Modern Pathology

Total Page:16

File Type:pdf, Size:1020Kb

Modern Pathology VOLUME 32 | SUPPLEMENT 2 | MARCH 2019 MODERN PATHOLOGY 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. ” Modern Pathology 2019; 32 (s u p pl 2): pa ge# ! !!"## $%&&'(')*%+,#-./0120/12+*%3.,420,%)'#54.,*(+)/&'(+/'#6#7-895:6;#<=1('//%0)#90)&'(/# 5>>('//%?')'//#+)3#@)3'1')3')*,.#8('3%4*/#A'4B((')4'#%)#C(0*2',%+,#D,+33'(#9+(4%)0E+/## #$%&"'()*+,%-*.!/"'$%&0"'()*+(%.0!/"'-$*)"1%-$0!/"#(2*3%$"#+,%..456!"" !"#$%&'()*&+,&-.#/0+12+3$(*-*'$4+"#$%&'()*&4+5607/"" $%/4,0/B('/F"#$%&"'()*+,%-*.7"84&*9"'$%&0"'()*+(%.07"84&*9"'-$*)"1%-$07"84&*9"#(2*3%$"#+,%..4567"84&*" D+4G>(0B)3F":.42-*+;%+"<%.<;&4$%3"%.*"-;=-+0"-*2*.4=*&*453";&"2*.$3"4>"(;4+4=;<%+"(*-%?;4."@-;<-"<*.2%;&+0".*>+*<23");>>*.*&2"%&)"<4$A+*B" $*2%(4+;<"%&)"$4+*<5+%."A%2-@%03C" 84?*+"(;4$%.6*.3"2-%2"@;++"(*22*."%33;32"2-*"$%&%=*$*&2"4>"(+%))*."<%.<;&4$%3"%&)"-*+A"A.*);<2"A%2;*&23D"452<4$*"%.*"*%=*.+0"&**)*)C" E&=4;&=".*3*%.<-*3";&"2-*".*+%2;?*+0"&*@">;*+)"4>"+;A;)"$*2%(4+;3$"%.*"A.4$;3;&=";&"2-;3".*3A*<2C" F*<*&2+0/"4?*.*BA.*33;4&"4>"+034A-43A-%2;)0+<-4+;&*"%<0+2.%&3>*.%3*"!"GHIJ'K!L/"%"6*0"*&,0$*";&"+;A;)"$*2%(4+;3$/"-%3"(**&";$A+;<%2*)";&" 2-*"A%2-4=*&*3;3"%&)"A.4=.*33;4&"4>"3*?*.%+"25$4.3C"M4@*?*./"2-*"32%253"%&)"<+;&;<%+"3;=&;>;<%&<*"4>"HIJ'K!"*BA.*33;4&";&"5.;&%.0"(+%))*." <%.<;&4$%3"-%3".*$%;&*)"5&*BA+4.*)C" $'/%>)F"N*"*?%+5%2*)"HIJ'K!";$$5&4-;324<-*$;<%+"*BA.*33;4&";&"OP"#=0A2;%&"A%2;*&23"@;2-"5.42-*+;%+"(+%))*."<%.<;&4$%3"G:QJ3L"%&)" 32%2;32;<%++0"<4..*+%2*)";23"*BA.*33;4&"@;2-"42-*."<+;&;<4A%2-4+4=;<%+"A%.%$*2*.3";&<+5);&="A%2;*&23R"452<4$*C"K@*&20"&4&S&*4A+%32;<"(+%))*." 2;335*3"3*.?*)"%3"%"<4&2.4+"=.45AC" A'/B,*/F"T&":QJ3/"2@4");32;&<2"A%22*.&3"4>"HIJ'K!"*BA.*33;4&"@*.*")*2*<2*)/";&"UVPW"4>"25$4."<*++3/"%&)"@*.*")*3;=&%2*)"%3"32.4&="%&)" @*%6"&5<+*%."*BA.*33;4&"G1;=C"!XY".*3A*<2;?*+0LC" Z2.4&="HIJ'K!"&5<+*%."*BA.*33;4&"@%3"&42*)";&"%++"&4&S&*4A+%32;<"2;335*3"%&)";2"@%3"%334<;%2*)"@;2-"+4@"=.%)*"%&)"&4&S;&?%3;?*"25$4.3/" -4@*?*./"2-;3">;&);&="@%3"&42"32%2;32;<%++0"3;=&;>;<%&2C"T&2*.*32;&=+0/";2"@%3"3;=&;>;<%&2+0"%334<;%2*)"@;2-"-;=-*.".*<5..*&<*".%2*";&"(42-"+4@"%&)" -;=-"=.%)*"25$4.3"G7[PCPP\"X"7[PCPP]L"%&)";2"*$*.=*)"%3"%&";&)*A*&)*&2"A.*);<24."4>"25$4.".*<5..*&<*"G7[PCP!^LC" J4&?*.3*+0/"@*%6"HIJ'K!"&5<+*%."*BA.*33;4&"@%3"*B<+53;?*+0"&42*)";&"&*4A+%32;<"2;335*3"G78PCPPYL"%&)";2"@%3"3;=&;>;<%&2+0"%334<;%2*)" @;2-"-;=-"=.%)*"G789:9;<L"%&)";&?%3;?*"G789:9!;L"25$4.3C" 1;=5.*"!"S"__O"" 1;=5.*"Y"S"__O"" " " 90)4,B/%0)/F"N*"<4&<+5)*"2-%2"HIJ'K!")4@&.*=5+%2;4&"$;=-2"(*";&?4+?*)";&"5.42-*+;%+"<%.<;&4$%"25$4.;=*&*3;3"%&)"$;=-2"<4&2.;(52*"24" 25$4."%==.*33;?*"A-*&420A*"%&)"(*-%?;4.C"F*2%;&*)"HIJ'K!"*BA.*33;4&";&"5.42-*+;%+"<%.<;&4$%3";3"%&";&)*A*&)*&2"A.*);<24."4>"25$4." .*<5..*&<*"%&)"2-53";2".*A.*3*&23"%"A.4$;3;&="&4?*+"A.4=&432;<"$%.6*."@-;<-"$;=-2"-*+A"3*+*<2;4&"4>"<%&);)%2*3">4."32.;<2*."35.?*;++%&<*" $*2-4)3C""E5."325)0"35AA4.23"2-*"A4325+%2;4&"2-%2"%+2*.%2;4&3";&"+;A;)"$*2%(4+;3$"%AA%.*&2+0"A+%0");>>*.*&2".4+*3")5.;&=");>>*.*&2"32%=*3"4>" <%&<*."*?4+?*$*&2C" ! !" ! !!!####@)*'>(+*%?'#E0,'4B,+(#1(0&%,%)>#0&#1(0/*+*%4#3B4*+,#+3')04+(4%)0E+#('?'+,/#+#3%/*%)4*#E0,'4B,+(# /1'4*(BEH#%)4,B3%)>#&('IB')*#+4*%?+*%)>#8@JKL5K:#+)3#MN:#1+*2O+.#+,*'(+*%0)/## #$%&"'()5+>%2%-!/"`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" b4+*<5+%."1*%25.*3" e5<2%+"G'"["!_L"
