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Article: Novel dual action PARP and microtubule polymerization inhibitor AMXI-5001 powerfully inhibits growth of esophageal carcinoma both alone and in combination with radiotherapy.

Brand, Nathan R / Yang, Yi-Wei / Ding, Vivianne / Dutta, Hannah / Peto, Csaba J / Lemjabbar-Alaoui, Hassan / Jablons, David M

American journal of cancer research

2024 Volume 14, Issue 1, Page(s) 378–389

Abstract: Esophageal cancer is one of the leading causes of cancer deaths globally with an incidence that is concentrated in specific hot spots in Eastern Asia, the Middle East, Eastern Africa, and South America. 10-year overall survival for patients treated with ... ...

Abstract	Esophageal cancer is one of the leading causes of cancer deaths globally with an incidence that is concentrated in specific hot spots in Eastern Asia, the Middle East, Eastern Africa, and South America. 10-year overall survival for patients treated with standard of care chemoradiation followed by surgical resection is below 40% highlighting the need for novel therapeutics to treat this disease. We assessed the effect of AMXI-5001, a novel small molecule poly ADP-Ribose polymerase (PARP) inhibitor and microtubule polymerization inhibitor on tumor growth inhibition in both
Language	English
Publishing date	2024-01-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2589522-9
ISSN	2156-6976
ISSN	2156-6976
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Article ; Online: Comparative genomics between matched solid and lepidic portions of semi-solid lung adenocarcinomas.

Woodard, Gavitt A / Ding, Vivianne / Cho, Christina / Brand, Nathan R / Kratz, Johannes R / Jones, Kirk D / Jablons, David M

Lung cancer (Amsterdam, Netherlands)

2023 Volume 180, Page(s) 107211

Abstract: Background: Genetic changes that drive the transition from lepidic to invasive cancer development within a radiographic ground glass or semi-solid lung lesion (SSL) are not well understood. Biomarkers to predict the transition to solid, invasive cancer ... ...

Abstract	Background: Genetic changes that drive the transition from lepidic to invasive cancer development within a radiographic ground glass or semi-solid lung lesion (SSL) are not well understood. Biomarkers to predict the transition to solid, invasive cancer within SSL are needed. Methods: Patients with surgically resected SSL were identified retrospectively from a surgical database. Clinical characteristics and survival were compared between stage I SSL (n = 65) and solid adenocarcinomas (n = 120) resected during the same time period. Areas of normal lung, in situ lepidic, and invasive solid tumor were microdissected from within the same SSL specimens and next generation sequencing (NGS) and Affymetrix microarray of gene expression were performed. Results: There were more never smokers, Asian patients, and sub-lobar resections among SSL but no difference in 5-year survival between SSL and solid adenocarcinoma. Driver mutations found in both lepidic and solid invasive portion were EGFR (43%), KRAS (21%), and DNMT3A (5%). CEACAM5 was the most upregulated gene found in solid, invasive portions of SSL. Lepidic and invasive solid areas had many similarities in gene expression, however there were some significant differences with the gene SPP1 being a unique biomarker for the invasive component of a SSL. Conclusions: Common lung cancer driver mutations are present in in situ lepidic as well as invasive solid portions of a SSL, suggesting early development of driver mutations. CEACAM5 and SPP1 emerged as promising biomarkers of invasive potential in semi-solid lesions. Other studies have shown both genes to correlate with poor prognosis in lung cancer and their role in evolution of semi-solid lung lesions warrants further study.
MeSH term(s)	Humans ; Lung Neoplasms/pathology ; Retrospective Studies ; Adenocarcinoma of Lung/genetics ; Adenocarcinoma/pathology ; Genomics
Language	English
Publishing date	2023-04-21
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	632771-0
ISSN	1872-8332 ; 0169-5002
ISSN (online)	1872-8332
ISSN	0169-5002
DOI	10.1016/j.lungcan.2023.107211
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Article ; Online: Hedgehog Signaling in Lung Cancer: From Oncogenesis to Cancer Treatment Resistance.

Giroux-Leprieur, Etienne / Costantini, Adrien / Ding, Vivianne W / He, Biao

International journal of molecular sciences

2018 Volume 19, Issue 9

Abstract: Hedgehog signaling pathway is physiologically activated during embryogenesis, especially in lung development. It is also reactivated in many solid tumors. In lung cancer, Hedgehog pathway is closely associated with cancer stem cells (CSCs). Recent works ... ...

