DOCSLIB.ORG

Labcorp Diagnostic Immunohistochemical Staining Program

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Labcorp Diagnostic Immunohistochemical Staining Program LabCorp Diagnostic Immunohistochemical Staining Program To order, specify the option required, and supply the clinical information below. 484006 - Option I: Slides and controls are returned for your interpretation. 484006 - Option II: Slides and controls are returned with an immunostain interpretation. 980004 - Option IV: Full surgical pathology consultation (can be ordered with Option II.) Note: Cytokeratin 903, Racemase, hematopoietic group, lymphoma group, and infectious disease group stains are available only as Option I or Option II with Option IV. These stains cannot be ordered as Option II. Carcinoma Group Breast Carcinoma Sarcoma Group Liver Group Neuroendocrine Non-Hodgkin Group Group Lymphoma Group CD31 Ber-EP4 AFP Chromogranin BCL-2 CU-18 CD34 CDX2 A AT BCL-6 1 Pancytokeratin ER CD68 CEA CD117 LMW Cytokeratin NSE Kappa light chain PR (CAM 5.2) CK 7 Desmin Lambda light chain Serotonin HAM 56 CK 20 GCDFP-15 Factor VIII-related CD3 antigen Somatostatin Thyroid Group CU-18 E-Cadherin Factor XIIIa CD4 Synaptophysin LMW Cytokeratin Prostate Group HHV-8 Thyroglobulin CD5 (CAM 5.2) Germ Cell Tumor Myoglobulin Group Calcitonin CD7 HMW Cytokeratin Cytokeratin 903 Muscle-specific Actin AFP CD 8 Pancytokeratin PSA S-100 CEA β-hCG CD10 E-Cadherin Smooth-muscle Actin PSAP Chromogranin CEA CD20 EMA Vimentin Racemase Mesothelioma vs TTF-1 Pancytokeratin CD23 NSE Carcinoma Group CD43, MT1 P63 Hematopoietic PLAP OC125 Ber-EP4 Group CD45, Leukocyte PIN-3 Triple stain Infectious Disease B72.3 common antigen (LCA) PSA CD1a Group Melanoma Group Calretinin CD45 RA Helicobacter pylori PSAP CEA CD117 CD45 RO, UCHL-1 HMB45 HSV I & II (Cocktail) (T cell) P16 CK 5 & 6 Myeloperoxidase CD74 Melan-A Hodgkin Disease ProEx C Pancytokeratin Group CD79a Super Pancytokeratin Mel-5 E-Cadherin TdT CD30 (AE1/AE3, CAM 5.2) CD138 EMA S-100 CD34 TTF-1 CD20 CD15 Cyclin D1 Vimentin CD68 Villin Vimentin CD15 Ki67 Patient’s Name ______________________________________________ Surgical Pathology Case Number: _________________ Requesting Physician ___________________________________________________ Telephone: _________________________ For program options II and IV, please submit an H&E slide and complete the following information: Differential Diagnosis: ______________________________________________________________________________________ _________________________________________________________________________________________________________ Site of Specimen: __________________________________________________________________________________________ Clinical Information: ________________________________________________________________________________________ _________________________________________________________________________________________________________ Alphabetical Index A1AT (α1-antitrypsin) EMA (Epithelial membrane antigen) AFP (α-fetoprotein) ER (Estrogen receptor) B72.3 Factor VIII-related antigen BCL-2 Factor XIIIa BCL-6 GCDFP-15 Ber-EP4 HAM 56 β-hCG Helicobacter pylori Calcitonin HHV-8 