Norman L. Lehman

ORCID: 0000-0001-8394-2607
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About
Contact & Profiles
Research Areas
  • Glioma Diagnosis and Treatment
  • Microtubule and mitosis dynamics
  • Cancer Genomics and Diagnostics
  • Cancer, Hypoxia, and Metabolism
  • Meningioma and schwannoma management
  • Cancer-related Molecular Pathways
  • RNA modifications and cancer
  • Mitochondrial Function and Pathology
  • Epigenetics and DNA Methylation
  • Advanced Proteomics Techniques and Applications
  • Genomics and Chromatin Dynamics
  • Ferroptosis and cancer prognosis
  • Neurofibromatosis and Schwannoma Cases
  • Cancer-related molecular mechanisms research
  • Bioinformatics and Genomic Networks
  • Pituitary Gland Disorders and Treatments
  • RNA Research and Splicing
  • Molecular Biology Techniques and Applications
  • Genetic factors in colorectal cancer
  • Pancreatic and Hepatic Oncology Research
  • Brain Metastases and Treatment
  • Ubiquitin and proteasome pathways
  • Neurogenesis and neuroplasticity mechanisms
  • Cancer Immunotherapy and Biomarkers
  • Cancer Treatment and Pharmacology

Baylor Scott & White Medical Center - Temple
2024-2025

Baylor College of Medicine
2024-2025

Baylor Medical Center at Garland
2025

University of Louisville
2018-2024

Medical University of Lublin
2023-2024

The Ohio State University Wexner Medical Center
2014-2019

The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute
2014-2018

The Ohio State University
2013-2018

ETH Zurich
2018

SIB Swiss Institute of Bioinformatics
2018

Roger E. McLendon Allan H. Friedman D D Bigner Erwin G. Van Meir Daniel J. Brat and 95 more Gena M. Mastrogianakis Jeffrey J. Olson Tom Mikkelsen Norman L. Lehman Ken Aldape W.K. Alfred Yung Oliver Bögler John N. Weinstein Scott Vandenberg Mitchel S. Berger Michael D. Prados Donna M. Muzny Margaret Morgan Stephen W. Scherer Aniko Sabo Lynn Nazareth Lora Lewis Otis Hall Yiming Zhu Yanru Ren Omar Alvi Jiqiang Yao Alicia Hawes Shalini N. Jhangiani Gerald Fowler Anthony San Lucas Christie Kovar Andrew Cree Huyen Dinh Jireh Santibanez Vandita Joshi Manuel L. Gonzalez‐Garay Christopher A. Miller Aleksandar Milosavljevic L A Donehower David A. Wheeler Richard A. Gibbs Kristian Cibulskis Carrie Sougnez Tim Fennell Scott Mahan Jane Wilkinson Liuda Ziaugra Robert C. Onofrio Toby Bloom Robert Nicol Kristin Ardlie Jennifer N. Baldwin Stacey Gabriel Eric S. Lander Jun Li Robert S. Fulton Michael D. McLellan John Wallis David E. Larson Xiaoqi Shi Rachel M. Abbott Lucinda Fulton Ken Chen Daniel C. Koboldt Michael C. Wendl Rick Meyer Yuzhu Tang Ling Lin John R. Osborne Brian H. Dunford-Shore Tracie L. Miner Kim D. Delehaunty Chris Markovic G.M. Swift William Courtney Craig Pohl Scott Abbott Amy Hawkins Shin Leong Carrie A. Haipek Heather K. Schmidt Maddy Wiechert Tammi L. Vickery S. P. Scott David J. Dooling Asif Chinwalla George M. Weinstock Elaine R. Mardis Richard K. Wilson Gad Getz Wendy Winckler Roel G.W. Verhaak Michael S. Lawrence Michael O’Kelly Jim Robinson Gabriele Alexe Rameen Beroukhim Scott L. Carter Derek Y. Chiang

10.1038/nature07385 article EN Nature 2008-09-04
Michele Ceccarelli Floris P Barthel Tathiane M. Malta Thaís S. Sabedot Sofie R. Salama and 95 more Bradley A. Murray Olena Morozova Yulia Newton Amie Radenbaugh Stefano Maria Pagnotta Samreen Anjum Jiguang Wang Ganiraju C. Manyam Pietro Zoppoli Shiyun Ling Arjun A. Rao Mia Grifford Andrew D. Cherniack Hailei Zhang Laila Poisson Carlos Gilberto Carlotti Daniela Pretti da Cunha Tirapelli Arvind Rao Tom Mikkelsen Ching C. Lau W. K. Alfred Yung Raúl Rabadán Jason T. Huse Daniel J. Brat Norman L. Lehman Jill S. Barnholtz‐Sloan Siyuan Zheng Kenneth R. Hess Ganesh Rao Matthew Meyerson Rameen Beroukhim Lee Cooper Rehan Akbani Margaret Wrensch David Haussler Kenneth D. Aldape Peter W. Laird David H. Gutmann Houtan Noushmehr Antonio Iavarone Roel G.W. Verhaak Samreen Anjum Harindra Arachchi J. Todd Auman Miruna Balasundaram Saianand Balu Gene H. Barnett Stephen Baylin Sue Bell Christopher C. Benz Natalie Bir Keith L. Black Tom Bodenheimer Lori Boice Arnoud Boot Jay Bowen Christopher A. Bristow Yaron S.N. Butterfield Qingrong Chen Lynda Chin Juok Cho Eric Chuah Sudha Chudamani Simon G. Coetzee Mark L. Cohen Howard Colman Marta Couce Fulvio D’Angelo Tanja M. Davidsen Amy Davis John A. Demchok Karen Devine Li Ding Rebecca Duell J. Bradley Elder Jennifer Eschbacher Ashley Fehrenbach Martin L. Ferguson Scott Frazer Gregory N. Fuller Jordonna Fulop Stacey Gabriel Luciano Garofano Julie M. Gastier-Foster Nils Gehlenborg Mark Gerken Gad Getz Caterina Giannini William J. Gibson Angela Hadjipanayis D. Neil Hayes David I. Heiman Beth Hermes Joe Hilty Katherine A. Hoadley