Recommended publications
  • 8 Benign Neoplasms and Tumor-Like Lesions Roberto Maroldi, Marco Berlucchi, Davide Farina, Davide Tomenzoli, Andrea Borghesi, and Luca Pianta
    Benign Neoplasms and Tumor-Like Lesions 107 8 Benign Neoplasms and Tumor-Like Lesions Roberto Maroldi, Marco Berlucchi, Davide Farina, Davide Tomenzoli, Andrea Borghesi, and Luca Pianta CONTENTS 8.6.6 Follow-Up 131 8.7 Juvenile Angiofi broma 131 8.1 Osteoma 107 8.7.1 Defi nition, Epidemiology, Pattern of Growth 131 8.1.1 Defi nition, Epidemiology, Pattern of Growth 107 8.7.2 Clinical and Endoscopic Findings 132 8.1.2 Clinical and Endoscopic Findings 108 8.7.3 Treatment Guidelines 132 8.1.3 Treatment Guidelines 108 8.7.4 Key Information to Be Provided by Imaging 133 8.1.4 Key Information to Be Provided by Imaging 109 8.7.5 Imaging Findings 133 8.1.5 Imaging Findings 109 8.7.6 Follow-Up 141 8.1.6 Follow-Up 110 8.8 Pyogenic Granuloma 8.2 Fibrous Dysplasia and Ossifying Fibroma 110 (Lobular Capillary Hemangioma) 145 8.2.1 Defi nition, Epidemiology, Pattern of Growth 110 8.8.1 Defi nition, Epidemiology, Pattern of Growth 145 8.2.2 Clinical and Endoscopic Findings 111 8.8.2 Treatment Guidelines 145 8.2.3 Treatment Guidelines 112 8.8.3 Key Information to Be Provided by Imaging 146 8.2.4 Key Information to Be Provided by Imaging 112 8.8.4 Imaging Findings 146 8.2.5 Imaging Findings 112 8.9 Unusual Benign Lesions 147 8.2.6 Follow-Up 114 8.9.1 Pleomorphic Adenoma (Mixed Tumor) 147 8.3 Aneurysmal Bone Cyst 114 8.9.2 Schwannoma 149 8.3.1 Defi nition, Epidemiology, Pattern of Growth 114 8.9.3 Leiomyoma 150 8.3.2 Clinical and Endoscopic Findings 115 8.9.4 Paraganglioma 151 8.3.3 Treatment Guidelines 115 References 152 8.3.4 Key Information to Be Provided
    [Show full text]
  • Immune Function of Mir-214 and Its Application Prospects As Molecular Marker
    Immune function of miR-214 and its application prospects as molecular marker Qiuyuan Wang, Yang Liu, Yiru Wu, Jie Wen and Chaolai Man College of Life Science and Technology, Harbin Normal University, Harbin, China ABSTRACT MicroRNAs are a class of evolutionary conserved non-coding small RNAs that play key regulatory roles at the post-transcriptional level. In recent years, studies have shown that miR-214 plays an important role in regulating several biological processes such as cell proliferation and differentiation, tumorigenesis, inflammation and immunity, and it has become a hotspot in the miRNA field. In this review, the regulatory functions of miR-214 in the proliferation, differentiation and functional activities of immune- related cells, such as dendritic cells, T cells and NK cells, were briefly reviewed. Also, the mechanisms of miR-214 involved in tumor immunity, inflammatory regulation and antivirus were discussed. Finally, the value and application prospects of miR-214 as a molecular marker in inflammation and tumor related diseases were analyzed briefly. We