DOCSLIB.ORG

Genitourinary Pathology (Including Renal Tumors)

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read 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. Br at K wun Wah Wen , Pat h ol o gist-i n- Trai ni n g Ashley M. Ci mino- Mathe ws ABSTRACT REVIE W B OARD Benja min Ada m Ta mara Giorgadze Ta mara Lotan Steven Salvatore Mi c h ell e Af k h a mi Raul Gonzalez Anthony Magliocco Souzan Sanati Narasi mhan ( Narsi) Agara m Purva Gopal Kr uti M a ni ar Sandro Santagata R o u b a Ali- F e h mi Anuradha Gopalan Jonathan Marotti A nj ali S a qi G h a s s a n All o Jennifer Gordetsky E mil y M a s o n Frank Schneider Isabel Alvarado- Cabrero Rondell Graha m Jerri McLe more Jeanne Shen C hristi na Ar n ol d Alejandro Gru Bruce Mc Manus Ji a qi S hi Rohit Bhargava Nil e s h G u pt a David Meredith Wun-Ju Shieh Justin Bishop Ma mta Gupta A n n e Mill s G a bri el Si c a Jennifer Boland Kriszti na Ha nley Neda Moata med D e e pi k a Sir o hi Ele na Brac htel Douglas Hart man Sara Monaco K alli o pi Si zi o pi k o u M aril y n B ui Yael He her Atis Muehlenbachs Lauren S mith S helley Calt har p Walter He nricks Bit a N ai ni Sara Szabo Joanna Chan J o h n Hi g gi n s Di a n n a N g J ulie Ter uya-Fel dstei n Jennifer Chap man M ai H o a n g Tony Ng Gaetano Thiene H ui C h e n M oj g a n H o s s ei ni Ericka Ol gaar d Khin Th way Yi n g b ei C h e n Aaron Huber Jac q ueli ne Parai Rash mi Tondon Benja min Chen P et er Ill ei Yan Peng Jose Torrealba Rebecca Chernock D oi n a I v a n D a vi d Pi s a pi a E vi V a ki a ni Bet h Clark W ei Ji a n g Alexandros Polydorides Christopher VandenBussche Ja mes Conner Vi c ki e J o Sona m Prakash Sonal Var ma Alejandro Contreras Kirk J o nes Manju Prasad E n di W a n g Cla u di u C otta Neerja Ka mbha m Peter Pytel Christopher Weber Ti mothy D’ Alfonso Chiah Sui ( Sunny) Kao Joseph Rabban Olga Weinberg Farbod Darvishian Dipti Kara mchandani Stanley Radio Sara Wobker Jessica Davis Darcy Kerr E mad Rakha Mi n a X u Heather Da wson Ashraf Khan Preetha Ra malinga m Shaofeng Yan Elizabeth De micco Rebecca King Pri y a R a o A nj a n a Y el d a n di Suzanne Dintzis Mi c h a el Kl u k Robyn Reed A ki hi k o Y o s hi d a Mi c h ell e D o w n e s Kristine Konopka Mi c h ell e R ei d Gl ori a Y o u n g D a ni el D y e Gre g or Kri n gs Natasha Rekht man Minghao Zhong Andre w Evans Asangi Ku marapeli Mi c h a el Ri v er a Y a oli n Z h o u Mi c h a el F e el y Alvaro Laga Mi c h a el R o h Hongfa Zhu De n nis Firc ha u Cheng- Han Lee Andres Ro ma Debra Zynger Larissa F urta d o Z ai b o Li Avi Rosenberg A