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Pulmonary Pathology (Including Mediastinal)

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Pulmonary Pathology (Including Mediastinal) ANNUAL MEETING ABSTRACTS 471A Results: We show identical molecular signature in the original leukemic blasts and the 1895 Norovirus Infection in Pediatric Small Intestine Allografts: A subsequent histiocytic neoplasms in two pediatric patients with TALL. Using FISH, one Clinicopathological Study of a Cohort of 23 Patients case had the same biallelic deletion of the CDKN2A (TP16) locus on 9p21, while using Wei Xu, Stuart Kaufman, Joeffrey Chahine, Brandi Higgins, Nada Yazigi, Cal next generation sequencing, the other had the same G13D mutation in the NRAS gene. Matsumoto, Khalid Khan, Bhaskar VS Kallakury. Medstar Georgetown Univeristy Conclusions: This confirms a common clonal origin and highlights the need to perform Hospital, Washington, DC. appropriate molecular studies in such patients to better understand the mechanism Background: Human Norovirus in the family Caliciviridae is a major cause of and etiology behind histiocytic neoplasm seemingly born out of other hematopoietic epidemic gastroenteritis. Norovirus infections are typically acute and self-limited. malignancies. However, Norovirus infection, the most frequent cause of acute pediatric gastroenteritis in the era of Rotavirus vaccine, produces a prolonged and chronic diarrhea in immunocompromised host, particularly in pediatric small intestine transplant recipients. 1893 Assessment of PD-L1 Expression in Pediatric High-Grade This study aimed to characterize histological and immunohistochemical features of Gliomas Mariona Suñol, Iban Aldecoa, Ofelia Cruz, Angel Montero, Eva Rodríguez, Teresa small bowl allograft biopsies before and after Novovirus infection. Ribalta. Sant Joan de Déu Barcelona Children’s Hospital, Barcelona, Spain. Design: We retrospectively reviewed H&E slides and performed IHC staining for Background: Programmed death-ligand 1 (PD-L1) is an immune-inhibitory receptor proliferation index (Ki67), apoptosis (Caspase 3), T lymphocytes (CD3) on pre and expressed in some tumors, including high-grade gliomas (HGG). Expression of PD- post Novovirus enteritis (11 to 204 days from symptom onset to PCR diagnosis) in L1 has been associated with poorer outcomes and may predict response to anti-PD-1 23 small bowel transplant recipients at MGUH between 2007 and 2014. We studied agents. Immune checkpoint-inhibitor therapies can facilitate tumor regression and immunohistochemical features by counting the number of intraepithelial T lymphocytes, clinical studies of PD-1 blockade are now being initiated in pediatric patients with proliferation index and apoptotic bodies in both villi and crypts per 100 enterocytes. high-grade gliomas (HGG), however, little is known regarding PD-L1 expression in Results: Comparison was made between pre Novovirus infection group (controls) these childhood tumors. In the present study, we aimed to investigate the expression and PCR confirmed Novovirus infection group. Compared with controls, biopsies of PD-L1 in a series of pediatric HGGs of our institution. with Novovirus infection group showed significantly increased in intraepithelial Design: We measured the incidence of PD-L1 expression in 54 pediatric HGGs (ages T lymphocytes (15.1 ± 6.0 versus 7.7 ± 2.9 cells/100 enterocytes, P < .05), higher 0-17 y. o.). Whole slide sections were evaluated by IHC using the rabbit anti-PD-L1/ proliferation index in villi (7.3 ± 4.0 versus 2.9 ± 1.8 cells/100 enterocytes, P < .05) CD274 (clone SP142) monoclonal antibody. Nineteen of the tumors were autopsy and crypts (78.7 ± 12.1 versus 50.3 ± 11.7 cells /100 enterocytes, P < .05 ), higher cases. Tumor locations included pons (23), cerebral hemispheres (12), supratentorial apoptosis activity in superficial lamina propria (1.0 ± 0.5 versus 0.4 ± 0.3 cells/100 deep structures (7), spinal cord (4), and other (8). The percentage of PD-L1-expressing enterocytes, P < .05). There was no significant difference in crypts apoptosis activity cells was assessed semi-quantitatively. between Novovirus infection group and control group. Results: Fifty-seven percent (34/59) of tumors (28/40 biopsies; 6/19 autopsies) Conclusions: In summary, all Novovirus infection biopsies showed increased expressed PD-L1 in at least 1% of tumor cells. Staining was heterogeneous, with the intraepithelial T lymphocytes and villi blunting, increased proliferation index in vast majority of the cells demonstrating both membrane and cytoplasmic staining. both villi and crypts and increased lamina propria apoptosis, deemed characteristic Small clusters of strongly positive tumor cells were observed in 7 cases; a faint diffuse of Novovirus infection. These features may be helpful in designing a test group to cytoplasmic staining was seen in 7 cases and scattered positive cells were identified in differentiate Novovirus enteritis from mild acute rejection, warranting further study. 