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1,372 results on '"Camidge, D Ross"'

203. First-In-Human, First-In-Class, Phase I Trial of the Fucosylation Inhibitor SGN-2FF in Patients with Advanced Solid Tumors

Author

Do, Khanh T., primary, Chow, Laura Quan Man, additional, Reckamp, Karen, additional, Sanborn, Rachel E., additional, Burris, Howard, additional, Robert, Francisco, additional, Camidge, D. Ross, additional, Steuer, Conor E., additional, Strickler, John H., additional, Weise, Amy, additional, Specht, Jennifer M., additional, Gutierrez, Martin, additional, Haughney, Peter, additional, Hengel, Shawna, additional, Derleth, Christina Louise, additional, and Yap, Timothy A., additional

Published
2021
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204. Clinicopathologic Features and Response to Therapy ofNRG1Fusion–Driven Lung Cancers: The eNRGy1 Global Multicenter Registry

Author

Drilon, Alexander, primary, Duruisseaux, Michael, additional, Han, Ji-Youn, additional, Ito, Masaoki, additional, Falcon, Christina, additional, Yang, Soo-Ryum, additional, Murciano-Goroff, Yonina R., additional, Chen, Haiquan, additional, Okada, Morihito, additional, Molina, Miguel Angel, additional, Wislez, Marie, additional, Brun, Philippe, additional, Dupont, Clarisse, additional, Branden, Eva, additional, Rossi, Giulio, additional, Schrock, Alexa, additional, Ali, Siraj, additional, Gounant, Valérie, additional, Magne, Fanny, additional, Blum, Torsten Gerriet, additional, Schram, Alison M., additional, Monnet, Isabelle, additional, Shih, Jin-Yuan, additional, Sabari, Joshua, additional, Pérol, Maurice, additional, Zhu, Viola W., additional, Nagasaka, Misako, additional, Doebele, Robert, additional, Camidge, D. Ross, additional, Arcila, Maria, additional, Ou, Sai-Hong Ignatius, additional, Moro-Sibilot, Denis, additional, Rosell, Rafael, additional, Muscarella, Lucia Anna, additional, Liu, Stephen V., additional, and Cadranel, Jacques, additional

Published
2021
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210. Phase I Study of 2- or 3-Week Dosing of Telisotuzumab Vedotin, an Antibody–Drug Conjugate Targeting c-Met, Monotherapy in Patients with Advanced Non–Small Cell Lung Carcinoma

Author

Camidge, D. Ross, primary, Morgensztern, Daniel, additional, Heist, Rebecca S., additional, Barve, Minal, additional, Vokes, Everett, additional, Goldman, Jonathan W., additional, Hong, David S., additional, Bauer, Todd M., additional, Strickler, John H., additional, Angevin, Eric, additional, Motwani, Monica, additional, Parikh, Apurvasena, additional, Sun, Zhaowen, additional, Bach, Bruce Allen, additional, Wu, Jun, additional, Komarnitsky, Philip B., additional, and Kelly, Karen, additional

Published
2021
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212. Abstract CT179: Telisotuzumab vedotin (teliso-v) monotherapy in patients with previously treated c-Met+ advanced non-small cell lung cancer

Author

Camidge, D. Ross, primary, Moiseenko, Fedor, additional, Cicin, Irfan, additional, Horinouchi, Hidehito, additional, Filippova, Elena, additional, Bar, Jair, additional, Lu, Shun, additional, Tomasini, Pascale, additional, Ocampo, Christopher, additional, Sullivan, Danielle, additional, Maag, David, additional, and Goldman, Jonathan W., additional

Published
2021
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213. Abstract CT167: Pooled analysis of drug-related interstitial lung disease (ILD) in 8 single-arm trastuzumab deruxtecan (T-DXd) studies

Author

Powell, Charles A., primary, Modi, Shanu, additional, Iwata, Hiroji, additional, Takahashi, Shunji, additional, Smit, Egbert F., additional, Siena, Salvatore, additional, Chang, Dwan-Ying, additional, Fuchs, Charles S., additional, Nie, Kun, additional, Qin, Amy, additional, Singh, Jasmeet, additional, Taitt, Corina, additional, Verma, Sunil, additional, and Camidge, D. Ross, additional

Published
2021
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215. Abstract CT163: CD73 inhibitor oleclumab plus osimertinib for advanced EGFRm NSCLC: First report of a Phase 1b/2 study