hope it can provide reference for further study on the mechanism and application of miR-214. Subjects Biochemistry, Molecular Biology, Immunology Keywords miR-214, Immune cell, Tumor immunity, Inflammation, Virus, Molecular marker INTRODUCTION MicroRNAs (miRNAs) are a kind of high conserved non-coding small RNAs in evolution that bind to the 30-untranslated region (30-UTR) of target gene mRNA and regulate gene Submitted 18 September 2020 expression at post-transcriptional level. In immune responses, miRNAs act as signal- Accepted 20 January 2021 Published 16 February 2021 regulating molecules after immune-related receptors activation, and affect the expression Corresponding author of immune-related genes, thus extensively participating in various aspects of immune Chaolai Man, [email protected] response (Bosisio et al., 2019; Mehta & Baltimore, 2016).
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [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]
  • Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
    Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase
    [Show full text]
  • Transcriptomic and Proteomic Profiling Provides Insight Into
    BASIC RESEARCH www.jasn.org Transcriptomic and Proteomic Profiling Provides Insight into Mesangial Cell Function in IgA Nephropathy † † ‡ Peidi Liu,* Emelie Lassén,* Viji Nair, Celine C. Berthier, Miyuki Suguro, Carina Sihlbom,§ † | † Matthias Kretzler, Christer Betsholtz, ¶ Börje Haraldsson,* Wenjun Ju, Kerstin Ebefors,* and Jenny Nyström* *Department of Physiology, Institute of Neuroscience and Physiology, §Proteomics Core Facility at University of Gothenburg, University of Gothenburg, Gothenburg, Sweden; †Division of Nephrology, Department of Internal Medicine and Department of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan; ‡Division of Molecular Medicine, Aichi Cancer Center Research Institute, Nagoya, Japan; |Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden; and ¶Integrated Cardio Metabolic Centre, Karolinska Institutet Novum, Huddinge, Sweden ABSTRACT IgA nephropathy (IgAN), the most common GN worldwide, is characterized by circulating galactose-deficient IgA (gd-IgA) that forms immune complexes. The immune complexes are deposited in the glomerular mesangium, leading to inflammation and loss of renal function, but the complete pathophysiology of the disease is not understood. Using an integrated global transcriptomic and proteomic profiling approach, we investigated the role of the mesangium in the onset and progression of IgAN. Global gene expression was investigated by microarray analysis of the glomerular compartment of renal biopsy specimens from patients with IgAN (n=19) and controls (n=22). Using curated glomerular cell type–specific genes from the published literature, we found differential expression of a much higher percentage of mesangial cell–positive standard genes than podocyte-positive standard genes in IgAN. Principal coordinate analysis of expression data revealed clear separation of patient and control samples on the basis of mesangial but not podocyte cell–positive standard genes.
