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LABORATORY INVESTIGATION THE BASIC AND TRANSLATIONAL PATHOLOGY RESEARCH JOURNAL LI VOLUME 98 | SUPPLEMENT 1 | MARCH 2018 2018 ABSTRACTS GENITOURINARY PATHOLOGY (894-1126) 107TH ANNUAL MEETING GEARED TO LEARN Vancouver Convention Centre MARCH 17-23, 2018 Vancouver, BC, Canada PLATFORM & 2018 ABSTRACTS POSTER PRESENTATIONS EDUCATION COMMITTEE Jason L. Hornick, Chair Amy Chadburn Rhonda Yantiss, Chair, Abstract Review Board Ashley M. Cimino-Mathews and Assignment Committee James R. Cook Laura W. Lamps, Chair, CME Subcommittee Carol F. Farver Steven D. Billings, Chair, Interactive Microscopy Meera R. Hameed Shree G. Sharma, Chair, Informatics Subcommittee Michelle S. Hirsch Raja R. Seethala, Short Course Coordinator Anna Marie Mulligan Ilan Weinreb, Chair, Subcommittee for Rish Pai Unique Live Course Offerings Vinita Parkash David B. Kaminsky, Executive Vice President Anil Parwani (Ex-Officio) Deepa Patil Aleodor (Doru) Andea Lakshmi Priya Kunju Zubair Baloch John D. Reith Olca Basturk Raja R. Seethala Gregory R. Bean, Pathologist-in-Training Kwun Wah Wen, Pathologist-in-Training Daniel J. Brat ABSTRACT REVIEW BOARD Narasimhan Agaram Mamta Gupta David Meredith Souzan Sanati Christina Arnold Omar Habeeb Dylan Miller Sandro Santagata Dan Berney Marc Halushka Roberto Miranda Anjali Saqi Ritu Bhalla Krisztina Hanley Elizabeth Morgan Frank Schneider Parul Bhargava Douglas Hartman Juan-Miguel Mosquera Michael Seidman Justin Bishop Yael Heher Atis Muehlenbachs Shree Sharma Jennifer Black Walter Henricks Raouf Nakhleh Jeanne Shen Thomas Brenn John Higgins Ericka Olgaard Steven Shen Fadi Brimo Jason Hornick Horatiu Olteanu Jiaqi Shi Natalia Buza Mojgan Hosseini Kay Park Wun-Ju Shieh Yingbei Chen David Hwang Rajiv Patel Konstantin Shilo Benjamin Chen Michael Idowu Yan Peng Steven Smith Rebecca Chernock Peter Illei David Pisapia Lauren Smith Andres Chiesa-Vottero Kristin Jensen Jenny Pogoriler Aliyah Sohani James Conner Vickie Jo Alexi Polydorides Heather Stevenson-Lerner Claudiu Cotta Kirk Jones Sonam Prakash Khin Thway Tim D’Alfonso Chia-Sui Kao Manju Prasad Evi Vakiani Leona Doyle Ashraf Khan Bobbi Pritt Sonal Varma Daniel Dye Michael Kluk Peter Pytel Marina Vivero Andrew Evans Kristine Konopka Charles Quick Yihong Wang Alton Farris Gregor Krings Joseph Rabban Christopher Weber Dennis Firchau Asangi Kumarapeli Raga Ramachandran Olga Weinberg Ann Folkins Frank Kuo Preetha Ramalingam Astrid Weins Karen Fritchie Alvaro Laga Priya Rao Maria Westerhoff Karuna Garg Robin LeGallo Vijaya Reddy Sean Williamson James Gill Melinda Lerwill Robyn Reed Laura Wood Anthony Gill Rebecca Levy Michelle Reid Wei Xin Ryan Gill Zaibo Li Natasha Rekhtman Mina Xu Tamara Giorgadze Yen-Chun Liu Michael Rivera Rhonda Yantiss Raul Gonzalez Tamara Lotan Mike Roh Akihiko Yoshida Anuradha Gopalan Joe Maleszewski Marianna Ruzinova Xuefeng Zhang Jennifer Gordetsky Adrian Marino-Enriquez Peter Sadow Debra Zynger Ilyssa Gordon Jonathan Marotti Safia Salaria Alejandro Gru Jerri McLemore Steven Salvatore To cite abstracts in this publication, please use the following format: Author A, Author B, Author C, et al. Abstract title (abs#). Laboratory Investigation 2018; 98 (suppl 1): page# GENITOURINARY PATHOLOGY microdissection (LCM). LCM was performed to isolate HGPIN, IDCP, and the major higher and lower grade components of IC using the p63 (INCLUDING RENAL TUMORS) IHC as a guide. DNA and RNA were isolated and the corresponding libraries were prepared. NGS was performed on Ion S5XL sequencer using OCP 143-gene panel. Variants were called using Ion Reporter 894 Prostate Cancer with Cribriform Pattern (CFPC) is analysis tool (ThermoFisher). Associated with Adverse Clinical and Pathological Results: Sequencing results are presented in the table. Sequencing Features in Prostate Biopsies (Bx) with Gleason revealed a common set of aberrations present in all microdissected Score (GS) 7 (3+4) Prostate Cancer (PC) components. IDCP and IC show a similar genetic profile, which is Eman Abdulfatah1, Dongping Shi2, Rohith Arcot3, Hui Guan3, Elisabeth more complex than that of concurrent HGPIN. 