Calretinin HMB45 CD1a HMW Cytokeratin (34ßE12) CD3 HSV I & II (cocktail) CD4 Kappa light chain CD5 Ki67 (MIB-1) CD7 Lambda light chain CD8 (T cell) LMW Cytokeratin (CAM 5.2) CD10 Mel-5 CD15 (LeuM1) Melan-A CD20 (B cell, L26) Muscle-specific Actin CD23 Myeloperoxidase CD30 (Ki-1 antigen/BerH2) Myoglobulin CD31 NSE (Neuron-specific enolase) CD34 OC125 (Celomic ovarian antigen) CD43, MT1 (T cell) P16 CD45 RA P63 CD45 RO, UCHL-1 (T cell) Pancytokeratin (AE1/AE3 & PCK26) CD45, Leukocyte common antigen (LCA) PIN-3 Triple stain (p504S/P63/HMW Cytokeratin) CD68 (KP-1) PLAP (Placental alkaline phosphatase) CD74, LN2 (B cell) PR (Progesterone receptor) CD79a (B cell) ProEx C CD117 PSA (Prostate-specific antigen) CD138 PSAP (Prostate-specific acid phosphatase) CDX2 Racemase (P504S) CEA (Carcinoembryonic antigen) S-100 Chromogranin Serotonin CK 5 & 6 Smooth-muscle Actin CK 7 Somatostatin CK 20 Super Pancytokeratin (AE1/AE3, CAM 5.2) CU-18 (Breast-related antigen) Synaptophysin Cyclin D1 TdT Cytokeratin 903 Thyroglobulin Desmin TTF-1 (Thyroid transcription factor-1) E-Cadherin Villin Vimentin Center for Molecular Biology and Pathology 1912 Alexander Drive Research Triangle Park, NC 27709 Customer Service: 800-735-4087 ©2008 Laboratory Corporation of America® Holdings All rights reserved. L6067-0408-1 Fax: 919-361-7201.
Load more

Recommended publications
  • EP3 Prostate Adenocarcinoma Metastasis to the Bilateral Ureters
    Autopsy, Forensic, Grossing 004 Id: EP3 Prostate Adenocarcinoma Metastasis to the Bilateral Ureters: An Unusual Pattern Suvra Roy, MD, L. Maximilian Buja, MD, University of Texas Health Science Center at Houston We report an autopsy of a patient with prostate cancer who had hydronephrosis and sepsis due to obstruction from Downloaded from https://academic.oup.com/ajcp/article/144/suppl_2/A004/1772163 by guest on 23 September 2021 bilateral ureteral metastasis of prostate adenocarcinoma. He was an 82-year-old man who presented to the emergency department with weakness and shortness of breath. Fifteen years earlier, he had been diagnosed with prostate cancer , underwent chemotherapy, and was in remission for 10 years. Eighteen months ago, he developed a recurrence and began chemotherapy again but, because of his worsening renal condition, stopped the chemotherapy about 4 months ago. On admission, he was found to have chronic kidney disease, stage 5, and sepsis. Abdominal CT was negative for genitourinary mass. His condition deteriorated rapidly and he developed bradycardia and then pulseless electrical activity (PEA). He went into cardiac arrest for 30 minutes without return of pulse and remained in PEA. His poor prognosis was explained to his family and, per the family’s wishes, resuscitation was stopped, and the patient died. Autopsy revealed bilateral dilated renal pelvis, trabeculated urinary bladder and enlarged prostate. No gross evidence of metastasis was identified in lymph nodes or bone. However, the openings of the ureters revealed papillary masses involving the distal ureters bilaterally, but not involving the bladder. Microscopic examination of the masses revealed atypical tumor cells with highly pleomorphic features.