    [Show full text]
  • Mitochondria Are Transported Along Microtubules in Membrane
    Shen et al. Cell Death and Disease (2018) 9:81 DOI 10.1038/s41419-017-0145-x Cell Death & Disease ARTICLE Open Access Mitochondria are transported along microtubules in membrane nanotubes to rescue distressed cardiomyocytes from apoptosis Jing Shen1,2,3,4, Jiang-Hui Zhang1,2,3,4,HanXiao1,2,3,4,Ji-MinWu1,2,3,4,Kang-MinHe1,2,3,4,Zhi-ZhenLv1,2,3,4, Zi-Jian Li1,2,3,4, Ming Xu1,2,3,4 and You-Yi Zhang1,2,3,4 Abstract Membrane nanotubes (MNTs) act as “highways” between cells to facilitate the transfer of multiple signals and play an important role in many diseases. Our previous work reported on the transfer of mitochondria via MNTs between cardiomyocytes (CMs) and cardiac myofibroblasts (MFs); however, the elucidation of the underlying mechanism and pathophysiological significance of this transfer requires additional study. In this study, we determined that the mean movement velocity of mitochondria in MNTs between CMs and MFs was approximately 17.5 ± 2.1 nm/s. Meanwhile, treatment with microtubule polymerisation inhibitors nocodazole or colcemid in cell culture decreased mitochondrial velocity, and knockdown of the microtubule motor protein kinesin family member 5B (KIF5B) led to a similar effect, indicating that mitochondrial movement was dependent on microtubules and the motor protein KIF5B. Furthermore, we showed that hypoxia/reoxygenation-induced CM 1234567890 1234567890 apoptosis was attenuated by coculture with intact or hypoxia/reoxygenation-treated MFs, which transferred mitochondria to CMs. This rescue was prevented either by separating the cells using Transwell culture or by impairing mitochondrial transfer with nocodazole or colcemid treatment.
    [Show full text]
  • Poster: Publikace 2008
    Publikované Práce lékařů Šiklova Patologicko – anatomického ústavu a bioPtické laboratoře s.r.o. za rok 2008 Časopisy s „impact“ faktorem syringofibroadenoma associated with well-differentiated squamous cell 28. Kuroda N., Katto K., Yamaguchi T., Kawada T., ImamuraY., Hes O., Michal M., 42. Vazmitel M., Spagnolo D.V., Němcová J., Michal M., Kazakov D.V.: 1. Alvarado-Cabrero I., Perez-Montiel D.M., Hes, O.: Multicystic urothelial carcinoma. Am J Dermatopathol, 30, 572-574, 2008. Shuin T., Lee G.H.: Chromophobe renal cell carcinoma: Diagnostic ancillary Hidradenoma papilliferum with a ductal carcinoma in situ component. Case report and review of the literature. Am J Dermatopathol, 30, 392-394, 2008. carcinoma of the bladder with gland-like lumina and with signet-ring cells. 17. Kacerovska D., Michal M., Kreuzberg B., Mukensnabl P., Kazakov DV.: application of imprint cytology and fluorescencein situ hybridization of Acral calcified vascular leiomyoma of the skin: a rare clinicopathological chromosomes 10 and 21 in two cases of typical and eosinophilic variants. 43. Vazmitel M., Michal M., Kazakov D.V.: Merkel cell carcinoma with a A case report. Diagn Pathol, 3, 36, 2008. follicular lymphocytic infiltrate: report of two cases. Am J Dermatopathol, 2. Beneš Z., Chlumská A., Antoš Z., Kohout P., Sequens R.: Detection of variant of cutaneous vascular leiomyomas: report of 3 cases. J Amer Acad Med Mol Morphol, 41, 227-232, 2008. 29. Kuroda N., Kato K., Tamura M., Shiotsu T., Hes O., Michal M., Hagashima 30, 389-391, 2008. carcinoma by means of endoscopic cytoscopy in the area of ulcerative colitis. Dermatology, 59,1000-1004, 2008.
