Labinvest201321.Pdf

Total Page:16

File Type:pdf, Size:1020Kb

Labinvest201321.Pdf 190A ANNUAL MEETING ABSTRACTS Sensitivity, specificity, positive/negative predictive value, and the odds ratio of the SCC (0/33) by FISH. No difference of overall survival time was observed between 2 markers were summarized in Table 1. There was no difference in p16 expression amplified and non-amplified groups in EAC patients. between the DG and control group. Conclusions: ALK amplification was present in 7% of EAC cases, but ALK Table 1. Summary of sensitivity, specificity, PPV, NPV, and OR. rearrangement and expression was not present. No ALK amplification, rearrangement Sensitivity (%) Specificity (%) PPV (%) NPV (%) OR and expression were detected in SCC. ALK amplification is not associated with EAC beta-catenin 92.3 76.9 80.0 90.9 40.0 patients’ overall survival. c-met 69.2 61.5 64.3 66.7 3.6 Either 100.0 53.8 68.4 100.0 13.9* Both 61.5 92.3 88.9 70.6 19.2 785 Mitosis-Specific Marker PHH3 Immunostain Is a More Sensitive NPV, negative predictive value; PPV, positive predictive value; OR, odds ratio. *, estimated OR. and Efficient Method To Evaluate the Mitotic Activity in Gastrointestinal Conclusions: The combination of c-met and beta-catenin provides a relatively specific Stromal Tumor (GIST) panel to identify patients with BE who are at increased risk for future development S Zhu, F Lin, ZE Chen. Geisinger Medical Center, Danville, PA. of dysplasia. Background: Mitotic activity is an important prognostic factor in GIST. The accurate identification of mitotic figures on the H&E stained slides could be challenging due to 783 Microfibrillar Associated Protein 5 (MFAP 5): A Marker for processing artifact, degeneration, apoptosis, or lymphocytic infiltration. Mitosis-specific Desmoplasia That Facilitates the Distinction between an Invasive marker PHH3 was proven as a sensitive and reliable method to assess the mitotic activity Component and Pseudoinvasion in Colonic Adenomas in various tumors. The aim of the current study was to compare the PHH3-stained mitotic L Zhao, T Antic, S-Y Xiao, C VanSlambrouck, J Hart. University of Chicago, Chicago, IL. counts and the time for counting on immunostained slides with the mitotic counts and & Background: Distinction between invasive adenocarcinoma and submucosal the time for counting on H E stained slides in GIST. & displacement of adenomatous mucosa in colonic polyps can be problematic in clinical Design: Immunohistochemical stain for PHH3 and routine H E staining were practice. Recent microarray studies have demonstrated that tumor stroma exhibits performed on 45 cases (41 non-malignant and 4 malignant at the time of sampling) of & reproducible gene-expression changes compared to normal stromal tissue. MFAP5, a 25- GIST. The mitotic counts were assessed on both immunostaining slides and H E stained kD glycoprotein that is involved in elastic microfibril assembly, has been demonstrated slides. The PHH3-stained mitotic counts were compared to the mitotic counts on the & to be significantly down regulated in tumorous stroma [Jia et al. Cancer Res 2011]. H E stained slides. The time to count the mitosis by two methods was recorded too. & The aim of this study is to confirm the reduced expression of MFAP5 in tumor stroma Results: For 41 non-malignant GIST cases, the mean mitotic count on the H E by immunohistochemistry and evaluate the utility of MFAP5 as a diagnostic marker. stained slides was 1.9 per 50 high power fields and the mean PHH-stained mitotic Design: An immunohistochemical stain for MFAP 5 (Sigma) was first performed on count was 4.9 (p < 0.001) per 50 high power fields. For 4 malignant GIST cases, the & ten invasive colon cancer resection specimens to compare the its expression pattern in mean mitotic count on the H E stained slides was 47.5 per 50 high power fields and invasive tumor and in the surrounding lamina propria and submucosa. Then a total of the mean PHH-stained mitotic count was 90 