Author

Kim, Dong-Wan, primary, Kim, Sang-We, additional, Camidge, D. Ross, additional, Rizvi, Naiyer A., additional, Marrone, Kristen A., additional, Le, Xiuning, additional, Blakely, Collin, additional, Park, Keunchil, additional, Chang, Gee-Chen, additional, Patel, Sandip Pravin, additional, Cooper, Zachary A., additional, Kumar, Rakesh, additional, Samadani, Ramin, additional, McCombs, Rebecca, additional, Pluta, Michael, additional, Wu, Kevin Yufeng, additional, and Ramalingam, Suresh, additional

Published
2021
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216. PPD01.02 Repotrectinib in Patients With ROS1Fusion-Positive (ROS1+) NSCLC: Update From the Pivotal Phase 1/2 TRIDENT-1 Trial

Author

Drilon, Alexander, Camidge, D. Ross, Lin, Jessica J., Kim, Sang-We, Solomon, Benjamin, Dziadziuszko, Rafal, Besse, Benjamin, Goto, Koichi, Johannes de Langen, Adrianus, Wolf, Jürgen, Lee, Ki Hyeong, Popat, Sanjay, Springfeld, Christoph, Nagasaka, Misako, Felip, Enriqueta, Yang, Nong, Lu, Shun, Kao, Steven, Velcheti, Vamsidhar, Cheema, Parneet, Stopatschinskaja, Shanna, Mehta, Minal, Trone, Denise, Ades, Felipe, Calvet, Christophe Y., and Cho, Byoung Chul

Published
2024
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217. Brigatinib (BRG) in ALK+ crizotinib (CRZ)-refractory non-small cell lung cancer (NSCLC): Final results of the phase 1/2 and phase 2 (ALTA) trials.:Journal of Clinical Oncology

Author

Gettinger, Scott N., Huber, Rudolf M., Kim, Dong-Wan, Bazhenova, Lyudmila, Holmskov Hansen, Karin, Tiseo, Marcello, Langer, Corey J., Paz-Ares, Luis G., West, Howard, Reckamp, Karen L., Weiss, Glen J., Smit, Egbert F., Hochmair, Maximilian, Kim, Sang-We, Ahn, Myung-Ju, Kim, Edward S., Groen, Harry J.M., Pye, Joanna, Vranceanu, Florin, and Camidge, D. Ross

Abstract

9071Background: BRG is a kinase inhibitor approved for the treatment of patients (pts) with ALK+ metastatic NSCLC; specific details for BRG use vary by indication and country. We report long-term efficacy and safety results of the Phase 1/2 and Phase 2 (ALTA) trials of BRG. Methods: The Phase 1/2 study was a single-arm, open-label trial (NCT01449461) of BRG 30?300 mg/d in pts with advanced malignancies. ALTA (NCT02094573) randomized pts with CRZ-refractory ALK+ NSCLC to receive BRG at 90 mg qd (arm A) or 180 mg qd with 7-d lead-in at 90 mg (arm B). For the Phase 1/2 study, investigator assessments of confirmed objective response rate (cORR; RECIST v1.1), duration of response (DoR), progression-free survival (PFS), overall survival (OS), and safety in pts with ALK+ NSCLC are reported. The primary endpoint of ALTA was cORR per investigator; secondary endpoints included cORR per independent review committee (IRC), DoR, PFS, and OS. Results: In the Phase 1/2 study, 137 pts received BRG; of these, 79 pts had ALK+ NSCLC (71/79 had prior CRZ; 28/79 received 180 mg qd [7-d lead-in at 90 mg]; 14/79 received 90 mg qd). In ALTA, 222 pts with CRZ-refractory ALK+ NSCLC were randomized (n = 112/110, arm A/B). At the end of the Phase 1/2 study (Feb 18, 2020), with median 27.7 mo follow-up (?67 mo after last pt enrolled), 4 pts remained on BRG. At the end of ALTA (Feb 27, 2020), with median 19.6/28.3 mo follow-up in arm A/B (?53 mo after last pt enrolled), 10/17 pts in arm A/B were still on treatment. Table shows efficacy results from final analyses with long-term follow-up. In ALTA, the IRC-assessed intracranial cORR in pts with measurable baseline brain metastases was 50% (13/26) in arm A and 67% (12/18) in arm B; Kaplan-Meier (KM) estimated median intracranial DoR was 9.4 mo (95% CI, 3.7, not reached [NR]) in arm A and 16.6 mo (3.7, NR) in arm B. With long-term follow-up, no new safety signals were identified. Treatment-emergent adverse events led to dose interruption (Phase 1/2: 59%; ALTA arm A/B: 49%/61%), dose reduction (13%; 8%/33%), or discontinuation (10%; 4%/13%). Conclusions: BRG showed sustained long-term activity, PFS, and manageable safety in pts with CRZ-refractory ALK+ NSCLC. The 180 mg/d dose after 7-d lead-in at 90 mg/d led to numerically higher median PFS and OS. Final results are similar to those reported for other approved ALK tyrosine kinase inhibitors in this setting. Clinical trial information: NCT01449461, NCT02094573.Phase 1/2(n = 79)ALTA: A(n = 112)ALTA: B(n = 110)cORR, n (%) [95% CI]Per investigator53 (67) [56, 77]51 (46) [36, 55]63 (57) [48, 67]Per IRC?58 (52) [42, 61]62 (56) [47, 66]Median DoR (95% CI),a moPer investigator14.9 (9.9, 29.5)12.0 (9.2, 19.4)13.8 (10.8, 17.6)Per IRC?19.4 (9.2, 24.9)15.7 (13.6, 22.1)Median PFS (95% CI),a moPer investigator14.5 (10.8, 21.2)9.2 (7.4, 11.1)15.6 (11.1, 18.5)Per IRC?9.9 (7.4, 12.8)16.7 (11.6, 21.4)Median OS (95% CI),a mo47.6 (28.6, NR)25.9 (18.2, 45.8)40.6 (32.5, NR)OS at 5 yearsa42%31%43%aKM estimates.