nt h o n y Gill H ai y a n Li u Est her ( Dia na) R ossi R y a n Gill Xi uli Li u Peter Sado w P a ul a Gi nt er Yen- Chun Liu S a i a S al ari a T o cit e a b str a ct s i n t hi s p u bli c ati o n, pl e a s e u s e t h e f oll o wi n g f or m at: A ut h or A, A ut h or B, A ut h or C, et al. A b str a ct titl e ( a b s #). I n “ Fil e Titl e. ” Laboratory Investigation 2019; 99 (s u p pl 1): pa ge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`4$%+"`5&)*.Y/"Z;$A%"Z%+%$;]/"HC"I.;0%"`5&a5\/"'&=*+%"N5V/"F4-;2"b*-.%Y/"Z<422"K4$+;&3Y/"'%.4&":)%=*.]"" !=)1>>$+?1*'/$+,&)@>4+3A4+BC'*D$)>*/0+12+3*-E*6&'4+"''+")F1)4+3A4+;C'*D$)>*/0+12+3*-E*6&'+3$(*-&#+G-E11#4+"''+")F1)4+ 3A4+HC'*D$)>*/0+12+3*-E*6&'+I1>7*/&#4+"''+")F1)4+3A4+<"''+")F1)4+3A"" $%/4,0/B('/F"#$%&"'()5+>%2%-7"84&*9"`4$%+"`5&)*.7"84&*9"Z;$A%"Z%+%$;7"84&*9"HC"I.;0%"`5&a57"84&*9"'&=*+%"N57"84&*9"F4-;2"b*-.%7" 84&*9"Z<422"K4$+;&37"J1'>.#/&'//"M4+4=;<cd*&SI.4(*9"3&K1)+GE&)$E1#($)/"Z2.%2%"E&<4+4=09"3&K1)+GE&)$E1#($)/"Z2.%2%"E&<4+4=09"'%.4&" :)%=*.7"84&*" D+4G>(0B)3F"I.432%2;<")5<2%+"%)*&4<%.<;&4$%"GIe'L";3"%&"5&<4$$4&/"%==.*33;?*"?%.;%&2"4>"A.432%2*"<%&<*.C"Ie'"20A;<%++0"$%&;>*323"%3" %"$;B*)"25$4.";&"<4$(;&%2;4&"@;2-"<4&?*&2;4&%+"%<;&%."%)*&4<%.<;&4$%"%&)"4&+0".%.*+0"4<<5.3";&"%"A5.*">4.$C"E?*."2-*"A%32"2@4")*<%)*3/" 2.*$*&)453"%)?%&<*3"-%?*"(**&"$%)*";&"45."5&)*.32%&);&="4>"2-*"$4+*<5+%."A%2-4+4=0"4>"A.432%2*"<%&<*./"%+2-45=-"Ie'".*$%;&3" .*+%2;?*+0"5&)*.325);*)C"K-53/";&"2-;3"325)0/"@*"52;+;,*)"2%.=*2*)"&*B2S=*&*.%2;4&"e8'"%&)"F8'"3*f5*&<;&="24"*BA+4.*"2-*"$4+*<5+%." 3A*<2.5$"4>"Ie'C" $'/%>)F"Ie'"GA5.*"4."$;B*)"@;2-"%&"%<;&%."<4$A4&*&2L"%&)"%?%;+%(+*"%334<;%2*)"$5+2;>4<%+"%<;&%."25$4.3"@*.*".*2.43A*<2;?*+0";)*&2;>;*)" >.4$"%"3;&=+*"+%.=*"%<%)*$;<";&32;252;4&C"MX#"3+;)*3">.4$"%++"<%3*3"@*.*".*?;*@*)"(0"%2"+*%32"2@4"=*&;245.;&%.0"A%2-4+4=;323/"%&)" .*A.*3*&2%2;?*">4.$%+;&S>;B*)"A%.%>>;&S*$(*))*)"G11I#L"2;335*"@%3"3*+*<2*)">4."2%.=*2*)"&*B2S=*&*.%2;4&"e8'"%&)"F8'"3*f5*&<;&="4&"%&" T4&"K4..*&2"I.424&"3*f5*&<*."53;&="2-*"E&<4$;&*"J4$A.*-*&3;?*"'33%0"%&)"%"<5324$"A.432%2*"<%&<*.S>4<53*)"A%&*+/".*3A*<2;?*+0C" I.;4.;2;,*)"34$%2;<"?%.;%&23"%&)"<4A0"&5$(*."%+2*.%2;4&3"GJ8'L"%&)"#KZ"=*&*">53;4&"32%253"@*.*"$%&5%++0"<5.%2*)"53;&="*32%(+;3-*)";&S -453*"(;4;&>4.$%2;<3"A;A*+;&*3C" A'/B,*/F"E?*.%++/"!_")5<2%+"%&)"YO"%<;&%."25$4."3%$A+*3"@*.*"%?%;+%(+*">4."2-;3"325)0C"b4+*<5+%.">*%25.*3"%.*"35$$%.;,*)";&"2-*"K%(+*C" e5<2%+"25$4.3"3-4@*)"3;=&;>;<%&2+0"-;=-*."$52%2;4&%+"(5.)*&"%&)"=*&4$;<"<4$A+*B;20"2-%&"%<;&%."25$4.39";&"A%.2;<5+%./"%<2;?%2;&="$4+*<5+%." %+2*.