per 50 high power fields. The mean time & 24 diagnostically challenging adenomatous polypectomy specimens (6 with an invasive to count the mitotic figures for 50 high power fields on the H E stained slides was 2 focus and 18 with pseudoinvasion) were used to evaluate the diagnostic value of MFAP5. minutes and 50 seconds. The mean time to count the PHH3-stained mitotic figures for Results: In all 10 colon cancer resection cases there was no reactivity in the 50 high power fields was 40 seconds (p < 0.001). desmoplastic stroma surrounding the invasive component, while the uninvolved Conclusions: PHH3 immunostain is a more sensitive and efficient method to evaluate lamina propria and submucosa exhibited strong diffuse reactivity in stromal cells. the mitotic activity in GIST. The malignant GISTs demonstrate significant higher mitotic counts by both PHH3 immunostain and H&E stained slides. 786 Etiology and Histomorphology of Esophagogastric Junction Intramucosal Adenocarcinoma (IMC): In Comparison to Esophageal IMC H Zhu, Z Li, H Xie, TW Rice, LA Rybicki, JR Goldblum, X Liu. Cleveland Clinic Foundation, Cleveland, OH; Second Military Medical University, Shanghai, China. Background: While it is clear Barrett Esophagus (BE) predisposes to esophageal adenocarcinoma, controversy exists regarding the etiology of esophagogastric junction (EGJ) adenocarcinoma. The aim of this study is to evaluate the clinical and pathologic features of EGJ IMC and compare them to IMC of the distal esophagus, as these tumors are smaller than more deeply invasive ones and allow for a better comparison of the In 16 out of 18 polypectomy specimens with pseudoinvasion, strong reactivity was surrounding mucosal changes which are often obscured by larger tumors. preserved in the stroma surrounding the displaced adenomatous mucosa (left panel of Design: 149 cases of IMC from an esophagectomy database (1983 – 2010) were figure below). Lack of staining in the stroma surrounding small foci of invasive tumor identified by reviewing medical charts and slides from these resection specimens. was observed in all 6 malignant polyps (right panel of figure below). Clinicopathologic features were compared between IMC arising in the esophagus versus EGJ. Results: Of these 149 cases; 54 cases (36.2%) were EGJ and 95 (63.7%) were esophageal IMC. Mean age and gender were not significantly different between these two groups [(61.8 yrs vs. 64.7, p=0.12; 92.6% male vs. 83.2%, p=0.14)]. Hiatal hernia was present in 87.5% and 90.5% of EGJ and esophageal IMC (p=0.51); hiatal hernia length was shorter in patients with EGJ IMC [median: 3 cm vs. 4 cm, p = 0.007)]. Compared with esophageal IMC, intestinal metaplasia (IM) in the esophagus was absent in 8 of 54 EGJ IMC (14.8% vs. 0%, p<0.001) and lack of dysplasia in IM of the esophagus was noted in patients with EGJ IMC (18.8% vs. 4.2%, p=0.012). Tumor histomorphologic features including macroscopic abnormalities, focality, size, depth of invasion, grade, Conclusions: MFAP5 is a useful marker to demonstrate tumor associated desmoplastic and lymphovascular invasion were similar. Both EGJ and esophageal IMC had low rates stromal proliferation. It facilitates the distinction between pseudoinvasion and true of nodal metastasis (0% and 1.1%). Of the 8 EGJ IMC patients without esophageal IM, invasive cancer in colonic adenomatous polyps with high sensitivity and specificity. 3 had long-standing GERD, 3 had cardia/EGJ IM associated with chronic gastritis (2) and reflux (1), 1 had a clinical history of familial adenomatous polyposis (FAP), and 1 had no apparent gastric or esophageal diseases. 