    [Show full text]
  • Germ Cell Origin of Testicular Carcinoid Tumors Phillip H
    Imaging, Diagnosis, Prognosis Germ Cell Origin of Testicular Carcinoid Tumors Phillip H. Abbosh,1Shaobo Zhang,1Gregory T.MacLennan,3 Rodolfo Montironi,4 Antonio Lopez-Beltran,5 Joseph P. Rank,6 LeeAnn Baldridge,1and Liang Cheng1, 2 Abstract Purpose: Carcinoids are neuroendocrine tumors and most frequently occur within tissues derived from the embryonic gut.These tumors can occur in any organ site but are rare in the testis. The cell type giving rise to testicular carcinoid is unknown.We hypothesized that testicular carci- noid may have a germ cell origin. Experimental Design: We describe our analysis of protein and genetic markers of germ cell neoplasia, using immunohistochemistry and fluorescence in situ hybridization, in four testicular carcinoid tumors. Results: All four cases of testicular carcinoid tumor arose in a background of mature teratoma. Isochromosome 12p was identified in carcinoid tumor cells in all four samples. 12p overrepresen- tation was also observed in three cases. Isochromosome 12p and 12p overrepresentation were present in cells of coexisting mature teratoma in three cases. Carcinoid tumors showed strong immunoreactivity for synaptophysin and chromogranin, but no immunoreactivity for OCT4, CD30, c-kit,TTF-1, and CDX2. Membranous and cytoplasmic staining for h-catenin was detected in three cases. Conclusion: Our findings suggest that testicular carcinoid represents a phenotypic expression of testicular teratoma and is of germ cell origin. Testicular carcinoid tumor is rare. It was originally reported in Materials and Methods 1954 by Simon (1) who described it as part of a cystic teratoma, and additional cases have been subsequently reported. All Patients. We analyzed four cases of testicular carcinoid tumor.
    [Show full text]
  • Neuroendocrine Differentiation of Prostatic Adenocarcinoma
    J Lab Med 2019; 43(2): 123–126 Laboratory Case Report Cátia Iracema Morais*, João Lobo, João P. Barreto, Cláudia Lobo and Nuno D. Gonçalves Neuroendocrine differentiation of prostatic adenocarcinoma – an important cause for castration-resistant disease recurrence https://doi.org/10.1515/labmed-2018-0190 awareness of this entity is crucial due to its underdiagno- Received December 3, 2018; accepted December 12, 2018; previously sis and adverse prognosis. published online February 15, 2019 Keywords: carcinoma; castration-resistant (D064129); cell Abstract transformation; neoplastic (D002471); neuroendocrine (D018278); prostate (D011467); prostatic neoplasms. Background: Neuroendocrine differentiation of prostatic carcinoma is a rare entity associated with metastatic castration-resistant disease. Among useful biomarkers of neuroendocrine differentiation, chromogranin A, sero- Introduction tonin, synaptophysin and neuron-specific enolase stand out, while total prostate-specific antigen (PSA) levels are Neuroendocrine prostatic carcinoma is a rare and often low or undetectable. underdiagnosed histologic subtype. Despite the low Case presentation: We report a case of prostatic adenocar- incidence rate of primary neuroendocrine prostatic cinoma recurrence after a 6-year disease-free follow-up, in carcinoma (which represents under 1% of all prostate which increased serum chromogranin A levels and unde- cancers at diagnosis), 30–40% of patients who develop tectable total PSA provided a prompt indication of neu- metastasized castration-resistant
    [Show full text]
  • Transiently Structured Head Domains Control Intermediate Filament Assembly
    Transiently structured head domains control intermediate filament assembly Xiaoming Zhoua, Yi Lina,1, Masato Katoa,b,c, Eiichiro Morid, Glen Liszczaka, Lillian Sutherlanda, Vasiliy O. Sysoeva, Dylan T. Murraye, Robert Tyckoc, and Steven L. McKnighta,2 aDepartment of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390; bInstitute for Quantum Life Science, National Institutes for Quantum and Radiological Science and Technology, 263-8555 Chiba, Japan; cLaboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0520; dDepartment of Future Basic Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara, Japan; and eDepartment of Chemistry, University of California, Davis, CA 95616 Contributed by Steven L. McKnight, January 2, 2021 (sent for review October 30, 2020; reviewed by Lynette Cegelski, Tatyana Polenova, and Natasha Snider) Low complexity (LC) head domains 92 and 108 residues in length are, IF head domains might facilitate filament assembly in a manner respectively, required for assembly of neurofilament light (NFL) and analogous to LC domain function by RNA-binding proteins in the desmin intermediate filaments (IFs). As studied in isolation, these IF assembly of RNA granules. head domains interconvert between states of conformational disor- IFs are defined by centrally located α-helical segments 300 to der and labile, β-strand–enriched polymers. Solid-state NMR (ss-NMR) 350 residues in length. These central, α-helical segments are spectroscopic studies of NFL and desmin head domain polymers re- flanked on either end by head and tail domains thought to be veal spectral patterns consistent with structural order.