Abstract	Hedgehog signaling pathway is physiologically activated during embryogenesis, especially in lung development. It is also reactivated in many solid tumors. In lung cancer, Hedgehog pathway is closely associated with cancer stem cells (CSCs). Recent works have shown that CSCs produced a full-length Sonic Hedgehog (Shh) protein, with paracrine activity and induction of tumor development. Hedgehog pathway is also involved in tumor drug resistance in lung cancer, as cytotoxic chemotherapy, radiotherapy, and targeted therapies. This review proposes to describe the activation mechanisms of Hedgehog pathway in lung cancer, the clinical implications for overcoming drug resistance, and the perspectives for further research.
MeSH term(s)	Animals ; Carcinogenesis/genetics ; Carcinogenesis/metabolism ; Drug Resistance, Neoplasm ; Hedgehog Proteins/genetics ; Hedgehog Proteins/metabolism ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/radiotherapy ; Radiation Tolerance ; Signal Transduction
Chemical Substances	Hedgehog Proteins
Language	English
Publishing date	2018-09-19
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms19092835
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Article ; Online: Genetic and immunologic features of recurrent stage I lung adenocarcinoma.

Kratz, Johannes R / Li, Jack Z / Tsui, Jessica / Lee, Jen C / Ding, Vivianne W / Rao, Arjun A / Mann, Michael J / Chan, Vincent / Combes, Alexis J / Krummel, Matthew F / Jablons, David M

Scientific reports

2021 Volume 11, Issue 1, Page(s) 23690

Abstract: Although surgery for early-stage lung cancer offers the best chance of cure, recurrence still occurs between 30 and 50% of the time. Why patients frequently recur after complete resection of early-stage lung cancer remains unclear. Using a large cohort ... ...

Abstract	Although surgery for early-stage lung cancer offers the best chance of cure, recurrence still occurs between 30 and 50% of the time. Why patients frequently recur after complete resection of early-stage lung cancer remains unclear. Using a large cohort of stage I lung adenocarcinoma patients, distinct genetic, genomic, epigenetic, and immunologic profiles of recurrent tumors were analyzed using a novel recurrence classifier. To characterize the tumor immune microenvironment of recurrent stage I tumors, unique tumor-infiltrating immune population markers were identified using single cell RNA-seq on a separate cohort of patients undergoing stage I lung adenocarcinoma resection and applied to a large study cohort using digital cytometry. Recurrent stage I lung adenocarcinomas demonstrated higher mutation and lower methylation burden than non-recurrent tumors, as well as widespread activation of known cancer and cell cycle pathways. Simultaneously, recurrent tumors displayed downregulation of immune response pathways including antigen presentation and Th1/Th2 activation. Recurrent tumors were depleted in adaptive immune populations, and depletion of adaptive immune populations and low cytolytic activity were prognostic of stage I recurrence. Genomic instability and impaired adaptive immune responses are key features of stage I lung adenocarcinoma immunosurveillance escape and recurrence after surgery.
MeSH term(s)	Adenocarcinoma of Lung/diagnosis ; Adenocarcinoma of Lung/genetics ; Adenocarcinoma of Lung/immunology ; Biomarkers, Tumor ; Computational Biology/methods ; Disease Susceptibility ; Epigenesis, Genetic ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genetic Variation ; Humans ; Male ; Mutation ; Neoplasm Recurrence, Local ; Neoplasm Staging ; Prognosis ; Proportional Hazards Models ; Tumor Microenvironment/genetics
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2021-12-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-02946-0
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Article: Spotlight on afatinib and its potential in the treatment of squamous cell lung cancer: the evidence so far.

Xu, Yijun / Ding, Vivianne W / Zhang, Hong / Zhang, Xun / Jablons, David / He, Biao

Therapeutics and clinical risk management

2016 Volume 12, Page(s) 807–816

Abstract: Compared to adenocarcinoma, fewer effective treatment options are available for advanced or metastatic squamous cell carcinoma (SCC) of the lung. Afatinib is an orally administered, irreversible EGFR antagonist. As a second-generation tyrosine kinase ... ...