784 ALK Status in Esophageal Adenocarcinoma and Squamous Conclusions: Similar to esophageal IMC, most EGJ IMC arise in patients with reflux Carcinoma Studied by DNA Microarray, FISH and Immunohistochemistry disease and intestinal metaplasia with hiatal hernia, but hiatal hernias were shorter Z Zhou, S Bandla, J Ye, L Li, T Godfrey, N Wang. University of Rochester Medical compared with esophageal IMC patients. About 7.5% EGJ IMC occurred in patients Center, Rochester, NY. without GERD and may be associated with H. pylori infection or genetic predilection. Background: The anaplastic lymphoma kinase (ALK) gene encodes a tyrosine kinase Our study supports the current view that EGJ and esophageal IMC in the USA share receptor that belongs to the insulin receptor superfamily. The 3’-tyrosine kinase domain similar etiology, tumor morphology and clinical behavior. is fused to a variety of partners such as NPM-ALK or EML4-ALK leading to express fusion proteins that play oncogenic roles in a variety of malignancies. Using mass spectroscopy alone, TPM4-ALK fusion protein was detected in esophageal squamous cell carcinoma (SCC). To verify the possible role of ALK in SCC and esophageal Genitourinary adenocarcinoma (EAC), we use different approaches to study ALK gene arrangement, amplification or expression. 787 “More Cocktails, More Cancer”; Do Pathologists Who Use Design: Genomic DNA from 116 EAC (95 M and 21 F) fresh tissue was analyzed Immunohistochemistry More Frequently on Prostate Biopsies, Diagnose for copy number aberrations using Affymetrix SNP 6.0 arrays. Tissue microarrays Prostate Cancer More Frequently? constructed at the University of Rochester between 1997 and 2005 included squamous S Al Diffalha, W Roquiz, GA Barkan, EM Wojcik, MM Picken, SE Pambuccian. Loyola mucosa (SE), EAC and SCC. ALK amplification and rearrangement were detected by University Chicago, Maywood, IL. FISH and ALK expression was tested by immunohistochemistry (IHC). Background: Atypical small acinar proliferations (ASAP), found in 1.5-5% of all Results: By genomic analysis, ALK amplification was found in 7% (8/116) EAC frozen prostate biopsies, are very small foci of atypical glands (usually <10 glands and <0.5 mm), tissue cases by SNP analysis which was confirmed by FISH test in TMA cases (7%; which show no definite histologic features of malignancy and cannot be reproducibly 5/74).
Recommended publications
  • Potential High-Impact Interventions Report Priority Area 02: Cancer
    AHRQ Healthcare Horizon Scanning System – Potential High-Impact Interventions Report Priority Area 02: Cancer Prepared for: Agency for Healthcare Research and Quality U.S. Department of Health and Human Services 540 Gaither Road Rockville, MD 20850 www.ahrq.gov Contract No. HHSA290201000006C Prepared by: ECRI Institute 5200 Butler Pike Plymouth Meeting, PA 19462 December 2012 Statement of Funding and Purpose This report incorporates data collected during implementation of the Agency for Healthcare Research and Quality (AHRQ) Healthcare Horizon Scanning System by ECRI Institute under contract to AHRQ, Rockville, MD (Contract No. HHSA290201000006C). The findings and conclusions in this document are those of the authors, who are responsible for its content, and do not necessarily represent the views of AHRQ. No statement in this report should be construed as an official position of AHRQ or of the U.S. Department of Health and Human Services. This report’s content should not be construed as either endorsements or rejections of specific interventions. As topics are entered into the System, individual topic profiles are developed for technologies and programs that appear to be close to diffusion into practice in the United States. Those reports are sent to various experts with clinical, health systems, health administration, and/or research backgrounds for comment and opinions about potential for impact. The comments and opinions received are then considered and synthesized by ECRI Institute to identify interventions that experts deemed, through the comment process, to have potential for high impact. Please see the methods section for more details about this process. This report is produced twice annually and topics included may change depending on expert comments received on interventions issued for comment during the preceding 6 months.