Published
2021

218. Clinicopathologic Features and Response to Therapy of NRG1 Fusion-Driven Lung Cancers : The eNRGy1 Global Multicenter Registry

Author

Drilon, Alexander, Duruisseaux, Michael, Han, Ji-Youn, Ito, Masaoki, Falcon, Christina, Yang, Soo-Ryum, Murciano-Goroff, Yonina R., Chen, Haiquan, Okada, Morihito, Molina, Miguel Angel, Wislez, Marie, Brun, Philippe, Dupont, Clarisse, Brandén, Eva, Rossi, Giulio, Schrock, Alexa, Ali, Siraj, Gounant, Valerie, Magne, Fanny, Blum, Torsten Gerriet, Schram, Alison M., Monnet, Isabelle, Shih, Jin-Yuan, Sabari, Joshua, Perol, Maurice, Zhu, Viola W., Nagasaka, Misako, Doebele, Robert, Camidge, D. Ross, Arcila, Maria, Ou, Sai-Hong Ignatius, Moro-Sibilot, Denis, Rosell, Rafael, Muscarella, Lucia Anna, Liu, Stephen, V, Cadranel, Jacques, Drilon, Alexander, Duruisseaux, Michael, Han, Ji-Youn, Ito, Masaoki, Falcon, Christina, Yang, Soo-Ryum, Murciano-Goroff, Yonina R., Chen, Haiquan, Okada, Morihito, Molina, Miguel Angel, Wislez, Marie, Brun, Philippe, Dupont, Clarisse, Brandén, Eva, Rossi, Giulio, Schrock, Alexa, Ali, Siraj, Gounant, Valerie, Magne, Fanny, Blum, Torsten Gerriet, Schram, Alison M., Monnet, Isabelle, Shih, Jin-Yuan, Sabari, Joshua, Perol, Maurice, Zhu, Viola W., Nagasaka, Misako, Doebele, Robert, Camidge, D. Ross, Arcila, Maria, Ou, Sai-Hong Ignatius, Moro-Sibilot, Denis, Rosell, Rafael, Muscarella, Lucia Anna, Liu, Stephen, V, and Cadranel, Jacques