Abstract	Compared to adenocarcinoma, fewer effective treatment options are available for advanced or metastatic squamous cell carcinoma (SCC) of the lung. Afatinib is an orally administered, irreversible EGFR antagonist. As a second-generation tyrosine kinase inhibitor, it has been applied in the treatment of patients with EGFR-mutant non-small-cell lung cancer. Recently, several clinical trials have shown that afatinib leads to a significant improvement in progression-free survival and overall survival of patients with SCC. Moving forward, afatinib should be one of the options among tyrosine kinase inhibitors, monoclonal antibodies, and cytotoxicity chemotherapy drugs for SCC.
Language	English
Publishing date	2016-05-24
Publishing country	New Zealand
Document type	Journal Article ; Review
ZDB-ID	2186560-7
ISSN	1178-203X ; 1176-6336
ISSN (online)	1178-203X
ISSN	1176-6336
DOI	10.2147/TCRM.S92996
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Article: GLI1 activation is a key mechanism of erlotinib resistance in human non-small cell lung cancer.

Dong, Zhouhuan / Wang, Yun / Ding, Vivianne / Yan, Xiang / Lv, Yali / Zhong, Mei / Zhu, Fengwei / Zhao, Po / He, Charlotte / Ding, Feng / Shi, Huaiyin

Oncology letters

2020 Volume 20, Issue 4, Page(s) 76

Abstract: Lung cancer is the leading cause of cancer-associated death worldwide. In recent years, the advancement of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) targeted therapies has provided clinical benefits for lung cancer patients ... ...

Abstract	Lung cancer is the leading cause of cancer-associated death worldwide. In recent years, the advancement of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) targeted therapies has provided clinical benefits for lung cancer patients with EGFR mutations. The response to EGFR-TKI varies in patients with lung cancer, and resistance typically develops during the course of the treatment. Therefore, understanding biomarkers which can predict resistance to EGFR-TKI is important. Overexpression of GLI causes activation of the Hedgehog (Hh) signaling pathway and plays a critical role in oncogenesis in numerous types of cancer. In the present study, the role of GLI1 in erlotinib resistance was investigated. GLI1 mRNA and protein expression levels were determined using reverse transcription-quantitative PCR and immunohistochemistry (IHC) in lung cancer cell lines and tumor specimens, respectively. GLI1 mRNA expression levels were found to be positively correlated with the IC
Language	English
Publishing date	2020-07-31
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2573196-8
ISSN	1792-1082 ; 1792-1074
ISSN (online)	1792-1082
ISSN	1792-1074
DOI	10.3892/ol.2020.11937
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Article ; Online: Deletion of Rbpj from postnatal endothelium leads to abnormal arteriovenous shunting in mice.

Nielsen, Corinne M / Cuervo, Henar / Ding, Vivianne W / Kong, Yupeng / Huang, Eric J / Wang, Rong A

Development (Cambridge, England)

2014 Volume 141, Issue 19, Page(s) 3782–3792

Abstract: Arteriovenous malformations (AVMs) are tortuous vessels characterized by arteriovenous (AV) shunts, which displace capillaries and shunt blood directly from artery to vein. Notch signaling regulates embryonic AV specification by promoting arterial, as ... ...