    [Show full text]
  • Limited Diagnostic Utility of Chromogranin a Measurements in Workup of Neuroendocrine Tumors
    diagnostics Article Limited Diagnostic Utility of Chromogranin A Measurements in Workup of Neuroendocrine Tumors Jonas Baekdal 1,2,*, Jesper Krogh 1,2, Marianne Klose 1,2, Pernille Holmager 1,2, Seppo W. Langer 1,3, Peter Oturai 1,4,5, Andreas Kjaer 1,4,5 , Birgitte Federspiel 1,6, Linda Hilsted 1,7, Jens F. Rehfeld 1,7, Ulrich Knigge 1,2,8 and Mikkel Andreassen 1,2 1 ENETS Neuroendocrine Tumor Centre of Excellence, Rigshospitalet, Copenhagen University Hospital, 2100 Copenhagen, Denmark; [email protected] (J.K.); [email protected] (M.K.); [email protected] (P.H.); [email protected] (S.W.L.); [email protected] (P.O.); [email protected] (A.K.); [email protected] (B.F.); [email protected] (L.H.); [email protected] (J.F.R.); [email protected] (U.K.); [email protected] (M.A.) 2 Department of Endocrinology, Rigshospitalet, Copenhagen University Hospital, 2100 Copenhagen, Denmark 3 Department of Oncology, Rigshospitalet, Copenhagen University Hospital, 2100 Copenhagen, Denmark 4 Department of Clinical Physiology, Nuclear Medicine & PET and Cluster for Molecular Imaging, Copenhagen University Hospital, 2100 Copenhagen, Denmark 5 Department of Biomedical Sciences, Rigshospitalet and University of Copenhagen, 2100 Copenhagen, Denmark 6 Department of Pathology, Rigshospitalet, Copenhagen University Hospital, 2100 Copenhagen, Denmark 7 Department of Clinical Biochemistry, Rigshospitalet, Copenhagen University Hospital, 2100 Copenhagen, Denmark 8 Department of Surgery and Transplantation, Rigshospitalet, Copenhagen University Hospital, 2100 Copenhagen, Denmark * Correspondence: [email protected]; Tel.: +45-6013-4687 Received: 11 October 2020; Accepted: 28 October 2020; Published: 29 October 2020 Abstract: Background: Plasma chromogranin A (CgA) is related to tumor burden and recommended in the follow-up of patients diagnosed with neuroendocrine tumors (NETs).
    [Show full text]
  • Small-Cell Neuroendocrine Tumors: Cell State Trumps the Oncogenic Driver Matthew G
    Published OnlineFirst January 26, 2018; DOI: 10.1158/1078-0432.CCR-17-3646 CCR Translations Clinical Cancer Research Small-Cell Neuroendocrine Tumors: Cell State Trumps the Oncogenic Driver Matthew G. Oser1,2 and Pasi A. Janne€ 1,2,3 Small-cell neuroendocrine cancers often originate in the lung SCCB and SCLC share common genetic driver mutations. but can also arise in the bladder or prostate. Phenotypically, Clin Cancer Res; 24(8); 1775–6. Ó2018 AACR. small-cell carcinoma of the bladder (SCCB) shares many simi- See related article by Chang et al., p. 1965 larities with small-cell lung cancer (SCLC). It is unknown whether In this issue of Clinical Cancer Research, Chang and colleagues ponent, suggesting that RB1 and TP53 loss occurs after the initial (1) perform DNA sequencing to characterize the mutational development of the urothelial carcinoma and is required for signature of small-cell carcinoma of the bladder (SCCB). They transdifferentiation from urothelial cancer to SCCB. This is rem- find that both SCCB and small-cell lung cancer (SCLC) harbor iniscent of a similar phenomenon observed in two other tumors near universal loss-of-function mutations in RB1 and TP53.In types: (i) EGFR-mutant lung cancer and (ii) castration-resistant contrast to the smoking mutational signature found in SCLC, prostate cancer, where RB1 and TP53 loss is necessary for the SCCB has an APOBEC mutational signature, a signature also transdifferentiation from an adenocarcinoma to a small-cell neu- found in urothelial carcinoma. Furthermore, they show that SCCB roendocrine tumor. EGFR-mutant lung cancers acquire RB1 loss as and urothelial carcinoma share many common mutations that are a mechanism of resistance to EGFR tyrosine kinase inhibitors (3), distinct from mutations found in SCLC, suggesting that SCCB and castration-resistant prostate cancers acquire RB1 and TP53 may arise from a preexisting urothelial cancer.