%2;4&3";&"2-*"IT]`c'`K"A%2-@%0"G;C*C/"?L5M/""NL/"?AN;J"/"%&)"?AN;O!L"%&)"N8K"A%2-@%0"G;C*C/"JLMMP!"%&)""?JL"@*.*"3;=&;>;<%&2+0" *&.;<-*)";&")5<2%+"25$4.3C"84"A.;4.;2;,*)"34$%2;<"?%.;%&23";&"$;3$%2<-".*A%;."=*&*3"@*.*";)*&2;>;*)C"#KZ"=*&*">53;4&3"@*.*"A.*3*&2";&"%" 35(3*2"4>")5<2%+"25$4.3/"(52"2-*">.*f5*&<0"4>"#KZ"=*&*3">53;4&3"@%3"&42"3;=&;>;<%&2");>>*.*&2"2-%&"%<;&%."25$4.3";&"2-;3"<4-4.2C"E>"2-*"^" Ie'"@;2-"%"$;B*)"%<;&%."<4$A4&*&2/";&2*=.%2;4&"4>"&*B2S=*&*.%2;4&"e8'"%&)"F8'"3*f5*&<;&=")%2%")*$4&32.%2*)"$5+2;<+4&%+;20";&"!"<%3*" %&)"<+4&%+;20";&"]"<%3*39"<+4&%+;20"<45+)"&42"(*")*>;&;2;?*+0")*2*.$;&*)";&"2-*"42-*."V"<%3*3C"
Load more

Recommended publications
  • Killer-Like Receptors and GPR56 Progressive Expression Defines Cytokine Production of Human CD4+ Memory T Cells
    ARTICLE https://doi.org/10.1038/s41467-019-10018-1 OPEN Killer-like receptors and GPR56 progressive expression defines cytokine production of human CD4+ memory T cells Kim-Long Truong1,7, Stephan Schlickeiser1,2,7, Katrin Vogt1, David Boës1, Katarina Stanko1, Christine Appelt1, Mathias Streitz1, Gerald Grütz1,2, Nadja Stobutzki1, Christian Meisel1, Christina Iwert1, Stefan Tomiuk3, Julia K. Polansky2,4, Andreas Pascher5, Nina Babel2,6, Ulrik Stervbo 6, Igor Sauer 5, Undine Gerlach5 & Birgit Sawitzki1,2 1234567890():,; All memory T cells mount an accelerated response on antigen reencounter, but significant functional heterogeneity is present within the respective memory T-cell subsets as defined by CCR7 and CD45RA expression, thereby warranting further stratification. Here we show that several surface markers, including KLRB1, KLRG1, GPR56, and KLRF1, help define low, high, or exhausted cytokine producers within human peripheral and intrahepatic CD4+ memory T-cell populations. Highest simultaneous production of TNF and IFN-γ is observed in KLRB1+KLRG1+GPR56+ CD4 T cells. By contrast, KLRF1 expression is associated with T-cell exhaustion and reduced TNF/IFN-γ production. Lastly, TCRβ repertoire analysis and in vitro differentiation support a regulated, progressive expression for these markers during CD4+ memory T-cell differentiation. Our results thus help refine the classification of human memory T cells to provide insights on inflammatory disease progression and immunotherapy development. 1 Institute of Medical Immunology, Charité – Universitätsmedizin Berlin, Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, 13353 Berlin, Germany. 2 Berlin-Brandenburg Center for Regenerative Therapies (BCRT), Charité – Universitätsmedizin Berlin, 13353 Berlin, Germany. 3 Milteny Biotec GmbH, 51429 Bergisch Gladbach, Germany.