Abstract

PURPOSE Although NRG1 fusions are oncogenic drivers across multiple tumor types including lung cancers, these are difficult to study because of their rarity. The global eNRGy1 registry was thus established to characterize NRG1 fusion-positive lung cancers in the largest and most diverse series to date. METHODS From June 2018 to February 2020, a consortium of 22 centers from nine countries in Europe, Asia, and the United States contributed data from patients with pathologically confirmed NRG1 fusion-positive lung cancers. Profiling included DNA-based and/or RNA-based next-generation sequencing and fluorescence in situ hybridization. Anonymized clinical, pathologic, molecular, and response (RECIST v1.1) data were centrally curated and analyzed. RESULTS Although the typified never smoking (57%), mucinous adenocarcinoma (57%), and nonmetastatic (71%) phenotype predominated in 110 patients with NRG1 fusion-positive lung cancer, further diversity, including in smoking history (43%) and histology (43% nonmucinous and 6% nonadenocarcinoma), was elucidated. RNA-based testing identified most fusions (74%). Molecularly, six (of 18) novel 5 ' partners, 20 unique epidermal growth factor domain-inclusive chimeric events, and heterogeneous 5 '/3 ' breakpoints were found. Platinum-doublet and taxane-based (post-platinum-doublet) chemotherapy achieved low objective response rates (ORRs 13% and 14%, respectively) and modest progression-free survival medians (PFS 5.8 and 4.0 months, respectively). Consistent with a low programmed death ligand-1 expressing (28%) and low tumor mutational burden (median: 0.9 mutations/megabase) immunophenotype, the activity of chemoimmunotherapy and single-agent immunotherapy was poor (ORR 0%/PFS 3.3 months and ORR 20%/PFS 3.6 months, respectively). Afatinib achieved an ORR of 25%, not contingent on fusion type, and a 2.8-month median PFS. CONCLUSION NRG1 fusion-positive lung cancers were molecularly, pathologically, and clinically more heterogeneous tha

Published
2021
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219. Activity and Safety of Mobocertinib (TAK-788) in Previously Treated Non-Small Cell Lung Cancer with EGFR Exon 20 Insertion Mutations from a Phase I/II Trial.

Author

Riely, Gregory J, Riely, Gregory J, Neal, Joel W, Camidge, D Ross, Spira, Alexander I, Piotrowska, Zofia, Costa, Daniel B, Tsao, Anne S, Patel, Jyoti D, Gadgeel, Shirish M, Bazhenova, Lyudmila, Zhu, Viola W, West, Howard L, Mekhail, Tarek, Gentzler, Ryan D, Nguyen, Danny, Vincent, Sylvie, Zhang, Steven, Lin, Jianchang, Bunn, Veronica, Jin, Shu, Li, Shuanglian, Jänne, Pasi A, Riely, Gregory J, Riely, Gregory J, Neal, Joel W, Camidge, D Ross, Spira, Alexander I, Piotrowska, Zofia, Costa, Daniel B, Tsao, Anne S, Patel, Jyoti D, Gadgeel, Shirish M, Bazhenova, Lyudmila, Zhu, Viola W, West, Howard L, Mekhail, Tarek, Gentzler, Ryan D, Nguyen, Danny, Vincent, Sylvie, Zhang, Steven, Lin, Jianchang, Bunn, Veronica, Jin, Shu, Li, Shuanglian, and Jänne, Pasi A

Abstract

Mobocertinib, an oral epidermal growth factor receptor (EGFR) inhibitor targeting EGFR gene mutations, including exon 20 insertions (EGFRex20ins), in non-small cell lung cancer, was evaluated in a phase I/II dose-escalation/expansion trial (ClinicalTrials.gov NCT02716116). Dose escalation identified 160 mg/d as the recommended phase 2 dose and maximum tolerated dose. Among 136 patients treated with 160 mg/d, the most common any-grade treatment-related adverse events (TRAE; >25%) were diarrhea (83%), nausea (43%), rash (33%), and vomiting (26%), with diarrhea (21%) the only grade ≥3 TRAE >5%. Among 28 EGFRex20ins patients treated at 160 mg/d, the investigator-assessed confirmed response rate was 43% (12/28; 95% confidence interval, 24%-63%) with median duration of response of 14 months (5.0-not reached) and median progression-free survival of 7.3 months (4.4-15.6). Mobocertinib demonstrated antitumor activity in patients with diverse EGFRex20ins variants with a safety profile consistent with other EGFR inhibitors. SIGNIFICANCE: No oral EGFR-targeted therapies are currently approved for patients with EGFRex20ins NSCLC. Mobocertinib demonstrated antitumor activity with manageable toxicity in patients with advanced EGFRex20ins NSCLC in this study, supporting additional development of mobocertinib in this patient population.See related commentary by Pacheco, p. 1617.This article is highlighted in the In This Issue feature, p. 1601.