    [Show full text]
  • Immunohistochemistry Stain Offerings
    immunohistochemistry stain offerings TRUSTED PATHOLOGISTS. INVALUABLE ANSWERS.™ MARCHMAY 20172021 www.aruplab.com/ap-ihcaruplab.com/ap-ihc InformationInformation in this brochurein this brochure is current is current as of as May of March 2021. 2017. All content All content is subject is subject to tochange. change. Please contactPlease ARUPcontact ClientARUP Services Client Services at 800-522-2787 at (800) 522-2787 with any with questions any questions or concerns.or concerns. ARUP LABORATORIES As a nonprofit, academic institution of the University of Utah and its Department We believe in of Pathology, ARUP believes in collaborating, sharing and contributing to laboratory science in ways that benefit our clients and their patients. collaborating, Our test menu is one of the broadest in the industry, encompassing more sharing and than 3,000 tests, including highly specialized and esoteric assays. We offer comprehensive testing in the areas of genetics, molecular oncology, pediatrics, contributing pain management, and more. to laboratory ARUP’s clients include many of the nation’s university teaching hospitals and children’s hospitals, as well as multihospital groups, major commercial science in ways laboratories, and group purchasing organizations. We believe that healthcare should be delivered as close to the patient as possible, which is why we support that provide our clients’ efforts to be the principal healthcare provider in the communities they serve by offering highly complex assays and accompanying consultative support. the best value Offering analytics, consulting, and decision support services, ARUP provides for the patient. clients with the utilization management tools necessary to prosper in this time of value-based care.
    [Show full text]
  • Neurod1 Regulation of Migration Accompanies the Differential Sensitivity of Neuroendocrine Carcinomas to Trkb Inhibition
    OPEN Citation: Oncogenesis (2013) 2, e63; doi:10.1038/oncsis.2013.24 & 2013 Macmillan Publishers Limited All rights reserved 2157-9024/13 www.nature.com/oncsis ORIGINAL ARTICLE NeuroD1 regulation of migration accompanies the differential sensitivity of neuroendocrine carcinomas to TrkB inhibition JK Osborne1, JE Larsen2, JX Gonzales1, DS Shames2,4, M Sato2,5, II Wistuba3, L Girard1,2, JD Minna1,2 and MH Cobb1 The developmental transcription factor NeuroD1 is anomalously expressed in a subset of aggressive neuroendocrine tumors. Previously, we demonstrated that TrkB and neural cell adhesion molecule (NCAM) are downstream targets of NeuroD1 that contribute to the actions of neurogenic differentiation 1 (NeuroD1) in neuroendocrine lung. We found that several malignant melanoma and prostate cell lines express NeuroD1 and TrkB. Inhibition of TrkB activity decreased invasion in several neuroendocrine pigmented melanoma but not in prostate cell lines. We also found that loss of the tumor suppressor p53 increased NeuroD1 expression in normal human bronchial epithelial cells and cancer cells with neuroendocrine features. Although we found that a major mechanism of action of NeuroD1 is by the regulation of TrkB, effective targeting of TrkB to inhibit invasion may depend on the cell of origin. These findings suggest that NeuroD1 is a lineage-dependent oncogene acting through its downstream target, TrkB, across multiple cancer types, which may provide new insights into the pathogenesis of neuroendocrine cancers. Oncogenesis (2013) 2, e63; doi:10.1038/oncsis.2013.24; published online 19 August 2013 Subject Categories: Cellular oncogenes Keywords: NeuroD1; neuroendocrine; TrkB; migration INTRODUCTION increased expression of NeuroD1, possibly in a lineage-dependent Aberrant expression of basic helix loop helix transcription factors manner.
