Katherine E. Arensmeyer
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Katherine E. Arensmeyer has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Alessandro Russo
Department of Onco-Hematology, Papardo Hospital, Messina, Italy
1 shared publication - Ana Rita Lopes
Marlene and Stewart Greenebaum Comprehensive Cancer Center, University of Maryland School of Medicine, 22 S Greene Street Rm. N9E08, Baltimore, MD, 21201, USA
1 shared publication - Christian Rolfo
The Ohio State University Comprehensive Cancer Center, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James), Columbus, OH, USA
1 shared publication - Giuseppina Rosaria Rita Ricciardi
Department of Onco-Haematology, Papardo Hospital, 98100 Messina, Italy
1 shared publication - Katherine Scilla
University of Maryland School of Medicine, Greenebaum Comprehensive Cancer Center, Baltimore, MD
1 shared publication - Michael G. McCusker
University of Maryland Medical Center, Greenebaum Comprehensive Cancer Center, Baltimore, MD, USA
1 shared publication
Latest Publications
- 16 April 2020
- Published by Springer Nature in Current Oncology Reports
- Vol. 22 (5) , 1-14
New Targets in Lung Cancer (Excluding EGFR, ALK, ROS1)
Purpose of Review Over the last two decades, the identification of targetable oncogene drivers has revolutionized the therapeutic landscape of non-small cell lung cancer (NSCLC). The extraordinary progresses made in molecular biology prompted the identification of several rare molecularly defined subgroups. In this review, we will focus on the novel and emerging actionable oncogenic drivers in NSCLC. Recent Findings Recently, novel oncogene drivers emerged as promising therapeutic targets besides the well-established EGFR mutations, and ALK/ROS1 rearrangements, considerably expanding the list of potential exploitable genetic aberrations. However, the therapeutic algorithm in these patients is far less defined. Summary The identification of uncommon oncogene drivers is reshaping the diagnostic and therapeutic approach to NSCLC. The introduction of novel highly selective inhibitors is expanding the use of targeted therapies to rare and ultra-rare subsets of patients, further increasing the therapeutic armamentarium of advanced NSCLC.
- 16 April 2020
- Published by Springer Nature in Current Oncology Reports
- Vol. 22 (5) , 1-14
New Targets in Lung Cancer (Excluding EGFR, ALK, ROS1)
Purpose of Review Over the last two decades, the identification of targetable oncogene drivers has revolutionized the therapeutic landscape of non-small cell lung cancer (NSCLC). The extraordinary progresses made in molecular biology prompted the identification of several rare molecularly defined subgroups. In this review, we will focus on the novel and emerging actionable oncogenic drivers in NSCLC. Recent Findings Recently, novel oncogene drivers emerged as promising therapeutic targets besides the well-established EGFR mutations, and ALK/ROS1 rearrangements, considerably expanding the list of potential exploitable genetic aberrations. However, the therapeutic algorithm in these patients is far less defined. Summary The identification of uncommon oncogene drivers is reshaping the diagnostic and therapeutic approach to NSCLC. The introduction of novel highly selective inhibitors is expanding the use of targeted therapies to rare and ultra-rare subsets of patients, further increasing the therapeutic armamentarium of advanced NSCLC.