    [Show full text]
  • A Case Report of Nasal Adenoid Cystic Carcinoma Rahim H1*, Bencheikh R2, Gliti MA1, Harmouch A3, Benbouzid MA2, Essakali L2
    Saudi Journal of Medical and Pharmaceutical Sciences Abbreviated Key Title: Saudi J Med Pharm Sci ISSN 2413-4929 (Print) |ISSN 2413-4910 (Online) Scholars Middle East Publishers, Dubai, United Arab Emirates Journal homepage: https://saudijournals.com Case Report A Case Report of Nasal Adenoid Cystic Carcinoma Rahim H1*, Bencheikh R2, Gliti MA1, Harmouch A3, Benbouzid MA2, Essakali L2 1Resident physician in otorhinolaryngology, Department of Otorhinolaryngology, Head and Neck Surgery, Ibn Sina University Hospital, Faculty of Medicine, Mohammed V University, Rabat, Morocco 2Professor of otorhinolaryngology, Department of Otorhinolaryngology, Head and Neck Surgery, Ibn Sina University Hospital, Faculty of Medicine, Mohammed V University, Rabat, Morocco 3Professor of Anatomopathology, Ibn Sina University Hospital, Faculty of Medicine, Mohammed V University, Rabat, Morocco DOI: 10.36348/sjmps.2020.v06i11.007 | Received: 22.08.2020 | Accepted: 29.08.2020 | Published: 28.11.2020 *Corresponding author: Rahim Hanaa Abstract The adenoid cystic carcinoma is a rare tumor in the region of the head and neck, it's the common malignant tumor of the salivary glands. Its location in the nasal cavity is exceptional. We report in our study a case of adenoid cystic carcinoma of the nasal cavity of a 68-year-old patient who presents nasal symptoms. The CT- scan shows a tissue process in the right nasal cavity, the endoscopy showed a process in the right nasal cavity extending to the lower cornet. The histology confirmed the adenoid cystic carcinoma. The surgical treatment consisted on the excision of the entire tumor followed by radiation therapy. Keywords: Adenoid cystic carcinoma – nasal cavity. Copyright © 2020 The Author(s): This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License (CC BY-NC 4.0) which permits unrestricted use, distribution, and reproduction in any medium for non-commercial use provided the original author and source are credited.
    [Show full text]
  • Tumors in the Kidney (Pdf)
    Systemicist Pathology.. Lecture # 8 Title :Tumors In The Kidney Done by: Dema Mhmd Khdier A man may die, nations may rise and fall…….But an idea lives on Classification PRIMARY **Benign: 1)Papillary adenoma (in the cortex). 2)Oncocytoma 3)Medullary fibroma (interstitial cell T) **Malignant: 1)Renal cell carcinoma (most common): •Clear cell renal cell carcinoma. •Papillary renal cell carcinoma. •Chromophobe renal cell carcinoma. 2) Nephroblastoma (Wilms tumor). 3) Urothelial carcinoma of renal pelvis. SECONDARY **Benign renal tumors** _ Angiomyolipoma: Consists of vessels, smooth muscles & fat. Seen in 25-50% of patients with (Tuberous Sclerosis). **Malignant renal tumors** 1)Renal cell carcinoma (RCC) Tumors are derived from the renal tubular epithelium. • Most cases are sporadic. • 2-3% of all visceral cancers. ~85% of all renal cancer. • M:F = 2:1. Commonly 60-70 years. Risk factors 1) Smoking (most significant), obesity, HTN. 2)Unopposed estrogen Rx 3)Cadmium, petroleum products & heavy metals. 4)CRF & acquired cystic disease** (30 folds ) 5)Familial (4%) most are AD: _Von Hippel-Lindau (VHL) syndrome _Hereditary clear cell carcinoma _Hereditary papillary carcinoma Morphology of RCC Grossly: ▫ Mainly arise in cortex > polar & spherical. ▫ May extend into renal vein. ▫ Orange – yellow OR tan–brown, variegated tumor with hemorrhagic, necrotic & cystic areas. Classified according to the histological picture: 1)Clear cell carcinoma (70-80%). 2)Papillary carcinoma (10-15%). 3)Chromophobe renal carcinoma (5%). 4)Sarcomatoid carcinoma. A. Clear cell carcinoma • Most common RCC subtype. • Arise from proximal convoluted tubules. • Majority are sporadic & unilateral. • Familial forms, associated with germ-line mutation of the VHL tumor suppressor gene on 3p: *von Hippel-Lindau: rare tumor of adrenal gland tissue.