    [Show full text]
  • Glycosylation: Rising Potential for Prostate Cancer Evaluation
    cancers Review Glycosylation: Rising Potential for Prostate Cancer Evaluation Anna Kałuza˙ * , Justyna Szczykutowicz and Mirosława Ferens-Sieczkowska Department of Chemistry and Immunochemistry, Wroclaw Medical University, Sklodowskiej-Curie 48/50, 50-369 Wroclaw, Poland; [email protected] (J.S.); [email protected] (M.F.-S.) * Correspondence: [email protected]; Tel.: +48-71-770-30-66 Simple Summary: Aberrant protein glycosylation is a well-known hallmark of cancer and is as- sociated with differential expression of enzymes such as glycosyltransferases and glycosidases. The altered expression of the enzymes triggers cancer cells to produce glycoproteins with specific cancer-related aberrations in glycan structures. Increasing number of data indicate that glycosylation patterns of PSA and other prostate-originated proteins exert a potential to distinguish between benign prostate disease and cancer as well as among different stages of prostate cancer development and aggressiveness. This review summarizes the alterations in glycan sialylation, fucosylation, truncated O-glycans, and LacdiNAc groups outlining their potential applications in non-invasive diagnostic procedures of prostate diseases. Further research is desired to develop more general algorithms exploiting glycobiology data for the improvement of prostate diseases evaluation. Abstract: Prostate cancer is the second most commonly diagnosed cancer among men. Alterations in protein glycosylation are confirmed to be a reliable hallmark of cancer. Prostate-specific antigen is the biomarker that is used most frequently for prostate cancer detection, although its lack of sensitivity and specificity results in many unnecessary biopsies. A wide range of glycosylation alterations in Citation: Kałuza,˙ A.; Szczykutowicz, prostate cancer cells, including increased sialylation and fucosylation, can modify protein function J.; Ferens-Sieczkowska, M.
    [Show full text]
  • PROPOSED REGULATION of the STATE BOARD of HEALTH LCB File No. R057-16
    PROPOSED REGULATION OF THE STATE BOARD OF HEALTH LCB File No. R057-16 Section 1. Chapter 457 of NAC is hereby amended by adding thereto the following provision: 1. The Division may impose an administrative penalty of $5,000 against any person or organization who is responsible for reporting information on cancer who violates the provisions of NRS 457. 230 and 457.250. 2. The Division shall give notice in the manner set forth in NAC 439.345 before imposing any administrative penalty 3. Any person or organization upon whom the Division imposes an administrative penalty pursuant to this section may appeal the action pursuant to the procedures set forth in NAC 439.300 to 439. 395, inclusive. Section 2. NAC 457.010 is here by amended to read as follows: As used in NAC 457.010 to 457.150, inclusive, unless the context otherwise requires: 1. “Cancer” has the meaning ascribed to it in NRS 457.020. 2. “Division” means the Division of Public and Behavioral Health of the Department of Health and Human Services. 3. “Health care facility” has the meaning ascribed to it in NRS 457.020. 4. “[Malignant neoplasm” means a virulent or potentially virulent tumor, regardless of the tissue of origin. [4] “Medical laboratory” has the meaning ascribed to it in NRS 652.060. 5. “Neoplasm” means a virulent or potentially virulent tumor, regardless of the tissue of origin. 6. “[Physician] Provider of health care” means a [physician] provider of health care licensed pursuant to chapter [630 or 633] 629.031 of NRS. 7. “Registry” means the office in which the Chief Medical Officer conducts the program for reporting information on cancer and maintains records containing that information.