    [Show full text]
  • Prostate Carcinoma in Transgenic Lewis Rats - a Tumor Model for Evaluation of Immunological Treatments
    Original Article Page 1 of 9 Prostate carcinoma in transgenic Lewis rats - a tumor model for evaluation of immunological treatments Laura E. Johnson, Jordan T. Becker, Jason A. Dubovsky, Brian M. Olson, Douglas G. McNeel University of Wisconsin Carbone Cancer Center, Madison, WI 53705, USA Corresponding to: Douglas G. McNeel. 7007 Wisconsin Institutes for Medical Research, 1111 Highland Avenue, Madison, WI 53705, USA. Email: [email protected]. Abstract: Transgenic rodent models of prostate cancer have served as valuable preclinical models to evaluate novel treatments and understand malignant disease progression. In particular, a transgenic rat autochthonous model of prostate cancer using the SV40 large T antigen expressed under a prostate-specific probasin promoter was previously developed as a model of androgen-dependent prostate cancer (TRAP). In the current report, we backcrossed this strain to the Lewis strain, an inbred rat strain better characterized for immunological analyses. We demonstrate that Lewis transgenic rats (Lew-TRAP) developed prostate adenocarcinomas with 100% penetrance by 25 weeks of age. Tumors were predominantly androgen- dependent, as castration prevented tumor growth in the majority of animals. Finally, we demonstrate that Lew-TRAP rats could be immunized with a DNA vaccine encoding a human prostate tumor antigen (prostatic acid phosphatase) with the development of Lewis strain-specific T-cell responses. We propose that this Lew- TRAP strain, and prostate tumor cell lines derived from this strain, can be used as a future prostate cancer immunotherapy model. Key Words: Lewis rat; transgenic; prostate cancer; vaccine Submitted Nov 09, 2012. Accepted for publication Nov 16, 2012. DOI: 10.3978/j.issn.2304-3865.2012.11.06 Scan to your mobile device or view this article at: http://www.thecco.net/article/view/1210/1922 Introduction is expressed downstream of the prostate-specific probasin promoter (TRAMP, transgenic adenocarcinoma of mouse Prostate cancer remains a worldwide health problem, prostate) (2).
    [Show full text]
  • Synaptophysin Immunoreactivity in Adrenocortical Adenomas
    European Journal of Endocrinology (2009) 161 939–945 ISSN 0804-4643 CLINICAL STUDY Synaptophysin immunoreactivity in adrenocortical adenomas: a correlation between synaptophysin and CYP17A1 expression Kazuto Shigematsu, Noriyuki Nishida1, Hideki Sakai2, Tsukasa Igawa2, Kan Toriyama, Akira Nakatani, Osamu Takahara and Kioko Kawai3 Department of Pathology, Japanese Red-Cross Nagasaki Atomic Bomb Hospital, Nagasaki 852-8511, Japan, 1Divisions of Molecular Microbiology and Immunology, 2Nephro-Urology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan and 3Department of Pathology, Nagasaki Prefecture Medical Health Operation Group, Isahaya 859-0401, Japan (Correspondence should be addressed to K Shigematsu; Email: [email protected]) Abstract Design and methods: The adrenal cortex is not considered to be an intrinsic part of the diffuse neuroendocrine system, but adrenocortical neoplasms possess neuroendocrine properties. In this study, we examined synaptophysin (SYP) and neural cell adhesion molecule (NCAM) expression in adrenocortical adenomas in relation to adrenal function. Results: Immunohistochemical analysis showed that 50.7 and 98.6% of the cortical adenomas showed SYP and NCAM immunoreactivities respectively. There was no apparent difference in NCAM immunoreactivity among the adenomas. However, the immunostaining for SYP was significantly stronger in cortisol-producing adenomas (CPA) than in aldosterone-producing adenomas (APA), nonfunctioning adenomas (NFA), showing no clinical or endocrinological