10.1016/j.cell.2015.12.028 article EN publisher-specific-oa Cell 2016-01-01

Abstract The objective of this study was to demonstrate 1 H MR spectroscopy (MRS) changes in cerebral metabolites after acute head trauma. Twenty‐five patients (12 children, 13 adults) were examined with quantitative MRS closed injury. Clinical grade (Glasgow Coma Scale [GCS]) and outcome (Rancho Los Amigos Medical Center Outcome Score [ROS]) correlated neurochemical findings. N‐acetylas‐partate (NAA), a neuronal axonal marker, reduced ( P < .03−.001). In NAA/creatine plus phosphocreatine...

10.1002/jmri.1880080412 article EN Journal of Magnetic Resonance Imaging 1998-07-01

The periodic destruction of mitotic cyclins is triggered by the activation anaphase-promoting complex/cyclosome (APC/C) in mitosis. Although ability APC/C to recognize box (D-box) substrates oscillates throughout cell cycle, mechanism regulating binding D-box remains unclear. Here, we show that inhibitor Emi1 tightly binds both and its Cdh1 activator, receptor site on , competes with for binding. itself contains a conserved C-terminal D-box, which provides APC/C-binding affinity,...

10.1101/gad.1454006 article EN Genes & Development 2006-08-18

Tumor-infiltrating lymphocytes (TIL) have prognostic significance in many cancers, yet their roles glioblastoma not been fully defined. We hypothesized that TILs are associated with molecular alterations, histologies, and survival.

10.1158/1078-0432.ccr-13-0551 article EN Clinical Cancer Research 2013-07-18

Background and Purpose— Axonal remodeling is critical to brain repair after stroke. The present study investigated axonal outgrowth stroke the signaling pathways mediating in cortical neurons. Methods— Using a rodent model of middle cerebral artery occlusion, we examined high-molecular weight neurofilament (NFH) immunoreactive axons myelin basic protein-positive oligodendrocytes peri-infarct area. In vitro, using cultured neurons microfluidic chamber challenged by oxygen-glucose deprivation...

10.1161/strokeaha.111.646224 article EN Stroke 2012-05-24

We characterized the expression and function of endoplasmic reticulum protein GRP78 in glial tumors. is highly expressed glioblastomas but not oligodendrogliomas, its inversely correlated with median patient survival. Overexpression glioma cells decreases caspase 7 activation renders resistant to etoposide- cisplatin-induced apoptosis, whereas silencing cell growth sensitizes etoposide, cisplatin, gamma-radiation. Thus, contributes increased apoptosis resistance may provide a target for...

10.1215/15228517-2008-006 article EN Neuro-Oncology 2008-04-11

Astroblastoma (AB) is a rare CNS tumor demonstrating abundant astroblastomatous pseudorosettes. Its molecular features have not been comprehensively studied and its status as entity controversial. We analyzed cohort of 27 histologically-defined ABs using DNA methylation profiling, copy number analysis, FISH site-directed sequencing. Most cases demonstrated mutually exclusive MN1 rearrangements (n = 10) or BRAFV600E mutations 7). Two additional harbored RELA rearrangements. Other lacked these...

10.1186/s40478-019-0689-3 article EN cc-by Acta Neuropathologica Communications 2019-03-15

Resistance to genotoxic therapies is a primary cause of treatment failure and tumor recurrence. The underlying mechanisms that activate the DNA damage response (DDR) allow cancer cells escape lethal effects remain unclear. Here, we uncover an unexpected mechanism through which pyruvate kinase M2 (PKM2), highly expressed PK isoform in master regulator metabolic reprogramming, integrates with DDR directly promote double-strand break (DSB) repair. In ionizing radiation oxidative stress, ATM...

10.1038/s41422-018-0086-7 article EN cc-by Cell Research 2018-10-08

Engineered oncolytic viruses are used clinically to destroy cancer cells and have the ability boost anticancer immunity. Phosphatase tensin homolog deleted on chromosome 10 loss is common across a broad range of malignancies, implicated in immune escape. The N-terminally extended isoform, phosphatase alpha (PTENα), regulates cellular functions including protein kinase B signaling mitochondrial adenosine triphosphate production. Here we constructed HSV-P10, replicating, PTENα expressing...

