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Journal Thoracic Oncology

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Abstracts <strong>Journal</strong> of <strong>Thoracic</strong> <strong>Oncology</strong> • Volume 12 Issue S1 January 2017<br />

United States of America, 7 Pathology, St. Francis Hospital, Memphis/TN/United<br />

States of America, 8 Pathology, Jackson-Madison County General Hospital, Jackson/<br />

TN/United States of America, 9 Pathology, Methodist Healthcare, Memphis/TN/<br />

United States of America, 10 Pathology, Doctors Anatomic Pathology, Jonesboro/AR/<br />

United States of America, 11 Pathology, North Mississippi Medical Center, Tupelo/<br />

MS/United States of America<br />

Background: Incomplete retrieval of intrapulmonary lymph nodes and missed<br />

nodal metastasis are associated with worse-than-expected survival after<br />

(NSCLC) resection. We tested the nodal yield from a novel gross dissection<br />

method. Methods: multi-institutional prospective cohort study of<br />

intrapulmonary (stations 11-14) lymph node yield from lobectomy/greater<br />

NSCLC resection specimens from 11 US hospitals from 2009-2016. A novel gross<br />

dissection protocol was used in 2 hospital pathology departments from June<br />

2012 onwards. Intrapulmonary lymph node yields from all lobectomy or greater<br />

resections before and after the new protocol in the intervention hospitals were<br />

compared to yields from 9 non-intervention hospitals over the same time-span,<br />

using Wilcoxon-Mann-Whitney. From February 2015, some randomly selected<br />

discarded remnant lung specimens in the intervention hospitals were<br />

re-dissected for inadvertently discarded lymph nodes as a quality control<br />

measure. Results: Intrapulmonary lymph node yields in the 2 groups of<br />

hospitals was similar at baseline, followed by a significant increase in the<br />

intervention hospitals with the novel dissection protocol (Table 1).<br />

Subsequently, in 112 specimens re-dissected for independent quality control<br />

after application of the novel dissection protocol, discarded lymph nodes were<br />

found in 30 (27%), down from 90% historically; discarded lymph nodes with<br />

metastasis in 6 (5%), down from 29% historically; and missed N1 nodal<br />

metastasis was found in 1 of 67 (1.5%) pN0 patients, down from 12% historically.<br />

The median number of missed intrapulmonary lymph nodes was 0 (down from 6<br />

historically), the mean (standard deviation) was 0.88 (2.58). The gross<br />

dissection protocol required a median of 15 minutes (range 10 – 24).<br />

Conclusion: A novel gross dissection protocol significantly improves the<br />

thoroughness of intrapulmonary lymph node retrieval and can be successfully<br />

implemented in community-level pathology departments, providing a pathway<br />

for quality improvement in pathologic nodal staging of resected NSCLC.<br />

Keywords: Quality of care, Pathologic staging, lymph nodes, lung cancer<br />

surgery<br />

POSTER SESSION 3 – P3.01: BIOLOGY/PATHOLOGY<br />

MORPHOLOGY –<br />

WEDNESDAY, DECEMBER 7, 2016<br />

P3.01-032 PELP1 EXPRESSION IN MOLECULARLY CLASSIFIED LUNG<br />

ADENOCARCINOMAS<br />

Charuhas Deshpande 1 , Shweta Patel 2 , Jan Silverman 2<br />

1 Pathology & Laboratory Medicine, University of Pennsylvania, Philadelphia/<br />

United States of America, 2 Pathology & Laboratory Medicine, Allegheny Health<br />

Network, Pittsburgh/PA/United States of America<br />

Background: Proline-, glutamic acid-, and leucine-rich protein 1 (PELP1) is a<br />

scaffolding protein which functions as a coregulator of several transcription<br />

factors and nuclear receptors. It has a histone-binding domain and plays<br />

essential roles in several pathways including hormonal signaling. PELP1 is a<br />

coregulator of estrogen receptor (ER) and has been shown to be deregulated,<br />

contributing to therapy resistance and is a prognostic biomarker in breast<br />

cancer survival, as well as in other hormone-dependent cancers. Estrogens are<br />

also known to enhance lung tumorigenesis by estrogen receptor pathway 1,<br />

2 . In this study, we investigated the expression of PELP1 in molecularly<br />

classified lung adenocarcinomas, specifically those with known EGFR and<br />

KRAS mutations. Methods: Tissue microarray (TMA) was created using 0.6<br />

mm tissue cores in triplicates from 62 resected lung adenocarcinoma cases<br />

(26 with EGFR mutation and 36 with KRAS mutation). PELP1 antibody (Clone<br />

EPR15212; ABCAM) immunostaining was performed after heat induced epitope<br />

retrieval. Nuclear immunoreactivity for PELP1 was scored for staining intensity<br />

as 0 (negative), 1+ (weak, nucleolar), 2+ (moderate, nucleolar/nuclear) and 3+<br />

(strong nucleolar/nuclear). For statistical analysis, binary split was done as<br />

negative (scores 0 and 1+) and positive (scores 2+ and 3+). These TMAs were<br />

also stained for estrogen receptor (ER) with SP1 rabbit monoclonal antibody<br />

and scored similarly. Results: In our study, 61 cases had evaluable tissue cores<br />

with tumor. Positive PELP1 expression was noted in 14/25 (56%) EGFR mutated<br />

and 30/36 (83%) in KRAS mutated lung adenocarcinomas (p

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