Published
2021

222. O10-2 Telisotuzumab vedotin monotherapy in Asian patients with c-Met–overexpressing advanced non-small cell lung cancer

Author

Horinouchi, Hidehito, Camidge, D. Ross, Bar, Jair, Goldman, Jonathan, Moiseenko, Fedor, Filippova, Elena, Cicin, Irfan, Bradbury, Penelope, Daaboul, Nathalie, Tomasini, Pascale, Ciuleanu, Tudor, Planchard, David, Moskovitz, Mor, Girard, Nicolas, Dunbar, Martin, Bolotin, Ellen, Looman, Jim, Ratajczak, Christine, and Lu, Shun

Published
2023
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224. Brief Report: Prospective observational study showing early pulmonary function changes associated with brigatinib initiation

Author

Ng, Terry L., Johnson, Amber, Nemenoff, Raphael A., Hsieh, Elena, Osypuk, Andrea Abeyta, van Bokhoven, Adrie, Li, Howard, Camidge, D. Ross, and Schenk, Erin L.

Subjects
Carbon Monoxide, Lung Neoplasms, Organophosphorus Compounds, Pyrimidines, Humans, Prospective Studies, respiratory system, Article
Abstract

Symptomatic early onset pulmonary events (EOPEs) were observed in 3% to 6% of patients within 1 week of starting brigatinib at 90 mg daily for 7 days followed by 180 mg daily. We conducted a prospective observational cohort study to measure pulmonary function changes on initiating brigatinib.Patients initiating brigatinib were eligible. Pulmonary function test (PFT) with diffusing capacity for carbon monoxide (DLCO), Borg dyspnea scale, six-minute walk test, and blood draw for cytometry by time-of-flight were performed at baseline, day 2, and day 8 plus or minus day 15 of brigatinib. The primary end point was the incidence of PFT-defined EOPEs, prespecified as greater than or equal to 20% DLCO reduction from baseline. An interim analysis was performed owing to a higher than expected incidence of DLCO reduction.A total of 90% (nine of 10) experienced DLCO reduction with the nadir occurring on day 2 or day 8. Median DLCO nadir was -13.33% from baseline (range: -34.44 to -5.00). Three participants met the PFT-defined EOPE criteria. All patients, including these three, were asymptomatic, none required brigatinib interruption or dose reduction, and all patients escalated to 180 mg without further issues. Despite continued dosing, by day 15, all assessed patients experienced DLCO recovery. Dyspnea and six-minute walk test results did not correlate with DLCO changes. Patients with a PFT-defined EOPE had significantly higher levels of activated neutrophils at baseline and day 8.DLCO reduction occurred in 90% during the first 8 days of brigatinib dosing without any related symptoms. DLCO improved in all six patients assessed at day 15 despite continued dosing and dose escalation. Pretreatment levels of neutrophil activation should be explored as a biomarker for developing EOPEs.

Published
2020

229. hnRNP L regulates the tumorigenic capacity of lung cancer xenografts in mice via caspase-9 pre-mRNA processing

Author

Goehe, Rachel Wilson, Shultz, Jacqueline C., Murudkar, Charuta, Usanovic, Sanja, Lamour, Nadia F., Massey, Davis H., Zhang, Lian, Camidge, D. Ross, Shay, Jerry W., Minna, John D., and Chalfant, Charles E.

Subjects
Post-translational modification -- Research, Ribonucleoproteins -- Physiological aspects -- Genetic aspects -- Research, Lung cancer, Non-small cell -- Genetic aspects -- Research, Apoptosis -- Health aspects -- Research, Health care industry
Abstract

Caspase-9 is involved in the intrinsic apoptotic pathway and suggested to play a role as a tumor suppressor. Little is known about the mechanisms governing caspase-9 expression, but post-transcriptional pre-mRNA processing generates 2 splice variants from the caspase-9 gene, pro-apoptotic caspase-9a and anti-apoptotic caspase-9b. Here we demonstrate that the ratio of caspase-9 splice variants is dysregulated in non-small cell lung cancer (NSCLC) tumors. Mechanistic analysis revealed that an exonic splicing silencer (ESS) regulated caspase-9 pre-mRNA processing in NSCLC cells. Heterogeneous nuclear ribonucleoprotein L (hnRNPL) interacted with this ESS, and downregulation of hnRNP L expression induced an increase in the caspase-9a/9b ratio. Although expression ofhnRNP L lowered the caspase-9a/9b ratio inNSCLCcells, expression ofhnRNP L produced the opposite effect in non-transformed cells, suggesting a post-translational modification specific for NSCLC cells. Indeed, [Ser.sup.52] was identified as a critical modification regulating the caspase-9a/9b ratio. Importantly, in a mouse xenograft model, downregulation of hnRNP L in NSCLC cells induced a complete loss of tumorigenic capacity that was due to the changes in caspase-9 pre-mRNA processing. This study therefore identifies a cancer-specific mechanism of hnRNP L phosphorylation and subsequent lowering of the caspase-9a/9b ratio, which is required for the tumorigenic capacity of NSCLC cells., Introduction Caspase-9 is a critical factor in the apoptotic pathway induced by various chemotherapies, stress agents, and radiation (1-9) and is implicated as a tumor suppressor (10). Although caspase-9 has [...]

