Pascal Oliver Zinn

Dr. Pascal Oliver Zinn


Research Focus & Metrics

Academic Career Length

15Years (2012-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
18 July 2019 in Nature Communications
Verified
Journal Article
Open access
PDF file
NENabil Elshafeey
Nabil Elshafeey
AKAikaterini Kotrotsou
Aikaterini Kotrotsou
AHAhmed Hassan
Ahmed Hassan
NENancy Elshafei
Nancy Elshafei
IHIslam Hassan
Islam Hassan
RCRivka R. Colen
Rivka R. Colen
Pseudoprogression (PsP) is a diagnostic clinical dilemma in cancer. In this study, we retrospectively analyse glioblastoma patients, and using their dynamic susceptibility contrast and dynamic contrast-enhanced perfusion MRI images we build a classifier using radiomic features obtained from both Ktrans and rCBV maps coupled with support vector machines. We achieve an accuracy of 90.82% (area under the curve (AUC) = 89.10%, sensitivity = 91.36%, 67 specificity = 88.24%, p = 0.017) in differentiating between pseudoprogression (PsP) and progressive disease (PD). The diagnostic performances of the models built using radiomic features from Ktrans and rCBV separately were equally high (Ktrans: AUC = 94%, 69 p = 0.012; rCBV: AUC = 89.8%, p = 0.004). Thus, this MR perfusion-based radiomic model demonstrates high accuracy, sensitivity and specificity in discriminating PsP from PD, thus provides a reliable alternative for noninvasive identification of PsP versus PD at the time of clinical/radiologic question. This study also illustrates the successful application of radiomic analysis as an advanced processing step on different MR perfusion maps.

16 August 2021 in Journal of Clinical Investigation
Verified
Journal Article
Closed access
PDF file
ACApeng Chen
Apeng Chen
YJYinan Jiang
Yinan Jiang
ZLZhengwei Li
Zhengwei Li
LWLingxiang Wu
Lingxiang Wu
USUlises Santiago
Ulises Santiago
BHBaoli Hu
Baoli Hu

14 May 2020 in Best Practice & Research Clinical Anaesthesiology
Verified
Journal Article
Closed access
MMMaks Mihalj
Maks Mihalj
TCThierry Pierre Carrel
Thierry Pierre Carrel
IGIgor D. Gregoric
Igor D. Gregoric
LALukas Andereggen
Lukas Andereggen
PZPascal Oliver Zinn
Pascal Oliver Zinn
Markus M LuediMarkus M Luedi
Markus M Luedi

6 January 2012 in Stem Cells
Verified
Journal Article
Open access
PDF file
MKMohamed Kamal
Mohamed Kamal
PSPratheesh Sathyan
Pratheesh Sathyan
SSSanjay K. Singh
Sanjay K. Singh
PZPascal Oliver Zinn
Pascal Oliver Zinn
AMAnantha L. Marisetty
Anantha L. Marisetty
SMSadhan Majumder
Sadhan Majumder
Glioblastoma multiforme (GBM) tumors are the most common malignant primary brain tumors in adults. Although many GBM tumors are believed to be caused by self-renewing, glioblastoma-derived stem-like cells (GSCs), the mechanisms that regulate self-renewal and other oncogenic properties of GSCs are only now being unraveled. Here we showed that GSCs derived from GBM patient specimens express varying levels of the transcriptional repressor repressor element 1 silencing transcription factor (REST), suggesting heterogeneity across different GSC lines. Loss- and gain-of-function experiments indicated that REST maintains self-renewal of GSCs. High REST-expressing GSCs (HR-GSCs) produced tumors histopathologically distinct from those generated by low REST-expressing GSCs (LR-GSCs) in orthotopic mouse brain tumor models. Knockdown of REST in HR-GSCs resulted in increased survival in GSC-transplanted mice and produced tumors with higher apoptotic and lower invasive properties. Conversely, forced expression of exogenous REST in LR-GSCs produced decreased survival in mice and produced tumors with lower apoptotic and higher invasive properties, similar to HR-GSCs. Thus, based on our results, we propose that a novel function of REST is to maintain self-renewal and other oncogenic properties of GSCs and that REST can play a major role in mediating tumorigenicity in GBM. STEM CELLS 2012;30:405–414

10 March 2022 in Frontiers in Oncology
Verified
Journal Article
Open access
JBJamison Beiriger
Jamison Beiriger
AHAhmed Habib
Ahmed Habib
NJNicolina Jovanovich
Nicolina Jovanovich
CKChowdari V. Kodavali
Chowdari V. Kodavali
LELincoln Edwards
Lincoln Edwards
PZPascal Oliver Zinn
Pascal Oliver Zinn
Glioblastoma (GBM) is a malignant tumor with a median survival rate of 15-16 months with standard care; however, cases of successful treatment offer hope that an enhanced understanding of the pathology will improve the prognosis. The cell of origin in GBM remains controversial. Recent evidence has implicated stem cells as cells of origin in many cancers. Neural stem/precursor cells (NSCs) are being evaluated as potential initiators of GBM tumorigenesis. The NSCs in the subventricular zone (SVZ) have demonstrated similar molecular profiles and share several distinctive characteristics to proliferative glioblastoma stem cells (GSCs) in GBM. Genomic and proteomic studies comparing the SVZ and GBM support the hypothesis that the tumor cells and SVZ cells are related. Animal models corroborate this connection, demonstrating migratory patterns from the SVZ to the tumor. Along with laboratory and animal research, clinical studies have demonstrated improved progression-free survival in patients with GBM after radiation to the ipsilateral SVZ. Additionally, key genetic mutations in GBM for the most part carry regulatory roles in the SVZ as well. An exciting avenue towards SVZ modeling and determining its role in gliomagenesis in the human context is human brain organoids. Here we comprehensively discuss and review the role of the SVZ in GBM genesis, maintenance, and modeling.

1 January 2023 in Neuro-Oncology Advances
Verified
Journal Article
Open access
PDF file
NJNicolina Jovanovich
Nicolina Jovanovich
AHAhmed Habib
Ahmed Habib
JHJeffery Head
Jeffery Head
FHFarrukh Hameed
Farrukh Hameed
SASameer Agnihotri
Sameer Agnihotri
PZPascal Oliver Zinn
Pascal Oliver Zinn
Diffuse midline glioma (DMG) is a pediatric cancer that originates in the midline structures of the brain. Prognosis of DMG patients remains poor due to the infiltrative nature of these tumors and the protection they receive from systemically delivered therapeutics via an intact blood–brain barrier (BBB), making treatment difficult. While the cell of origin remains disputed, it is believed to reside in the ventral pons. Recent research has pointed toward epigenetic dysregulation inducing an OPC-like transcriptomic signature in DMG cells. This epigenetic dysregulation is typically caused by a mutation (K27M) in one of two histone genes—H3F3A or HIST1H3B –and can lead to a differentiation block that increases these cells oncogenic potential. Standard treatment with radiation is not sufficient at overcoming the aggressivity of this cancer and only confers a survival benefit of a few months, and thus, discovery of new therapeutics is of utmost importance. In this review, we discuss the cell of origin of DMGs, as well as the underlying molecular mechanisms that contribute to their aggressivity and resistance to treatment. Additionally, we outline the current standard of care for DMG patients and the potential future therapeutics for this cancer that are currently being tested in preclinical and clinical trials.