10.1038/s41467-018-07344-1 article EN cc-by Nature Communications 2018-11-21

Abstract Cancer stem cells (CSCs) are characterized by their self-renewing potential and ability to differentiate phenocopy the original tumor in orthotopic xenografts. Long-term propagation of glioblastoma (GBM) serum-containing medium results loss CSCs outgrowth genetically biologically divergent from parental tumors. In contrast, use a neurosphere assay, serum-free culture for selection, central nervous system-derived allows selection subpopulation containing CSCs. Gliosarcoma (GS),...

10.1002/stem.264 article EN Stem Cells 2009-11-23

Abstract Purpose To retrospectively correlate various diffusion tensor imaging (DTI) metrics in patients with glioblastoma multiforme (GBM) patient survival analysis and also degree of tumor proliferation index determined histologically. Materials Methods Thirty‐four histologically confirmed treatment naive GBMs underwent DTI on a 3.0 Tesla (T) scanner. Region‐of‐interest was placed the whole lesion including enhancing as well nonenhancing component to determine metrics. Kaplan‐Meier...

10.1002/jmri.22304 article EN Journal of Magnetic Resonance Imaging 2010-09-29

Abstract Ependymomas originate in posterior fossa ( PF ), supratentorial ST ) or spinal cord SC compartments. At present, grading schemes are applied independent of anatomic site. We performed detailed histological examination on 238 W orld H ealth O rganization grade II and III ependymomas. Among ependymomas, the presence hypercellular areas, necrosis, microvascular proliferation elevated mitotic rate (all P < 0.01) were significantly associated with worse progression‐free survival PFS...

10.1111/bpa.12050 article EN Brain Pathology 2013-03-04

Aurora A is critical for mitosis and overexpressed in several neoplasms. Its overexpression transforms cultured cells, both its knockdown cause genomic instability. In transgenic mice, haploinsufficiency, not overexpression, leads to increased malignant tumor formation. thus appears have tumor-promoting tumor-suppressor functions. Here, we report that protein, measured by quantitative protein gel blotting, differentially expressed major glioma types lineage-specific patterns. levels WHO...

10.4161/cc.11.3.18996 article EN Cell Cycle 2012-02-01

Abstract Background. Astroblastomas (ABs) are rare glial tumors showing overlapping features with astrocytomas, ependymomas, and sometimes other neoplasms, may be challenging to diagnose. Methods. We examined clinical, histopathological, molecular in 28 archival formalin-fixed, paraffin-embedded AB cases performed survival analyses using Cox proportional hazards Kaplan–Meier methods. Results. Unlike ependymomas angiocentric gliomas, ABs demonstrate abundant distinctive astroblastic...

10.1093/neuonc/now118 article EN Neuro-Oncology 2016-07-14

Abstract Papillary tumor of the pineal region (PTPR) is an uncommon with distinctive histopathologic and molecular characteristics. Experience limited respect to its heterogeneity clinical Here, we describe 39 new cases combine these 37 previously published for a cohort 76 PTPR’s, all confirmed by methylation profiling. As reported, two main groups were identified (PTPR-A PTPR-B). In our analysis extended subtyping into three subtypes: PTPR-A, PTPR-B1 PTPR-B2 supported DNA profile genomic...

10.1186/s40478-024-01781-4 article EN cc-by Acta Neuropathologica Communications 2024-07-16

Abstract Glioblastoma remains a devastating disease for which novel therapies are urgently needed. Here, we report that the Aurora-A kinase inhibitor alisertib exhibits potent efficacy against glioblastoma neurosphere tumor stem–like cells in vitro and vivo. Many treated with short periods undergo apoptosis, although some regain proliferative activity upon drug removal. Extended treatment, however, results complete irreversible loss of cell proliferation. Moreover, caused to partially...

10.1158/0008-5472.can-14-0386 article EN Cancer Research 2014-08-09

The quality of cancer genomic and proteomic data relies upon the clinical specimens examined. Here, we show that derived from non-microdissected glioblastoma multiforme tumor tissue is either masked or not accurate, producing correlations between lead to false classifications for therapeutic stratification. We analyzed level 133 key signaling proteins phosphoproteins in laser capture microdissected (LCM) primary tumors a study set tissues used Cancer Genome Atlas (TCGA) profiling efforts,...

10.1158/0008-5472.can-13-2172 article EN Cancer Research 2013-12-18

Brain intraparenchymal schwannoma is a rare clinical entity, generally curable with adequate resection. We describe case in male patient first presenting at 19 months of age, the youngest reported age for this lesion. It also appears to be connected germline TSC2 p.1510del mutation autism-like symptoms. Although tuberous sclerosis not associated increased risk schwannoma, mTORC1 activity, which inhibited by intact TSC1/TSC2 complex, involved progression. This patient's tumor harbored...

10.1007/s11033-024-10201-8 article EN cc-by-nc-nd Molecular Biology Reports 2025-01-10
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