Published
2010
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230. Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer

Author

Kwak, Eunice L., Ynng-Jue Bang, Camidge, D. Ross, Shaw, Alice T., Solomon, Benjamin, Maki, Robert G., Sai-Hong I. Ou, Dezube, Bruce J., Janne, Pasi A., Costa, Daniel B., Varella-Garcia, Marileila, Woo-Ho Kim, Lynch, Thomas J., Fidias, Panos, Stubbs, Hannah, Engelman, Jeffrey A., Sequist, Lecia V., WeiWei Tan, Gandhi, Leena, Mino-Kenudson, Mari, Wei, Greg C., Shreeve, S. Martin, Ratain, Mark J., Settleman, Jeffrey, Christensen, James G., Haber, Daniel A., Wilner, Keith, Salgia, Ravi, Shapiro, Geoffrey I., Clark, Jeffrey W., and Iafrate, A. John

Subjects
Lung cancer, Small cell -- Genetic aspects, Lung cancer, Small cell -- Diagnosis, Lung cancer, Small cell -- Care and treatment, Tyrosine -- Health aspects, Phosphotransferases -- Health aspects
Abstract

A study was conducted to evaluate the therapeutic efficacy of inhibition of anaplastic lymphoma kinase (ALK) in the case of non-small-cell lung cancer tumors. Results indicated that such ALK inhibition was effective in shrinkage of the tumor and stable disease in the case of most patients.

Published
2010

232. Using Multiplexed Assays of Oncogenic Drivers in Lung Cancers to Select Targeted Drugs

Author

Kris, Mark G., Johnson, Bruce E., Berry, Lynne D., Kwiatkowski, David J., Iafrate, A. John, Wistuba, Ignacio I., Varella-Garcia, Marileila, Franklin, Wilbur A., Aronson, Samuel L., Su, Pei-Fang, Shyr, Yu, Camidge, D. Ross, Sequist, Lecia V., Glisson, Bonnie S., Khuri, Fadlo R., Garon, Edward B., Pao, William, Rudin, Charles, Schiller, Joan, Haura, Eric B., Socinski, Mark, Shirai, Keisuke, Chen, Heidi, Giaccone, Giuseppe, Ladanyi, Marc, Kugler, Kelly, Minna, John D., and Bunn, Paul A.

Published
2014
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233. Ceritinib in ALK-Rearranged Non–Small-Cell Lung Cancer

Author

Shaw, Alice T., Kim, Dong-Wan, Mehra, Ranee, Tan, Daniel S.W., Felip, Enriqueta, Chow, Laura Q.M., Camidge, D. Ross, Vansteenkiste, Johan, Sharma, Sunil, De Pas, Tommaso, Riely, Gregory J., Solomon, Benjamin J., Wolf, Juergen, Thomas, Michael, Schuler, Martin, Liu, Geoffrey, Santoro, Armando, Lau, Yvonne Y., Goldwasser, Meredith, Boral, Anthony L., and Engelman, Jeffrey A.

Published
2014
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236. A phase 1b, open-label, single-arm study of cofetuzumab pelidotin (a PTK7-targeting antibody-drug conjugate) in patients with PTK7-expressing, recurrent non-small cell lung cancer (NSCLC).

Author

Schaefer, Eric S., primary, Camidge, D. Ross, additional, Yoh, Kiyotaka, additional, Zer, Alona, additional, Hernandez Guerrero, Tatiana, additional, Bar, Jair, additional, Okuma, Yusuke, additional, Peguero, Julio Antonio, additional, De Miguel, Maria, additional, Moskovitz, Mor Tal, additional, Morgensztern, Daniel, additional, Jeffries, Shawn, additional, Wang, Lan, additional, Lally, Satwant, additional, Conn, Christopher, additional, Xin, Xiaohua, additional, Jeng, Edwin E., additional, and Johnson, Melissa Lynne, additional

Published
2021
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237. Effect of continuing osimertinib with chemotherapy in the post-progression setting on progression-free survival among patients with metastatic epidermal growth factor receptor (EGFR) positive non-small cell lung cancer.