    [Show full text]
  • 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]
  • NK Cell Memory to Cytomegalovirus: Implications for Vaccine Development
    Review NK Cell Memory to Cytomegalovirus: Implications for Vaccine Development Calum Forrest 1 , Ariane Gomes 1 , Matthew Reeves 1,* and Victoria Male 2,* 1 Institute of Immunity & Transplantation, UCL, Royal Free Campus, London NW3 2PF, UK; [email protected] (C.F.); [email protected] (A.G.) 2 Department of Metabolism, Digestion and Reproduction, Imperial College London, Chelsea and Westminster Campus, London SW10 9NH, UK * Correspondence: [email protected] (M.R.); [email protected] (V.M.) Received: 24 June 2020; Accepted: 15 July 2020; Published: 20 July 2020 Abstract: Natural killer (NK) cells are innate lymphoid cells that recognize and eliminate virally-infected and cancerous cells. Members of the innate immune system are not usually considered to mediate immune memory, but over the past decade evidence has emerged that NK cells can do this in several contexts. Of these, the best understood and most widely accepted is the response to cytomegaloviruses, with strong evidence for memory to murine cytomegalovirus (MCMV) and several lines of evidence suggesting that the same is likely to be true of human cytomegalovirus (HCMV). The importance of NK cells in the context of HCMV infection is underscored by the armory of NK immune evasion genes encoded by HCMV aimed at subverting the NK cell immune response. As such, ongoing studies that have utilized HCMV to investigate NK cell diversity and function have proven instructive. Here, we discuss our current understanding of NK cell memory to viral infection with a focus on the response to cytomegaloviruses. We will then discuss the implications that this will have for the development of a vaccine against HCMV with particular emphasis on how a strategy that can harness the innate immune system and NK cells could be crucial for the development of a vaccine against this high-priority pathogen.
    [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]
  • BAP1: Case Report and Insight Into a Novel Tumor Suppressor Kanad Ghosh1, Badri Modi2, William D
    Ghosh et al. BMC Dermatology (2017) 17:13 DOI 10.1186/s12895-017-0065-6 CASEREPORT Open Access BAP1: case report and insight into a novel tumor suppressor Kanad Ghosh1, Badri Modi2, William D. James2 and Brian C. Capell1,2,3* Abstract Background: BRCA1-Associated-Protein 1 (BAP1) is a dynamic tumor suppressor which, when mutated, has been associated with an increased risk of uveal melanoma, cutaneous melanoma, mesothelioma, and several other cancers. Germline BAP1 mutations have been extensively studied, where they have been found to cause hereditary cancer susceptibility. However, their sporadic counterparts, tumors that display a loss of BAP1 expression due to somatically arising mutations in the BAP1 gene, remain a poorly described entity. Case presentation: Here we present the case of a 49-year-old female who presented with an asymptomatic dome-shaped pink papule on the dorsal foot which was found on biopsy to be deficient in the BAP1 tumor suppressor. While the patient’s family history did not suggest the presence of a familial cancer syndrome, germline genetic testing was performed and was negative. The patient underwent surgical excision of this sporadically appearing “BAPoma” by Mohs surgery. Conclusions: Given the relatively banal clinical appearance of these dome-shaped neoplasms, sporadic BAPomas may often be overlooked by clinicians and dermatologists. In addition to providing a representative case, here we also provide a synopsis of the current understanding of these neoplasms, both in terms of the histopathological features, as well as the molecular mechanisms underlying BAP1 function and its ability to prevent tumorigenesis. Keywords: BAP1, Tumor suppression, Familial cancer syndrome Background More recently, sporadic somatic BAP1 mutations have Within the last decade, the BRCA1-Associated-Protein 1 been shown to occur in the setting of both mesothelioma (BAP1) has been increasingly appreciated for its tumor sup- and uveal melanoma [3].