20 cases. Many of the scattered PD-L1 expressing cells had either the morphology of either normal neurons, or inflammatory cells. A combination of patterns was observed in 7 cases. Two cases showed a weak nuclear stain. Pulmonary Pathology Conclusions: Similar to adult HGG that have been recently profiled for PD-L1 expression, expression in our series of pediatric HGG patients using anti-PD-L1/CD274 (including Mediastinal) (clone SP142) is frequent, although is largely confined to a minority subpopulation of tumor cells. 1896 MET Exon 14 Splicing Mutations and Intragenic Deletions in Non-Small Cell Lung Cancer: A Study of Co-Occurring Genomic Mutations 1894 Histopathologic Correlation with the Newly Defined “Term” and Copy Number Alterations Deepu Alex, Joseph Montecalvo, William Travis, Maria E Arcila, Marc Ladanyi. Placenta Ashley N Vogel, Jordyn B Tumas, Dan de Cotiis, Amanda Roman, Joanna Chan. Thomas Memorial Sloan Kettering Cancer Center, New York, NY. Jefferson University, Philadelphia, PA; Einstein Medical Center, Philadelphia, PA. Background: Splicing mutations of MET exon 14 at the splice acceptor and donor sites Background: Previously, uncomplicated “term” pregnancies were considered a have been previously reported to cause exon skipping, resulting in loss of the CBL E3- homogeneous group defined as 37-41 weeks gestational age. However, neonatal ubiquitin ligase-binding site which is responsible of MET protein turnover. The presence outcomes, especially respiratory morbidity, varied significantly within this time frame. of these oncogenic mutations makes the tumor responsive to MET-targeted therapies. In 2013, the American Congress of Obstetrics and Gynecology (ACOG) reclassified Design: Comprehensive cancer genomic profiling was performed using a hybridization term pregnancy into early (37 0/7-38 6/7 weeks), full (39 0/7-40 6/7 weeks), late (41 capture-based next-generation sequencing (NGS) assay for targeted deep sequencing 0/7-41 6/7 weeks), and postterm (>42 0/7 weeks) pregnancies to reflect these clinical of all exons and selected introns (inclusive of MET) of 410 key cancer genes in differences. This study examines the correlation between this new stratification and formalin-fixed, paraffin-embedded tumors. Bar-coded libraries from patient-matched placental pathology. tumor and normal samples are captured, sequenced, and subjected to a custom analysis Design: From 2012-2016, 674 consecutive singleton placentas were evaluated for pipeline to identify somatic mutations, copy number alterations and select structural gestational age, placental weight, cord insertion, malperfusion, fetal/maternal vascular rearrangements. Next generation sequencing results from 1682 NSCLCs were reviewed stasis, meconium, fetal/maternal inflammatory response and decidual vasculopathy. to identify cases with MET exon 14 alterations. Statistical analysis used single and multiple variable ANOVA as well as single and Results: MET exon 14 alterations were detected in 58 patients [male=27, female=31] multiple variable logistical regression based on gestational age. When stratified into with a median age of 72 years (44-89). Tumor morphologies were variable and included early, full, and late term, data was evaluated using Chi-Square and Fischer exact test pleomorphic sarcoma, lung adenocarcinoma (lepidic, acinar and mixed patterns), analysis on a contingency table basis. squamous cell carcinoma and adenosquamous carcinoma. 42 cases had sequence variants Results: Retrospective evaluation shows that placental weight (p<0.0003) and at the splice donor site (6 not previously reported), 11 cases had sequence variants at the increased perivillous fibrin (p<0.001) directly correlate to gestational age. In addition, splice acceptor site and 5 cases had deletions within exon 14 that included the CBL E3- acute chorioamnionitis and funisitis correlate to increasing gestational age when ubiquitin ligase-binding site, Y1003 (3 not previously reported). Based on the analysis of compartmentalized as previously described (p<0.023 and p<0.001, respectively). The 410 genes of the sequencing panel, MET exon 14 mutated NSCLCs frequently showed remainder of the tested variables show no significant difference between early, full the following co-mutations: TP53 alterations (32%), MDM2 and CDK4 amplifications and late term placentas. (25 and 21% respectively), and TERT alterations (21%). Concurrent MET amplification Conclusions: Stratifying placentas by the new ACOG terminology significantly (as determined by the hybrid capture NGS assay) involving the mutated allele was correlates to placental weight, increased perivillous fibrin, chorioamnionitis and detected in 5 cases (9%). One case
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