Author

Patil, Tejas, primary, Tsui, David Chun Cheong, additional, Nicklawsky, Andrew, additional, Schenk, Erin Lynn, additional, Purcell, William T., additional, Bunn, Paul A., additional, Pacheco, Jose Maria, additional, and Camidge, D. Ross, additional

Published
2021
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238. Brigatinib (BRG) in ALK+ crizotinib (CRZ)-refractory non-small cell lung cancer (NSCLC): Final results of the phase 1/2 and phase 2 (ALTA) trials.

Author

Gettinger, Scott N., primary, Huber, Rudolf M., additional, Kim, Dong-Wan, additional, Bazhenova, Lyudmila, additional, Holmskov Hansen, Karin, additional, Tiseo, Marcello, additional, Langer, Corey J., additional, Paz-Ares, Luis G., additional, West, Howard, additional, Reckamp, Karen L., additional, Weiss, Glen J., additional, Smit, Egbert F., additional, Hochmair, Maximilian, additional, Kim, Sang-We, additional, Ahn, Myung-Ju, additional, Kim, Edward S., additional, Groen, Harry J.M., additional, Pye, Joanna, additional, Vranceanu, Florin, additional, and Camidge, D. Ross, additional

Published
2021
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239. Preliminary safety and efficacy results from phase 1 studies of DZD9008 in NSCLC patients with EGFR Exon20 insertion mutations.

Author

Yang, James Chih-Hsin, primary, Wang, Mengzhao, additional, Mitchell, Paul, additional, Fang, Jian, additional, Nian, Weiqi, additional, Chiu, Chao-Hua, additional, Zhou, Jianying, additional, Zhao, Yanqiu, additional, Su, Wu-Chou, additional, Camidge, D. Ross, additional, Yang, Tsung-Ying, additional, Zhu, Viola Weijia, additional, Millward, Michael, additional, Fan, Yun, additional, Huang, Wen Tsung, additional, Cheng, Ying, additional, Jiang, Liyan, additional, Zheng, Li, additional, Ye, Xiuhui, additional, and Janne, Pasi A., additional

Published
2021
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243. Indirect comparisons of brigatinib and alectinib for front-line -positive non-small-cell lung cancer.

Author

Reckamp, Karen L, Lin, Huamao M, Cranmer, Holly, Wu, Yanyu, Zhang, Pingkuan, Walton, Laura J, Kay, Stephen, Cichewicz, Allie, Neupane, Binod, Fahrbach, Kyle, Popat, Sanjay, and Camidge, D Ross

Subjects
LUNG cancer, DISEASE progression, PROTEIN kinase inhibitors, HETEROCYCLIC compounds, ORGANOPHOSPHORUS compounds, LUNG tumors, PIPERIDINE, RESEARCH funding
Abstract

Aim: To conduct an indirect treatment comparison (ITC) of the relative efficacy of brigatinib and alectinib for progression-free survival in people with tyrosine kinase inhibitor (TKI)-naive ALK-positive non-small-cell lung cancer (NSCLC). Methods: Final aggregate and patient-level data from the ALTA-1L trial comparing brigatinib to crizotinib and published aggregate data from ALEX (comparing alectinib to crizotinib) were contrasted using Bucher ITC and matching-adjusted indirect comparisons (MAICs). Results: No statistically significant differences were identified between brigatinib and alectinib in reducing the risk of disease progression overall and in patients with baseline central nervous system metastases. Conclusion: Brigatinib appeared similar to alectinib in reducing risk of disease progression for people with TKI-naive ALK-positive NSCLC. [ABSTRACT FROM AUTHOR]

Published
2022
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244. Effectiveness of crizotinib versus entrectinib in -positive non-small-cell lung cancer using clinical and real-world data.

Author

Tremblay, Gabriel, Groff, Michael, Iadeluca, Laura, Daniele, Patrick, Wilner, Keith, Wiltshire, Robin, Bartolome, Lauren, Usari, Tiziana, Cappelleri, Joseph C, and Camidge, D Ross

Subjects
LUNG cancer, PROTEINS, HETEROCYCLIC compounds, PROTEIN kinase inhibitors, LUNG tumors, PROTEIN-tyrosine kinases, RESEARCH funding, BENZAMIDE
Abstract