    [Show full text]
  • Hep Par 1 Expression in Carcinoma of the Cervix: Implications for Diagnosis and Prognosis T P Thamboo, a Wee
    48 ORIGINAL ARTICLE J Clin Pathol: first published as 10.1136/jcp.57.1.48 on 23 December 2003. Downloaded from Hep Par 1 expression in carcinoma of the cervix: implications for diagnosis and prognosis T P Thamboo, A Wee ............................................................................................................................... J Clin Pathol 2004;57:48–53 Aims: To determine the frequency and pattern of Hep Par 1 expression in cervical carcinomas of various histological types and to correlate expression with prognostic parameters. Methods: Twenty nine cervical carcinomas were analysed for tumour type, hepatoid and neuroendocrine See end of article for differentiation, and vascular invasion. A semiquantitative analysis was performed for Hep Par 1, authors’ affiliations ....................... a fetoprotein, chromogranin, and synaptophysin immunoreactivity. Results: Hep Par 1 expression was seen in seven of the 29 cervical carcinomas (three of seven Correspondence to: adenocarcinomas, one of 17 squamous cell carcinomas, one of two adenocarcinomas with Dr T P Thamboo, Department of Pathology, adenocarcinoma in situ, one of two adenocarcinomas in situ, and one of one large cell neuroendocrine National University of carcinoma with adenocarcinoma in situ). Normal looking endocervical epithelium was also positive in one Singapore, National case. Cases expressing Hep Par 1, with or without neuroendocrine coexpression, were associated with a University Hospital, 5 higher rate of vascular invasion and a worse prognosis. Three of the five cases expressing neuroendocrine Lower Kent Ridge Road, Singapore 119074, markers also coexpressed Hep Par 1. Republic of Singapore; Conclusions: Hep Par 1 expression in carcinoma of the cervix is not uncommon and is present in a variety [email protected] of histological types.
    [Show full text]
  • Organization and Reorganization of Neuromuscular Junctions in Mice Lacking Neural Cell Adhesion Molecule, Tenascin-C, Or Fibroblast Growth Factor-5
    The Journal of Neuroscience, February 15, 1998, 18(4):1465–1477 Organization and Reorganization of Neuromuscular Junctions in Mice Lacking Neural Cell Adhesion Molecule, Tenascin-C, or Fibroblast Growth Factor-5 Lisa M. Moscoso,1 Harold Cremer,2 and Joshua R. Sanes1 1Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110, and 2Developmental Biology Institute of Marseille, Campus de Luminy Case 907, 13288 Marseille Cedex 9, France Many proteins have been hypothesized to mediate intercellular mutant. In all other respects tested, however, the structure and interactions that regulate the formation, maturation, and main- molecular architecture of neuromuscular junctions were normal tenance of the skeletal neuromuscular junction. Three of the in all three single mutants and in the double mutant. We also best characterized of these are a membrane-associated adhe- tested the abilities of damaged motor axons to reinnervate sion molecule, neural cell adhesion molecule (N-CAM), an ex- mutant muscle after axotomy and of intact motor axons to tracellular matrix component, tenascin-C, and a soluble growth sprout after partial denervation. Again, no significant differ- factor, fibroblast growth factor-5 (FGF-5). To assess the roles of ences among genotypes were observed. Together, these re- these molecules in synaptogenesis in vivo, we examined neu- sults demonstrate that N-CAM, tenascin-C, and FGF-5 are romuscular junctions in homozygous mutant mice lacking dispensable for major aspects of synaptic
    [Show full text]