Abstract	Arteriovenous malformations (AVMs) are tortuous vessels characterized by arteriovenous (AV) shunts, which displace capillaries and shunt blood directly from artery to vein. Notch signaling regulates embryonic AV specification by promoting arterial, as opposed to venous, endothelial cell (EC) fate. To understand the essential role of endothelial Notch signaling in postnatal AV organization, we used inducible Cre-loxP recombination to delete Rbpj, a mediator of canonical Notch signaling, from postnatal ECs in mice. Deletion of endothelial Rbpj from birth resulted in features of AVMs by P14, including abnormal AV shunting and tortuous vessels in the brain, intestine and heart. We further analyzed brain AVMs, as they pose particular health risks. Consistent with AVM pathology, we found cerebral hemorrhage, hypoxia and necrosis, and neurological deficits. AV shunts originated from capillaries (and possibly venules), with the earliest detectable morphological abnormalities in AV connections by P8. Prior to AV shunt formation, alterations in EC gene expression were detected, including decreased Efnb2 and increased Pai1, which encodes a downstream effector of TGFβ signaling. After AV shunts had formed, whole-mount immunostaining showed decreased Efnb2 and increased Ephb4 expression within AV shunts, suggesting that ECs were reprogrammed from arterial to venous identity. Deletion of Rbpj from adult ECs led to tortuosities in gastrointestinal, uterine and skin vascular beds, but had mild effects in the brain. Our results demonstrate a temporal requirement for Rbpj in postnatal ECs to maintain proper artery, capillary and vein organization and to prevent abnormal AV shunting and AVM pathogenesis.
MeSH term(s)	Animals ; Arteriovenous Malformations/genetics ; Arteriovenous Malformations/pathology ; Endothelium, Vascular/metabolism ; Gene Deletion ; Gene Expression Profiling ; Image Processing, Computer-Assisted ; Immunoglobulin J Recombination Signal Sequence-Binding Protein/deficiency ; Immunoglobulin J Recombination Signal Sequence-Binding Protein/genetics ; Mice ; Microscopy, Fluorescence ; Real-Time Polymerase Chain Reaction ; Receptor, EphB4/metabolism ; Receptors, Notch/metabolism ; Signal Transduction/physiology
Chemical Substances	Immunoglobulin J Recombination Signal Sequence-Binding Protein ; Rbpj protein, mouse ; Receptors, Notch ; Ephb4 protein, mouse (EC 2.7.10.1) ; Receptor, EphB4 (EC 2.7.10.1)
Language	English
Publishing date	2014-09-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.108951
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Article ; Online: SARS-CoV-2 infection of airway organoids reveals conserved use of Tetraspanin-8 by Ancestral, Delta, and Omicron variants.

Hysenaj, Lisiena / Little, Samantha / Kulhanek, Kayla / Magnen, Melia / Bahl, Kriti / Gbenedio, Oghenekevwe M / Prinz, Morgan / Rodriguez, Lauren / Andersen, Christopher / Rao, Arjun Arkal / Shen, Alan / Lone, Jean-Christophe / Lupin-Jimenez, Leonard C / Bonser, Luke R / Serwas, Nina K / Mick, Eran / Khalid, Mir M / Taha, Taha Y / Kumar, Renuka /

Stem cell reports

2023 Volume 18, Issue 3, Page(s) 636–653

Abstract: Ancestral SARS coronavirus-2 (SARS-CoV-2) and variants of concern (VOC) caused a global pandemic with a spectrum of disease severity. The mechanistic explaining variations related to airway epithelium are relatively understudied. Here, we biobanked ... ...

Abstract	Ancestral SARS coronavirus-2 (SARS-CoV-2) and variants of concern (VOC) caused a global pandemic with a spectrum of disease severity. The mechanistic explaining variations related to airway epithelium are relatively understudied. Here, we biobanked airway organoids (AO) by preserving stem cell function. We optimized viral infection with H1N1/PR8 and comprehensively characterized epithelial responses to SARS-CoV-2 infection in phenotypically stable AO from 20 different subjects. We discovered Tetraspanin-8 (TSPAN8) as a facilitator of SARS-CoV-2 infection. TSPAN8 facilitates SARS-CoV-2 infection rates independently of ACE2-Spike interaction. In head-to-head comparisons with Ancestral SARS-CoV-2, Delta and Omicron VOC displayed lower overall infection rates of AO but triggered changes in epithelial response. All variants shared highest tropism for ciliated and goblet cells. TSPAN8-blocking antibodies diminish SARS-CoV-2 infection and may spur novel avenues for COVID-19 therapy.
MeSH term(s)	Humans ; COVID-19 ; SARS-CoV-2 ; Influenza A Virus, H1N1 Subtype ; Organoids ; Tetraspanins/genetics
Chemical Substances	Tetraspanins ; TSPAN8 protein, human
Language	English
Publishing date	2023-02-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2720528-9
ISSN	2213-6711 ; 2213-6711
ISSN (online)	2213-6711
ISSN	2213-6711
DOI	10.1016/j.stemcr.2023.01.011
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Article: SARS-CoV-2 infection studies in lung organoids identify TSPAN8 as novel mediator.