Aims: To compare clinical trial results for crizotinib and entrectinib in ROS1-positive non-small-cell lung cancer and compare clinical trial data and real-world outcomes for crizotinib. Patients & methods: We analyzed four phase I-II studies using a simulated treatment comparison (STC). A STC of clinical trial versus real-world evidence compared crizotinib clinical data to real-world outcomes. Results: Adjusted STC found nonsignificant trends favoring crizotinib over entrectinib: objective response rate, risk ratio = 1.04 (95% CI: 0.85-1.28); median duration of response, mean difference = 16.11 months (95% CI: -1.57- 33.69); median progression-free survival, mean difference = 3.99 months (95% CI: -6.27-14.25); 12-month overall survival, risk ratio = 1.01 (95% CI: 0.90-1.12). Nonsignificant differences were observed between the trial end point values and the real-world evidence for crizotinib. Conclusions: Crizotinib and entrectinib have comparable efficacy in ROS1-positive non-small-cell lung cancer. [ABSTRACT FROM AUTHOR]

Published
2022
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249. Co-occurring Alterations in the RAS-MAPK Pathway Limit Response to MET Inhibitor Treatment in MET Exon 14 Skipping Mutation-Positive Lung Cancer.

Author

Rotow, Julia K, Rotow, Julia K, Gui, Philippe, Wu, Wei, Raymond, Victoria M, Lanman, Richard B, Kaye, Frederic J, Peled, Nir, Fece de la Cruz, Ferran, Nadres, Brandon, Corcoran, Ryan B, Yeh, Iwei, Bastian, Boris C, Starostik, Petr, Newsom, Kimberly, Olivas, Victor R, Wolff, Alexander M, Fraser, James S, Collisson, Eric A, McCoach, Caroline E, Camidge, D Ross, Pacheco, Jose, Bazhenova, Lyudmila, Li, Tianhong, Bivona, Trever G, Blakely, Collin M, Rotow, Julia K, Rotow, Julia K, Gui, Philippe, Wu, Wei, Raymond, Victoria M, Lanman, Richard B, Kaye, Frederic J, Peled, Nir, Fece de la Cruz, Ferran, Nadres, Brandon, Corcoran, Ryan B, Yeh, Iwei, Bastian, Boris C, Starostik, Petr, Newsom, Kimberly, Olivas, Victor R, Wolff, Alexander M, Fraser, James S, Collisson, Eric A, McCoach, Caroline E, Camidge, D Ross, Pacheco, Jose, Bazhenova, Lyudmila, Li, Tianhong, Bivona, Trever G, and Blakely, Collin M

Abstract

PurposeAlthough patients with advanced-stage non-small cell lung cancers (NSCLC) harboring MET exon 14 skipping mutations (METex14) often benefit from MET tyrosine kinase inhibitor (TKI) treatment, clinical benefit is limited by primary and acquired drug resistance. The molecular basis for this resistance remains incompletely understood.Experimental designTargeted sequencing analysis was performed on cell-free circulating tumor DNA obtained from 289 patients with advanced-stage METex14-mutated NSCLC.ResultsProminent co-occurring RAS-MAPK pathway gene alterations (e.g., in KRAS, NF1) were detected in NSCLCs with METex14 skipping alterations as compared with EGFR-mutated NSCLCs. There was an association between decreased MET TKI treatment response and RAS-MAPK pathway co-occurring alterations. In a preclinical model expressing a canonical METex14 mutation, KRAS overexpression or NF1 downregulation hyperactivated MAPK signaling to promote MET TKI resistance. This resistance was overcome by cotreatment with crizotinib and the MEK inhibitor trametinib.ConclusionsOur study provides a genomic landscape of co-occurring alterations in advanced-stage METex14-mutated NSCLC and suggests a potential combination therapy strategy targeting MAPK pathway signaling to enhance clinical outcomes.

Published
2020

250. Activity and Safety of Mobocertinib (TAK-788) in Previously Treated Non–Small Cell Lung Cancer with EGFR Exon 20 Insertion Mutations from a Phase I/II Trial

Author

Riely, Gregory J., primary, Neal, Joel W., additional, Camidge, D. Ross, additional, Spira, Alexander I., additional, Piotrowska, Zofia, additional, Costa, Daniel B., additional, Tsao, Anne S., additional, Patel, Jyoti D., additional, Gadgeel, Shirish M., additional, Bazhenova, Lyudmila, additional, Zhu, Viola W., additional, West, Howard L., additional, Mekhail, Tarek, additional, Gentzler, Ryan D., additional, Nguyen, Danny, additional, Vincent, Sylvie, additional, Zhang, Steven, additional, Lin, Jianchang, additional, Bunn, Veronica, additional, Jin, Shu, additional, Li, Shuanglian, additional, and Jänne, Pasi A., additional

Published
2021
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