    [Show full text]
  • N35.12 Postinfective Urethral Stricture, NEC, Female N35.811 Other
    N35.12 Postinfective urethral stricture, NEC, female N35.811 Other urethral stricture, male, meatal N35.812 Other urethral bulbous stricture, male N35.813 Other membranous urethral stricture, male N35.814 Other anterior urethral stricture, male, anterior N35.816 Other urethral stricture, male, overlapping sites N35.819 Other urethral stricture, male, unspecified site N35.82 Other urethral stricture, female N35.911 Unspecified urethral stricture, male, meatal N35.912 Unspecified bulbous urethral stricture, male N35.913 Unspecified membranous urethral stricture, male N35.914 Unspecified anterior urethral stricture, male N35.916 Unspecified urethral stricture, male, overlapping sites N35.919 Unspecified urethral stricture, male, unspecified site N35.92 Unspecified urethral stricture, female N36.0 Urethral fistula N36.1 Urethral diverticulum N36.2 Urethral caruncle N36.41 Hypermobility of urethra N36.42 Intrinsic sphincter deficiency (ISD) N36.43 Combined hypermobility of urethra and intrns sphincter defic N36.44 Muscular disorders of urethra N36.5 Urethral false passage N36.8 Other specified disorders of urethra N36.9 Urethral disorder, unspecified N37 Urethral disorders in diseases classified elsewhere N39.0 Urinary tract infection, site not specified N39.3 Stress incontinence (female) (male) N39.41 Urge incontinence N39.42 Incontinence without sensory awareness N39.43 Post-void dribbling N39.44 Nocturnal enuresis N39.45 Continuous leakage N39.46 Mixed incontinence N39.490 Overflow incontinence N39.491 Coital incontinence N39.492 Postural
    [Show full text]
  • Genitourinary Pathology (Including Renal Tumors)
    LABORATORY INVESTIGATION THE BASIC AND TRANSLATIONAL PATHOLOGY RESEARCH JOURNAL LI VOLUME 99 | SUPPLEMENT 1 | MARCH 2019 2019 ABSTRACTS GENITOURINARY PATHOLOGY (INCLUDING RENAL TUMORS) (776-992) MARCH 16-21, 2019 PLATF OR M & 2 01 9 ABSTRACTS P OSTER PRESENTATI ONS EDUCATI ON C O M MITTEE Jason L. Hornick , C h air Ja mes R. Cook R h o n d a K. Y a nti s s, Chair, Abstract Revie w Board S ar a h M. Dr y and Assign ment Co m mittee Willi a m C. F a q ui n Laura W. La mps , Chair, C ME Subco m mittee C ar ol F. F ar v er St e v e n D. Billi n g s , Interactive Microscopy Subco m mittee Y uri F e d ori w Shree G. Shar ma , Infor matics Subco m mittee Meera R. Ha meed R aj a R. S e et h al a , Short Course Coordinator Mi c h ell e S. Hir s c h Il a n W ei nr e b , Subco m mittee for Unique Live Course Offerings Laksh mi Priya Kunju D a vi d B. K a mi n s k y ( Ex- Of ici o) A n n a M ari e M ulli g a n Aleodor ( Doru) Andea Ri s h P ai Zubair Baloch Vi nita Parkas h Olca Bast urk A nil P ar w a ni Gregory R. Bean , Pat h ol o gist-i n- Trai ni n g D e e p a P atil D a ni el J.
    [Show full text]
  • Variants of Acinar Adenocarcinoma of the Prostate Mimicking Benign Conditions Peter a Humphrey
    Modern Pathology (2018) 31, S64–S70 S64 © 2018 USCAP, Inc All rights reserved 0893-3952/18 $32.00 Variants of acinar adenocarcinoma of the prostate mimicking benign conditions Peter A Humphrey Department of Pathology, Yale School of Medicine, New Haven, CT, USA Histological variants of acinar adenocarcinoma of the prostate may be of significance due to difficulty in diagnosis or due to differences in prognosis compared to usual acinar adenocarcinoma. The 2016 World Health Organization classification of acinar adenocarcinoma includes four variants that are deceptively benign in histological appearance, such that a misdiagnosis of a benign condition may be made. These four variants are atrophic pattern adenocarcinoma, pseudohyperplastic adenocarcinoma, microcystic adenocarcinoma, and foamy gland adenocarcinoma. They differ from usual small acinar adenocarcinoma in architectural glandular structure and/or cytoplasmic and nuclear alterations. The variants are often admixed, in variable proportions, with usual small acinar adenocarcinoma that is often Gleason pattern 3 but may be high-grade pattern 4 in a minority of cases. Atrophic pattern adenocarcinoma can be identified in a sporadic setting or after radiation or hormonal therapy. This variant is characterized by cytoplasmic volume loss and can resemble benign glandular atrophy, an extremely common benign process in the prostate. The glands of pseudohyperplastic adenocarcinoma simulate usual epithelial hyperplasia, with gland complexity that is not typical of small acinar adenocarcinoma. These complex growth configurations include papillary infoldings, luminal undulations, and branching. Microcystic adenocarcinoma is characterized by cystic dilation of prostatic glands to a size that is much more commonly observed in cystic change in benign prostatic glands. Finally, the cells in foamy gland adenocarcinoma display cytoplasmic vacuolization and nuclear pyknosis, features that can found in benign glands and macrophages.
