Ryan Lena

ORCID: 0000-0003-1282-9492
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About
Contact & Profiles
Research Areas
  • Cancer Mechanisms and Therapy
  • NF-κB Signaling Pathways
  • Protein Tyrosine Phosphatases
  • FOXO transcription factor regulation
  • Protein Degradation and Inhibitors
  • Acute Myeloid Leukemia Research
  • Cell death mechanisms and regulation
  • RNA Interference and Gene Delivery
  • Advanced biosensing and bioanalysis techniques
  • Cancer-related Molecular Pathways
  • Chronic Lymphocytic Leukemia Research
  • Microbial Applications in Construction Materials
  • Mechanisms of cancer metastasis
  • Histone Deacetylase Inhibitors Research
  • Melanoma and MAPK Pathways
  • Multiple Myeloma Research and Treatments
  • Cancer Treatment and Pharmacology
  • ATP Synthase and ATPases Research
  • Viral Infectious Diseases and Gene Expression in Insects
  • Cancer Research and Treatment
  • Forensic Fingerprint Detection Methods
  • Multicomponent Synthesis of Heterocycles
  • Acute Lymphoblastic Leukemia research
  • Advanced Biosensing Techniques and Applications
  • Cell Image Analysis Techniques

Eutropics Pharmaceuticals (United States)
2011-2023

Translational Genomics Research Institute
2014

Cancer Treatment Centers of America
2014

The University of Texas MD Anderson Cancer Center
2013

Leukemia Research Foundation
2013

Synergistic molecular vulnerabilities enhancing hypomethylating agents in myeloid malignancies have remained elusive. RNA-interference drug modifier screens identified antiapoptotic BCL-2 family members as potent 5-Azacytidine-sensitizing targets. In further dissecting BCL-XL, and MCL-1 contribution to 5-Azacytidine activity, siRNA silencing of BCL-XL MCL-1, but not BCL-2, exhibited variable synergy with vitro. The BCL-w inhibitor ABT-737 sensitized most cell lines more potently compared the...

10.1038/leu.2014.44 article EN cc-by-nc-nd Leukemia 2014-01-23

Insensitivity to standard clinical interventions, including chemotherapy, radiotherapy, and tyrosine kinase inhibitor (TKI) treatment, remains a substantial hindrance towards improving the prognosis of patients with non-small cell lung cancer (NSCLC). The molecular mechanism therapeutic resistance poorly understood. TNF-like weak inducer apoptosis (TWEAK)-FGF-inducible 14 (TNFRSF12A/Fn14) signaling axis is known promote survival via NF-κB activation upregulation prosurvival Bcl-2 family...

10.1158/1541-7786.mcr-13-0458 article EN Molecular Cancer Research 2014-01-28

Abstract As acute myelogenous leukemia (AML) patient response to cytarabine-based standard-of-care treatment is variable, stratification into subgroups by biomarker-predicted may lead improved clinical outcomes. Here, we assess cell mitochondrial depolarization proapoptotic signaling BH3-only peptides as a surrogate for the function of Bcl-2 family proteins address therapy in patients with AML (N = 62). Peripheral blood mononuclear (PBMC) or bone marrow aspirate specimens were obtained from...

10.1158/1535-7163.mct-13-0692 article EN Molecular Cancer Therapeutics 2013-10-04

Abstract Introduction. Chronic lymphocytic leukemia (CLL) patients may benefit from personalized strategies targeting specific therapies to individuals with favorable molecular profiles. Many therapeutics exhibit response in a subset of patients, and factors such as age or cytogenetics are insufficient predict treatment success high accuracy. We assessed mitochondrial functionality apoptosis signaling for identification CLL likely clinical alvocidib. Effects this agent have been shown...

10.1158/1538-7445.am2014-907 article EN Cancer Research 2014-10-01

Abstract As numerous molecularly targeted agents are entering clinical trials, predictive testing is highly desirable. We investigated if response to certain correlates with the recently reported method of BH3 profiling (Chonghaile TN et al, Science, 2011), a functional assay developed by Letai's group that measures tumor cell mitochondrial priming measuring outer membrane permeabilization (MOMP) following exposure peptide-mimicking domains BH3-only proteins. Mitochondrial has been be...

10.1158/1538-7445.am2014-340 article EN Cancer Research 2014-10-01

Abstract Lung cancer is the leading cause of cancer-related mortality in world killing more than one million people each year. Therapeutic resistance remains a significant clinical hurdle, contributing to five-year survival rate less 5% advanced lung cancer. The mechanisms therapeutic remain poorly understood and thus difficult combat therapeutically. tumor necrosis factor-like weak inducer apoptosis (TWEAK)-fibroblast growth factor-inducible 14 (Fn14) signaling axis known promote cell via...

10.1158/1538-7445.am2014-338 article EN Cancer Research 2014-10-01

7087 Background: Chronic lymphocytic leukemia (CLL) patient outcomes may benefit from targeting therapies alone or in combination to individuals with favorable molecular profiles. Whether such personalized medicine approaches are best tailored patients treated single agent regimens using those agents is an underexplored question. Here, we assessed mitochondrial apoptosis signaling CLL lenalidomide, alvocidib, lenalidomide + alvocidib. Methods: Pretreatment blood mononuclear cell (PBMC)...

10.1200/jco.2014.32.15_suppl.7087 article EN Journal of Clinical Oncology 2014-05-20

Abstract Anti-apoptotic Bcl-2 family proteins are central to the regulation of intrinsic apoptotic pathway, and as such constitute an important group targets with great potential oncology therapeutics. The protein Mcl-1 has been demonstrated facilitate survival chemoresistance in multiple myeloma, AML, other cancers, agents which affect this pathway have become highly sought after. Currently, however, no therapies exist directly target Mcl-1. We identified compounds that may be characterized...

10.1158/1538-7445.am2013-2466 article EN Cancer Research 2013-04-01
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