    [Show full text]
  • Familial and Somatic BAP1 Mutations Inactivate ASXL1/2-Mediated Allosteric
    Author Manuscript Published OnlineFirst on December 28, 2017; DOI: 10.1158/0008-5472.CAN-17-2876 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited. Familial and Somatic BAP1 Mutations Inactivate ASXL1/2-Mediated Allosteric Regulation of BAP1 Deubiquitinase by Targeting Multiple Independent Domains Hongzhuang Peng1, Jeremy Prokop2, Jayashree Karar1, Kyewon Park1, Li Cao3, J. William Harbour4, Anne M. Bowcock5, S. Bruce Malkowicz6, Mitchell Cheung7, Joseph R. Testa7, and Frank J. Rauscher, 3rd1 1Wistar Institute, Philadelphia, PA, USA; 2HudsonAlpha Genome Sequencing Center, Huntsville AL, USA; 3Washington University in St Louis, St. Louis, MO; 4University of Miami School of Medicine, Miami, FL, USA; 5Icahn School of Medicine at Mount Sinai, New York, NY; 6University of Pennsylvania and Veterans Affairs Medical Center Philadelphia, Philadelphia PA, USA; 7Fox Chase Cancer Center, Philadelphia, PA, USA Running Title: BAP1 mutations disable ASXL1/2’s regulation of BAP1 activity Key Words: BAP1, PR-DUB, ASXL1/2, mutations, deubiquitinase, cancer, tumor susceptibility Correspondence: Frank J. Rauscher, 3rd, Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104; Phone: 215-898-0995; Fax: 215-898-3929; E-mail: [email protected]; Joseph R. Testa, 5Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA; Phone: 215-728- 2610; Fax: 215-214-1623; E-mail: [email protected] Précis: Combined computational and biochemical approaches demonstrate that the BAP1- ASXL2 interaction is direct and high affinity and that many BAP1 mutations act allosterically to inhibit BAP1-ASXL2 binding. 1 Downloaded from cancerres.aacrjournals.org on September 29, 2021. © 2017 American Association for Cancer Research. Author Manuscript Published OnlineFirst on December 28, 2017; DOI: 10.1158/0008-5472.CAN-17-2876 Author manuscripts have been peer reviewed and accepted for publication but have not yet been edited.
    [Show full text]
  • Monoclonal Antibody to CD161 / KLRB1 - Purified
    OriGene Technologies, Inc. OriGene Technologies GmbH 9620 Medical Center Drive, Ste 200 Schillerstr. 5 Rockville, MD 20850 32052 Herford UNITED STATES GERMANY Phone: +1-888-267-4436 Phone: +49-5221-34606-0 Fax: +1-301-340-8606 Fax: +49-5221-34606-11 [email protected] [email protected] SM1611PT Monoclonal Antibody to CD161 / KLRB1 - Purified Alternate names: C-type lectin domain family 5 member B, CLEC5B, HNKR-P1a, Killer cell lectin-like receptor subfamily B member 1, NKRP1A, Natural killer cell surface protein P1A Quantity: 25 µg Concentration: 1.0 mg/ml Background: Natural killer (NK) cells are lymphocytes that mediate cytotoxicity and secrete cytokines after immune stimulation. Several genes of the C-type lectin superfamily, including the rodent NKRP1 family of glycoproteins, are expressed by NK cells and may be involved in the regulation of NK cell function. The KLRB1 (CD161) protein contains an extracellular domain with several motifs characteristic of C type lectins, a transmembrane domain, and a cytoplasmic domain. The KLRB1 protein is classified as a type II membrane protein because it has an external C terminus. In mouse the NKRP1 family has three members, NKRP1A, B and C, whilst in human only one member has been identified. The human protein has received the designation CD161, and the mouse proteins have been referred to as CD161a, b and c. Engagement of CD161c has been reported to have activating function in NK cells, whilst engagement of CD161b is inhibitory. CD161 is expressed by almost all NK cells and with a small subset of CD3+ve T cells.
    [Show full text]
  • CD29 Identifies IFN-Γ–Producing Human CD8+ T Cells With
    + CD29 identifies IFN-γ–producing human CD8 T cells with an increased cytotoxic potential Benoît P. Nicoleta,b, Aurélie Guislaina,b, Floris P. J. van Alphenc, Raquel Gomez-Eerlandd, Ton N. M. Schumacherd, Maartje van den Biggelaarc,e, and Monika C. Wolkersa,b,1 aDepartment of Hematopoiesis, Sanquin Research, 1066 CX Amsterdam, The Netherlands; bLandsteiner Laboratory, Oncode Institute, Amsterdam University Medical Center, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands; cDepartment of Research Facilities, Sanquin Research, 1066 CX Amsterdam, The Netherlands; dDivision of Molecular Oncology and Immunology, Oncode Institute, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands; and eDepartment of Molecular and Cellular Haemostasis, Sanquin Research, 1066 CX Amsterdam, The Netherlands Edited by Anjana Rao, La Jolla Institute for Allergy and Immunology, La Jolla, CA, and approved February 12, 2020 (received for review August 12, 2019) Cytotoxic CD8+ T cells can effectively kill target cells by producing therefore developed a protocol that allowed for efficient iso- cytokines, chemokines, and granzymes. Expression of these effector lation of RNA and protein from fluorescence-activated cell molecules is however highly divergent, and tools that identify and sorting (FACS)-sorted fixed T cells after intracellular cytokine + preselect CD8 T cells with a cytotoxic expression profile are lacking. staining. With this top-down approach, we performed an un- + Human CD8 T cells can be divided into IFN-γ– and IL-2–producing biased RNA-sequencing (RNA-seq) and mass spectrometry cells. Unbiased transcriptomics and proteomics analysis on cytokine- γ– – + + (MS) analyses on IFN- and IL-2 producing primary human producing fixed CD8 T cells revealed that IL-2 cells produce helper + + + CD8 Tcells.