    [Show full text]
  • Supplementary Table 1) Immunohistochemical Protocol and Antibody Information Antibody Company Clone/# Clonality Dilution Incubat
    H. Reis et al: Differential proteomic and tissue expression analyses identify valuable diagnostic biomarkers of hepatocellular differentiation and hepatoid adenocarcinomas Suppl ementary Table 1) Immunohistochemical protocol and antibody information Antibody Company Clone/# Clonality Dilution Incubation Antigen retrieval Detection ABAT Abcam EPR4433 mono 1/3000 30 min, RT pH 9.0, WB, 95°C, 20 min. Zytomed Polymer HRP ACAA2 Abcam EPR6733 mono 1/100 30 min, RT pH 9.0, WB, 95°C, 20 min Zytomed Polymer HRP ACADM Abcam EPR3708 mono 1/3000 30 min, RT pH 9.0, WB, 95°C, 20 min Zytomed Polymer HRP ADH1B Abcam 4F12 mono 1/12.000 30 min, RT pH 9.0, WB, 95°C, 20 min Zytomed Polymer HRP Arginase1 Abcam EPR6672(B) mono 1/1000 30 min, RT pH 9.0, WB, 95°C, 20 min. Zytomed Polymer HRP BHMT Abcam EPR6782 mono 1/100 30 min, RT pH 9.0, WB, 95°C, 20 min. Zytomed Polymer HRP FABP1 Acris AIV\09011PU-S mono 1/15.000 30 min, RT pH 9.0, WB, 95°C, 20 min. Zytomed Polymer HRP HAOX1 Acris AP18044PU-N poly 1/100 30 min, RT pH 9.0, WB, 95°C, 20 min. Zytomed Polymer HRP HepPar1 Dako OCH1E5 mono 1/800 30 min, RT pH 9.0, WB, 95°C, 20 min. Zytomed Polymer HRP HMGCS2 Abcam Ab104807 poly 1/50 60 min, RT pH 9.0, WB, 95°C, 20 min Zytomed Polymer HRP H. Reis et al: Differential proteomic and tissue expression analyses identify valuable diagnostic biomarkers of hepatocellular differentiation and hepatoid adenocarcinomas Supplementary Table 2) Composition of the non-liver tumor TMA Diagnosis n % ADC 11 2.9 ADC Adenocarcinoma of the lung Carc.
    [Show full text]
  • 1 Effective January 1, 2018 ICD‐O‐3 Codes, Behaviors and Terms Are Site‐Specific Alpha Order Last Updat
    Effective January 1, 2018 ICD‐O‐3 codes, behaviors and terms are site‐specific Alpha Order Last updated 8/22/18 Status ICD‐O‐3 Term Reportable Comments Morphology Y/N Code New Term 8551/3 Acinar adenocarcinoma (C34. _) Y Lung primaries diagnosed prior to 1/1/2018 use code 8550/3 For prostate (all years) see 8140/3 New Term 8140/3 Acinar adenocarcinoma (C61.9 ONLY) Y For prostate only, do not use 8550/3 New Term 8572/3 Acinar adenocarcinoma, sarcomatoid (C61.9) Y New Term 8550/3 Acinar cell carcinoma Y Excludes C61.9‐ see 8140/3 New Term 8316/3 Acquired cystic disease‐associated renal cell carcinoma (RCC) Y (C64.9) New 8158/1 ACTH‐producing tumor N code/term New Term 8574/3 Adenocarcinoma admixed with neuroendocrine carcinoma (C53. _) Y Behavior 8253/2 Adenocarcinoma in situ, mucinous (C34. _) Y Important note: lung Code/term primaries ONLY: For cases diagnosed 1/1/2018 forward do not use code 8480 (mucinous adenocarcinoma) for in‐ situ adenocarcinoma, mucinous or invasive mucinous adenocarcinoma. 1 Status ICD‐O‐3 Term Reportable Comments Morphology Y/N Code Behavior 8250/2 Adenocarcinoma in situ, non‐mucinous (C34. _) Y code/term New Term 9110/3 Adenocarcinoma of rete ovarii (C56.9) Y New 8163/3 Adenocarcinoma, pancreatobiliary‐type (C24.1) Y Cases diagnosed prior to code/term 1/1/2018 use code 8255/3 Behavior 8983/3 Adenomyoepithelioma with carcinoma (C50. _) Y Code/term New Term 8620/3 Adult granulosa cell tumor (C56.9 ONLY) N Not reportable for 2018 cases New Term 9401/3 Anaplastic astrocytoma, IDH‐mutant (C71.