4 5 1 2 I Heath , Wael Sakr . Wayne State University, Detroit, MI, Wayne FOR TABLE DATA, SEE PAGE 403, FIG. 895 State University/Detroit Medical Center, Detroit, MI, 3Wayne State University, 4Karmanos Cancer Institute, Detroit, MI, 5Wayne State Conclusions: Our results show that synchronous HGPIN, invasive University/Harper University Hospital, Detroit, MI adenocarcinoma and IDCP within a single prostate share a group of core genetic abnormalities that are maintained throughout the Background: Gleason grade 4 (GG4) PC has different architectural process of tumor progression. Therefore, all the elements probably patterns with % of GG4 being an important prognosticator in arise from a single precursor (HGPIN). The genetic makeup of IDCP patients(pts) with GS 7(3+4) PC. Recent reports indicate that CFPC may closely resembles that of adjacent IC, supporting that IDCP represents be an additional, independent adverse risk factor in this PC category. ductal spread of coexisting IC. Alternatively, IDCP might arise as We aimed to explore the potential association of CFPC with aggressive a result of duct-confined progression of HGPIN that subsequently clinicopathologic parameters in men with GS 7(3+4) PC on Bx. develops invasion within a very short period of time, which would Design: All pts diagnosed with Bx GS 7(3+4) PC between 2005-2011 explain why IDCP is only exceptionally found alone. in our institution were included. PSA at diagnosis, no. of positive cores, % of core involvement, % of GG4 and presence of CFPC were documented. The presence of CFPC was correlated with post treatment 896 Identification and validation of novel long non- parameters; stage and margin status following radical prostatectomy coding RNA signatures of enzalutamide resistance (RP); biochemical recurrence(BR), distant metastasis(DM), progression in prostate cancer free survival(PFS) and cancer specific mortality(CSM) for all pts. 1 2 2 Statistical analyses were conducted using KM and regression analysis. John Aird , Steven G Gray , Anne-Marie Baird , Marvin Chang Jui Lim3, Ray McDermott4, Stephen Finn5. 1St. James’s Hospital, Dublin, Results: 283 pts qualified for analyses. We classified 74%,53%,26% 2St. James’s Hospital, 3University of Dublin, Trinity College, 4Adelaide and 21% of GG4 as fused glands, poorly formed glands, glomeruloid and Meath Hospital incorporating The National Children’s Hospital, and CFPC, respectively. At diagnosis, pts with CFPC had significantly 5University of Dublin, Trinity College, Dublin higher PSA, more positive cores, higher % core involvement and higher % of GG4 (P=0.03,P=0.001,P=0.001 and P=0.001,respectively). Forty Background: Despite significant advances, castration resistant percent of pts were treated with RP, 55% by radiation therapy(RT), 3% prostate cancer (CRPC) remains incurable. Sustained androgen- cryoablation and 2% chose active surveillance. receptor (AR) signalling despite low levels of circulating androgens is a key feature of CRPC. New drugs like enzalutamide target the AR After RP, GS was significantly upgraded for pts with CFPC(P=0.03). but drug resistance inevitably develops via sustained AR signalling. Median follow up was 89 (range 4-150)months. BR and DM were Although not yet fully understood, known mechanisms for sustained significantly higher in pts with CFPC compared to those without AR signalling include alternate AR splicing, AR gene overexpression/ (P=0.001 & P=0.001,respectively). On univariate regression analysis, amplification and AR gene mutations. CFPC was a significant predictor of BR(P=0.001), DM(P=0.003) and CSM(P=0.01). On multivariate analysis, CFPC was an independent Long non-coding RNAs (lncRNAs) are emerging as key modulators predictor of CSM(P=0.02). When stratifying pts based on treatment, of gene expression and have been shown to be associated with drug CFPC was significantly associated with BR(P=0.03) and an resistance in cancer. Our hypothesis is that lncRNAs are associated independent predictor of CSM(P=0.02) after RP. Following RT, BR was with resistance to enzalutamide in prostate cancer. also significantly higher in pts with CFPC(P=0.009). Design: Using a model of spontaneous resistance to enzalutamide in On KM analysis, pts with CFPC had significantly shorter BR free LNCaP cells previously developed by Korpal et al (Cancer Discovery, survival and PFS(P=0.001 and P=0.008, respectively). PFS was also September 2013) we profiled enzalutamide sensitive, and both significantly shorter in pts with CFPC who underwent RP(P=0.04), while weakly and strongly enzalutamide resistant clones for 40,173 well pts who received RT had shorter BRFS(P=0.001) and PFS(P=0.01). characterized lncRNAs using microarray technology. Differentially expressed lncRNAs with statistical significance were identified through Conclusions: Our data strongly suggest that CFPC, as a variant of GG4 Volcano Plot filtering. The threshold was fold change ≥ 2.0 and p-value PC, is significantly associated with poorer clinicopathololgic features. ≤ 0.05. False discovery rates were adjusted from all the p-values by Accounting for this variant has the potential of influencing prognostic Benjamini-Hochberg method for multiple testing correction. Both and management considerations. highly upregulated and candidate lncRNAs with strong biological relevance (known association with CRPC or with androgen signalling) were validated using qPCR. 895 Comparison of synchronous high grade prostate Results: Principal component
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