7 proteins and depends on the selection of which branch site. In general, E6*I splicing prefers the 30 ss-proximal branch site at nt 388 over the distal branch site at nt 384. Inactivation of the nt 388 branch site was found to activate a cryptic acceptor site at nt 636 for aberrant RNA splicing. Together, these data suggest that HPV18 modulates its production ratio of E6 and E7 proteins by alternative selection of the two mapped branch sites for the E6*I splicing, which could be beneficial in its productive or oncogenic infection according to the host cell environment.

关键词： Human papillomavirus 18 (HPV18) HPV splicing Branch point E6,E7,E6 intron HPV oncogenes