    [Show full text]
  • Development and Clinical Testing of Individual Immunoassays for the Quantification of Serum Glycoproteins to Diagnose Prostate Cancer
    RESEARCH ARTICLE Development and clinical testing of individual immunoassays for the quantification of serum glycoproteins to diagnose prostate cancer Kathrin Endt1, Jens Goepfert2, Aurelius Omlin3, Alcibiade Athanasiou1, Pierre Tennstedt4, Anna Guenther2, Maurizio Rainisio5, Daniel S. Engeler3, Thomas Steuber4, Silke Gillessen3, Thomas Joos2, Ralph Schiess1* a1111111111 a1111111111 1 ProteoMediX Inc., Schlieren, Switzerland, 2 NMI TuÈbingen, Reutlingen, Germany, 3 Cantonal Hospital St. Gallen, St. Gallen, Switzerland, 4 Martini-Klinik, Hamburg-Eppendorf, Germany, 5 Abanovus LLC, a1111111111 Sanremo, Italy a1111111111 a1111111111 * [email protected] Abstract OPEN ACCESS Prostate Cancer (PCa) diagnosis is currently hampered by the high false-positive rate of Citation: Endt K, Goepfert J, Omlin A, Athanasiou PSA evaluations, which consequently may lead to overtreatment. Non-invasive methods A, Tennstedt P, Guenther A, et al. (2017) with increased specificity and sensitivity are needed to improve diagnosis of significant Development and clinical testing of individual immunoassays for the quantification of serum PCa. We developed and technically validated four individual immunoassays for cathepsin glycoproteins to diagnose prostate cancer. PLoS D (CTSD), intercellular adhesion molecule 1 (ICAM1), olfactomedin 4 (OLFM4), and throm- ONE 12(8): e0181557. https://doi.org/10.1371/ bospondin 1 (THBS1). These glycoproteins, previously identified by mass spectrometry journal.pone.0181557 using a Pten mouse model, were measured in clinical serum samples for testing the capabil- Editor: Salvatore V Pizzo, Duke University School ity of discriminating PCa positive and negative samples. The development yielded 4 individ- of Medicine, UNITED STATES ual immunoassays with inter and intra-variability (CV) <15% and linearity on dilution of the Received: March 8, 2017 analytes. In serum, ex vivo protein stability (<15% loss of analyte) was achieved for a dura- Accepted: July 3, 2017 tion of at least 24 hours at room temperature and 2 days at 4ÊC.
    [Show full text]
  • Prostate Prostate Cancer Overview and Recent Advances: Overview
    Prostate Cancer Overview and Recent Advances: How Can a Common Disease Be So Controversial? Howard I. Scher, M.D. D. Wayne Calloway Chair in Urologic Oncology Chie f, Gen itouri nary Oncol ogy Servi ce Memorial Sloan-Kettering Cancer Center March 27, 2010 Prostate Cancer Overview and Recent Advances: How Can a Common Disease Be So Controversial? 1. The statistics : The pendulum is swinging. 2. A framework: 3. Risk adapted diagnostics: 4. Risk adapted prognostics to guide treatment: Page 1 2009 Cancer Statistics Estimated New Cases Estimated Deaths Jemal A, et al. CA Cancer J Clin. 2009;59:225-249. Cancer Incidence and Mortality Rates age adjusted, standardized over time Thun MJ et al. Cancer Statistics 2009. CA Cancer J Clin2009;59;225. Page 2 In an Aging Population, the Implications of “Detecting” And “Diagnosing” All Prostate Cancers Is Clear From Scardino and Kelman. Dr. Peter Scardino’s Prostate Book. Avery Press, 2005 (www.theprostatebook.com) The prostate produces seminal fluid that protects sperm. External Urinary Sphincter From Scardino and Kelman. Avery Press, 2005 (www.theprostatebook.com) Page 3 The Disease Usually Starts in the Peripheral Zone and is Often Multifocal, That May Limit the Role for Therapies That Do Not Treat the Whole Gland From Scardino and Kelman. Dr. Peter Scardino’s Prostate Book. Avery Press, 2005 (www.theprostatebook.com) Screening, Early Detection and Diagnosis: The Harder You Look, the More You Will Find From Scardino and Kelman. The Prostate Book. Avery Press, 2005 (www.theprostatebook.com) Page 4 TNM Staging 1. Characterizes disease at the time of diagnosis: Localized disease: TNM (+PSA) 2.
