Citations
2 citation(s) found for "Young, Lauren".
Integrated Molecular and Clinical Characterization of Pulmonary Large Cell Neuroendocrine Carcinoma
Chiang, Anne C. , Nassar, Amin H. , Kim, Chul , Farhat, Elias Bou , Matteson, Kelsey, Lau, Shun‐Fat , Gallegos, Jesús Antonio Ocejo , Ardeshir‐Larijani, Fatemeh , Leal, Ticiana, Alam, Sumaye, Gray, Jhanelle E. , Hicks, J. Kevin , Kaldas, David , Baena, Javier, Berjaga, María Zurera, Grohé, Christian , Leuders, Heike, Mingo, Emanuele Claudio , Pancirer, Danny, Cheung, Justin M., Lin, Jessica, Watson, Alexander, Camidge, D. Ross , Parikh, Kaushal , Aggarwal, Vanya , Ahmed, Murtaza, Zhang, Jun , Nagasaka, Misako , Awosika, Nichola, Alhamad, Khaled, Zaman, Unaiza, Gupta, Divya , Lau, Chelsea, Khan, Hina, Liauw, Justin , Brown, Tyiesha , Mosteiro, Miguel , Lopes, Gilberto , Patrick, C. , Young, Lauren K. , Aljumaily, Raid, Mirza, Haris , TAKEBE, Y., Baena, Javier , Nassar, Amin H. , Ocejo Gallegos, Jesus Antonio , Bou Farhat, Elias , Espinar, Javier Baena , Adeyelu, Tolulope Tosin , Abushukair, Hassan , Rakaee, Mehrdad , Takabe, Yamato J. , Ramalingam, Suresh S. , Alam, Sumaiya, Nana, Frank Aboubakar , Citarella, Fabrizio , Cortellini, Alessio , Das, Millie , Ellis-Caleo, Timothy John , Linehan, William Marston , Sridhar, Arthi , Crowley, Fionnuala , Marron, Thomas , Sankar, K. Nathan , Kawtharany, Hassan , Owen, Dwight H , Li, Mingjia , Pinato, David J. , Puri, Sonam , Velázquez, Ana I. , Moliner, Laura , Rocha, Pedro , Evans, Mark G. , Vanderwalde, Ari M. , Elliott, Andrew , Nieva, Jorgé , Patrick, C. , Borghaei, Hossein , Lee, Matthew , Kwiatkowski, David J. , Herbst, Roy S. , Flavell, Richard A. , Naqash, Abdul Rafeh
No container title available | May 16, 2025 | Volume: No volume available | Issue: No issue available | Pages: No page available
Abstract Pulmonary large cell neuroendocrine carcinoma (LCNEC) is a rare, aggressive lung tumor marked by significant molecular heterogeneity. In a study of 590 patients across two independent cohorts, we observed comparable overall survival across treatment regimens (chemotherapy, chemoimmunotherapy, immunotherapy) without unexpected adverse events. Genomic analysis identified distinct NSCLC-like (KEAP1, KRAS, STK11 mutations) and SCLC-like (RB1, TP53 mutations) LCNEC subtypes, with 80% aligning with SCLC transcriptional profiles. Serial sampling revealed stable mutational but shifting transcriptomic landscapes over time. NSCLC-like LCNECs showed elevated FGL-1 (a LAG-3 ligand) and SPINK1 expression, while SCLC-like subtypes expressed higher levels of DLL3. Immunofluorescence confirmed FGL-1 in NSCLC-like LCNECs, and H&E slide analyses indicated fewer tumor-infiltrating lymphocytes in LCNECs versus other lung cancers. These findings highlight LCNEC’s distinct immunogenomic profile, supporting future investigations into LAG-3, SPINK1, and DLL3-targeted therapies.
Precision medicine for gallbladder cancer using somatic copy number amplifications (SCNA) and DNA repair pathway gene alterations.
Javle, Milind , Catenacci, Daniel V.T. , Jain, Apurva , Young, Lauren , Wang, Kai , Chung, Jon , Schrock, Alexa B. , Gay, Laurie M. , Ahn, Daniel H. , Kelley, Robin Kate , Ganesan, Shridar , Stephens, Phil , Miller, Vincent A. , Ali, Siraj M. , Shroff, Rachna T. , Hezel, Aram F. , Goyal, Lipika , Bekaii‐Saab, Tanios , Ross, Jeffrey S
Journal of Clinical Oncology | July 6, 2017 | Volume: 35 | Issue: 15_suppl | Pages: 4076-4076
10.1200/jco.2017.35.15_suppl.4076
4076 Background: Gallbladder carcinoma (GBC) is commonly diagnosed at an advanced, unresectable disease stage and has a poor prognosis. Comprehensive genomic profiling (CGP) has a developing role in guiding systemic, precision anti-cancer therapy. Methods: We performed hybrid capture-based CGP on FFPE samples for 491 consecutive advanced GBCs. Mean coverage depth was >550X for up to 315 cancer-related genes plus 37 introns from 28 genes frequently rearranged in cancer. All 4 classes of genomic alterations (GA) were detected. Tumor mutational burden (TMB) was determined on up to 1.1 Mb of sequenced DNA. Results: Median age was 64 (range 25-88) and 69% (337/491) of patients were female. 96% (470), 2.9% (14), and 1.4% (7) of GBC patients had the diagnosis of adenocarcinoma, adenosquamous, or carcinoma not specified (NOS), respectively. Commonly altered genes were TP53 (62%), CDNK2A (31%), ARID1A (18%), and SMAD4 (15%), and most of the genetic aberrations (GA) were short variants. Potentially targetable SCNAs (including ERBB genes, MET, FGFRs, and the CCND1-FGF3/4/19 11q13 amplicon) were identified in 21% of cases (Table). Oncogenic BRAF, ALK, or FGFR2/3 rearrangements were found in 7 cases (1.4%). Moreover, 7.8% of cases had BRCA2 or ATM GA, and 0.8% had INI1loss suggesting benefit from PARP or EZH2 inhibitors, respectively. TMB was low; the 25th, 50th, and 75th percentiles were 2.5, 3.8 and 6.3 mutations/Mb, respectively. Less than 1% of cases had microsatellite instability. Radiological response to TKIs and immunotherapy was noted. Conclusions: In addition to the significant opportunity for anti-HER targeted therapies, other subsets of GBC cases harbored kinase GA (particularly SCNA), the 11q13 amplicon, or BRCA2/ ATM/ INI1mutations that are linked to therapeutic benefit. How the frequency of both driver SCNA and DNA repair alterations in GBC can be linked with inflammation awaits additional investigation. [Table: see text]