Hysenaj, Lisiena / Little, Samantha / Kulhanek, Kayla / Gbenedio, Oghenekevwe M / Rodriguez, Lauren / Shen, Alan / Lone, Jean-Christophe / Lupin-Jimenez, Leonard C / Bonser, Luke R / Serwas, Nina K / Bahl, Kriti / Mick, Eran / Li, Jack Z / Ding, Vivianne W / Matsumoto, Shotaro / Maishan, Mazharul / Simoneau, Camille / Fragiadakis, Gabriela / Jablons, David M /

Langelier, Charles R / Matthay, Michael / Ott, Melanie / Krummel, Matthew / Combes, Alexis J / Sil, Anita / Erle, David J / Kratz, Johannes R / Roose, Jeroen P

bioRxiv : the preprint server for biology

2021

Abstract: SARS coronavirus-2 (SARS-CoV-2) is causing a global pandemic with large variation in COVID-19 disease spectrum. SARS-CoV-2 infection requires host receptor ACE2 on lung epithelium, but epithelial underpinnings of variation are largely unknown. We ... ...

Abstract	SARS coronavirus-2 (SARS-CoV-2) is causing a global pandemic with large variation in COVID-19 disease spectrum. SARS-CoV-2 infection requires host receptor ACE2 on lung epithelium, but epithelial underpinnings of variation are largely unknown. We capitalized on comprehensive organoid assays to report remarkable variation in SARS-CoV-2 infection rates of lung organoids from different subjects. Tropism is highest for TUBA- and MUC5AC-positive organoid cells, but levels of TUBA-, MUC5A-, or ACE2- positive cells do not predict infection rate. We identify surface molecule Tetraspanin 8 (TSPAN8) as novel mediator of SARS-CoV-2 infection, which is not downregulated by this specific virus. TSPAN8 levels, prior to infection, strongly correlate with infection rate and TSPAN8-blocking antibodies diminish SARS-CoV-2 infection. We propose TSPAN8 as novel functional biomarker and potential therapeutic target for COVID-19.
Language	English
Publishing date	2021-06-02
Publishing country	United States
Document type	Preprint
DOI	10.1101/2021.06.01.446640
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Article: Activation of p53 by Dishevelled independent of Wnt or planar polarity pathways.

Ding, Vivianne W / Lin, Li-Ping / Chiang, Andrew L / McCormick, Frank

Journal of molecular medicine (Berlin, Germany)

2007 Volume 85, Issue 11, Page(s) 1281–1289

Abstract: Dishevelled is a key component of the Wnt signaling and planar polarity pathways. We discovered that in selective cell types, it potently activates the transcriptional activity of the tumor suppressor p53. This action, however, is not dependent on the ... ...

Abstract	Dishevelled is a key component of the Wnt signaling and planar polarity pathways. We discovered that in selective cell types, it potently activates the transcriptional activity of the tumor suppressor p53. This action, however, is not dependent on the downstream of either the Wnt or the planar polarity pathways. Dishevelled signals to the first 50 amino acids of p53, which is the transactivation domain. The level of phosphorylation on several serine residues within that region of p53 increases in response to disheveled activation, partially contributing to p53 activation. The MAP kinase pathway and E1B55k may also be involved in this dishevelled-p53 connection. Our data provide evidence that there is a novel signaling pathway from Dishevelled to p53.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Adenovirus E1B Proteins/metabolism ; Animals ; Cell Line ; DNA Damage ; Dishevelled Proteins ; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors ; Humans ; JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors ; MAP Kinase Signaling System/drug effects ; Mice ; Phosphoproteins/metabolism ; Phosphorylation/drug effects ; Protein Kinase Inhibitors/pharmacology ; Protein Structure, Tertiary ; Rats ; Signal Transduction/drug effects ; Transcriptional Activation/drug effects ; Transcriptional Activation/genetics ; Tumor Suppressor Protein p53/chemistry ; Tumor Suppressor Protein p53/genetics ; Wnt Proteins/metabolism ; beta Catenin/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Adenovirus E1B Proteins ; Dishevelled Proteins ; Phosphoproteins ; Protein Kinase Inhibitors ; Tumor Suppressor Protein p53 ; Wnt Proteins ; beta Catenin ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2007-11
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1223802-8
ISSN	1432-1440 ; 0946-2716
ISSN (online)	1432-1440
ISSN	0946-2716
DOI	10.1007/s00109-007-0228-8
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