    [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]
  • 1714 Gene Comprehensive Cancer Panel Enriched for Clinically Actionable Genes with Additional Biologically Relevant Genes 400-500X Average Coverage on Tumor
    xO GENE PANEL 1714 gene comprehensive cancer panel enriched for clinically actionable genes with additional biologically relevant genes 400-500x average coverage on tumor Genes A-C Genes D-F Genes G-I Genes J-L AATK ATAD2B BTG1 CDH7 CREM DACH1 EPHA1 FES G6PC3 HGF IL18RAP JADE1 LMO1 ABCA1 ATF1 BTG2 CDK1 CRHR1 DACH2 EPHA2 FEV G6PD HIF1A IL1R1 JAK1 LMO2 ABCB1 ATM BTG3 CDK10 CRK DAXX EPHA3 FGF1 GAB1 HIF1AN IL1R2 JAK2 LMO7 ABCB11 ATR BTK CDK11A CRKL DBH EPHA4 FGF10 GAB2 HIST1H1E IL1RAP JAK3 LMTK2 ABCB4 ATRX BTRC CDK11B CRLF2 DCC EPHA5 FGF11 GABPA HIST1H3B IL20RA JARID2 LMTK3 ABCC1 AURKA BUB1 CDK12 CRTC1 DCUN1D1 EPHA6 FGF12 GALNT12 HIST1H4E IL20RB JAZF1 LPHN2 ABCC2 AURKB BUB1B CDK13 CRTC2 DCUN1D2 EPHA7 FGF13 GATA1 HLA-A IL21R JMJD1C LPHN3 ABCG1 AURKC BUB3 CDK14 CRTC3 DDB2 EPHA8 FGF14 GATA2 HLA-B IL22RA1 JMJD4 LPP ABCG2 AXIN1 C11orf30 CDK15 CSF1 DDIT3 EPHB1 FGF16 GATA3 HLF IL22RA2 JMJD6 LRP1B ABI1 AXIN2 CACNA1C CDK16 CSF1R DDR1 EPHB2 FGF17 GATA5 HLTF IL23R JMJD7 LRP5 ABL1 AXL CACNA1S CDK17 CSF2RA DDR2 EPHB3 FGF18 GATA6 HMGA1 IL2RA JMJD8 LRP6 ABL2 B2M CACNB2 CDK18 CSF2RB DDX3X EPHB4 FGF19 GDNF HMGA2 IL2RB JUN LRRK2 ACE BABAM1 CADM2 CDK19 CSF3R DDX5 EPHB6 FGF2 GFI1 HMGCR IL2RG JUNB LSM1 ACSL6 BACH1 CALR CDK2 CSK DDX6 EPOR FGF20 GFI1B HNF1A IL3 JUND LTK ACTA2 BACH2 CAMTA1 CDK20 CSNK1D DEK ERBB2 FGF21 GFRA4 HNF1B IL3RA JUP LYL1 ACTC1 BAG4 CAPRIN2 CDK3 CSNK1E DHFR ERBB3 FGF22 GGCX HNRNPA3 IL4R KAT2A LYN ACVR1 BAI3 CARD10 CDK4 CTCF DHH ERBB4 FGF23 GHR HOXA10 IL5RA KAT2B LZTR1 ACVR1B BAP1 CARD11 CDK5 CTCFL DIAPH1 ERCC1 FGF3 GID4 HOXA11 IL6R KAT5 ACVR2A
    [Show full text]