    [Show full text]
  • Supplementary Table 1 Genes Tested in Qrt-PCR in Nfpas
    Supplementary Table 1 Genes tested in qRT-PCR in NFPAs Gene Bank accession Gene Description number ABI assay ID a disintegrin-like and metalloprotease with thrombospondin type 1 motif 7 ADAMTS7 NM_014272.3 Hs00276223_m1 Rho guanine nucleotide exchange factor (GEF) 3 ARHGEF3 NM_019555.1 Hs00219609_m1 BCL2-associated X protein BAX NM_004324 House design Bcl-2 binding component 3 BBC3 NM_014417.2 Hs00248075_m1 B-cell CLL/lymphoma 2 BCL2 NM_000633 House design Bone morphogenetic protein 7 BMP7 NM_001719.1 Hs00233476_m1 CCAAT/enhancer binding protein (C/EBP), alpha CEBPA NM_004364.2 Hs00269972_s1 coxsackie virus and adenovirus receptor CXADR NM_001338.3 Hs00154661_m1 Homo sapiens Dicer1, Dcr-1 homolog (Drosophila) (DICER1) DICER1 NM_177438.1 Hs00229023_m1 Homo sapiens dystonin DST NM_015548.2 Hs00156137_m1 fms-related tyrosine kinase 3 FLT3 NM_004119.1 Hs00174690_m1 glutamate receptor, ionotropic, N-methyl D-aspartate 1 GRIN1 NM_000832.4 Hs00609557_m1 high-mobility group box 1 HMGB1 NM_002128.3 Hs01923466_g1 heterogeneous nuclear ribonucleoprotein U HNRPU NM_004501.3 Hs00244919_m1 insulin-like growth factor binding protein 5 IGFBP5 NM_000599.2 Hs00181213_m1 latent transforming growth factor beta binding protein 4 LTBP4 NM_001042544.1 Hs00186025_m1 microtubule-associated protein 1 light chain 3 beta MAP1LC3B NM_022818.3 Hs00797944_s1 matrix metallopeptidase 17 MMP17 NM_016155.4 Hs01108847_m1 myosin VA MYO5A NM_000259.1 Hs00165309_m1 Homo sapiens nuclear factor (erythroid-derived 2)-like 1 NFE2L1 NM_003204.1 Hs00231457_m1 oxoglutarate (alpha-ketoglutarate)
    [Show full text]
  • Drosophila and Human Transcriptomic Data Mining Provides Evidence for Therapeutic
    Drosophila and human transcriptomic data mining provides evidence for therapeutic mechanism of pentylenetetrazole in Down syndrome Author Abhay Sharma Institute of Genomics and Integrative Biology Council of Scientific and Industrial Research Delhi University Campus, Mall Road Delhi 110007, India Tel: +91-11-27666156, Fax: +91-11-27662407 Email: [email protected] Nature Precedings : hdl:10101/npre.2010.4330.1 Posted 5 Apr 2010 Running head: Pentylenetetrazole mechanism in Down syndrome 1 Abstract Pentylenetetrazole (PTZ) has recently been found to ameliorate cognitive impairment in rodent models of Down syndrome (DS). The mechanism underlying PTZ’s therapeutic effect is however not clear. Microarray profiling has previously reported differential expression of genes in DS. No mammalian transcriptomic data on PTZ treatment however exists. Nevertheless, a Drosophila model inspired by rodent models of PTZ induced kindling plasticity has recently been described. Microarray profiling has shown PTZ’s downregulatory effect on gene expression in fly heads. In a comparative transcriptomics approach, I have analyzed the available microarray data in order to identify potential mechanism of PTZ action in DS. I find that transcriptomic correlates of chronic PTZ in Drosophila and DS counteract each other. A significant enrichment is observed between PTZ downregulated and DS upregulated genes, and a significant depletion between PTZ downregulated and DS dowwnregulated genes. Further, the common genes in PTZ Nature Precedings : hdl:10101/npre.2010.4330.1 Posted 5 Apr 2010 downregulated and DS upregulated sets show enrichment for MAP kinase pathway. My analysis suggests that downregulation of MAP kinase pathway may mediate therapeutic effect of PTZ in DS. Existing evidence implicating MAP kinase pathway in DS supports this observation.
    [Show full text]