    [Show full text]
  • Predicting Prostate Biopsy Outcome Using a PCA3-Based Nomogram in a Polish Cohort
    ANTICANCER RESEARCH 33: 553-558 (2013) Predicting Prostate Biopsy Outcome Using a PCA3-based Nomogram in a Polish Cohort MACIEJ SALAGIERSKI1, PETER MULDERS2 and JACK A. SCHALKEN2 1Urology Department, Medical University of Łódź, Poland; 2Department of Urology, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands Abstract. Background: Prostate Cancer Gene-3 (PCA3) is prostate tissues (1). As a consequence, the PCA3 gene, being highly prostate cancer (PCa)-specific and its application highly overexpressed in specific PCa cell lines and prostatic holds promise in identifying men with PCa. Aim: To tumors, constitutes today the most PCa-specific marker (2). determine whether the PCA3 score can be used relative to The urine Progensa PCA3 test (Gen-Probe, San Diego, PCa clinical variables to predict biopsy outcome. Patients CA, USA) has been clinically available since 2006. The and Methods: PCA3 scores were assessed in a group of 80 Progensa PCA3 assay is a non-invasive and highly specific patients using the Progensa assay (Gen-Probe, San Diego, test, which measures the expression of the PCA3 gene and CA, USA). The logistic regression algorithm was used to PSA mRNA concentrations in post-DRE urine. In many combine PCA3 results with the established biopsy risk factors studies, the PCA3 test was superior to PSA for the early including: age, prostate-specific antigen (PSA), digital rectal detection of PCa. The assay has been shown to be examination (DRE) and prostate volume (Pvol). Results: In particularly useful in patients with a previous negative univariate analyses, the Progensa PCA3 score outperformed biopsies and persistently elevated PSA levels (3, 4).
    [Show full text]
  • December 2020 E-Tips Solid Tumor Rules
    New Jersey State Cancer Registry December 2020 E-Tips Cancer Epidemiology Services http://www.nj.gov/health/ces (609) 633-0500 Solid Tumor Rules: December 2020 Update ICD-0-3.2 changes have also been added to applicable site modules. Most changes are minor: terminology, additional definitions, new notes and examples. In order to clarify histology coding instructions, new rules have been added and histology tables updated. These updates do not require review of already abstracted cases. The December 2020 rules replace the current rules and should be used now. SEER Strongly recommends reading the December 2020 Change Log to understand what changes were made. The updated Solid Tumor Rules may be accessed at: https://seer.cancer.gov/tools/solidtumor/ Reportability Changes for 2021 Radiation Coding Total Dose (1533) Starting 01/01/2021 the following terms are reportable: If doses across phases to a single point of region, code Sum of all phases. ** (see 2019 update below) Early or evolving melanoma in situ, or any other early or If doses are to multiple metastatic sites, code highest evolving melanoma, are reportable. dose site. If doses are to primary site and metastatic site, code dose All GIST tumors are reportable and classified as 8936/3 in from the primary site only. ICD-O-3.2. When you have two different sites, you cannot add the Nearly all thymomas are reportable; the exceptions are doses together to get the total dose. microscopic thymoma or thymoma benign (8580/0), micronodular thymoma with lymphoid stroma (8580/1), Radiation Tips and updates for 2019 and ectopic hamartomatous thymoma (8587/0).
    [Show full text]