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Article ; Online: Roles of Notch Signaling in the Tumor Microenvironment.

D'Assoro, Antonino B / Leon-Ferre, Roberto / Braune, Eike-Benjamin / Lendahl, Urban

International journal of molecular sciences

2022 Volume 23, Issue 11

Abstract: The Notch signaling pathway is an architecturally simple signaling mechanism, well known for its role in cell fate regulation during organ development and in tissue homeostasis. In keeping with its importance for normal development, dysregulation of ... ...

Abstract	The Notch signaling pathway is an architecturally simple signaling mechanism, well known for its role in cell fate regulation during organ development and in tissue homeostasis. In keeping with its importance for normal development, dysregulation of Notch signaling is increasingly associated with different types of tumors, and proteins in the Notch signaling pathway can act as oncogenes or tumor suppressors, depending on the cellular context and tumor type. In addition to a role as a driver of tumor initiation and progression in the tumor cells carrying oncogenic mutations, it is an emerging realization that Notch signaling also plays a role in non-mutated cells in the tumor microenvironment. In this review, we discuss how aberrant Notch signaling can affect three types of cells in the tumor stroma-cancer-associated fibroblasts, immune cells and vascular cells-and how this influences their interactions with the tumor cells. Insights into the roles of Notch in cells of the tumor environment and the impact on tumor-stroma interactions will lead to a deeper understanding of Notch signaling in cancer and inspire new strategies for Notch-based tumor therapy.
MeSH term(s)	Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Oncogenes ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Signal Transduction/physiology ; Tumor Microenvironment
Chemical Substances	Receptors, Notch
Language	English
Publishing date	2022-06-02
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/ijms23116241
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Article ; Online: Roles of Notch Signaling in the Tumor Microenvironment

Antonino B. D’Assoro / Roberto Leon-Ferre / Eike-Benjamin Braune / Urban Lendahl

International Journal of Molecular Sciences, Vol 23, Iss 6241, p

2022 Volume 6241

Abstract	The Notch signaling pathway is an architecturally simple signaling mechanism, well known for its role in cell fate regulation during organ development and in tissue homeostasis. In keeping with its importance for normal development, dysregulation of Notch signaling is increasingly associated with different types of tumors, and proteins in the Notch signaling pathway can act as oncogenes or tumor suppressors, depending on the cellular context and tumor type. In addition to a role as a driver of tumor initiation and progression in the tumor cells carrying oncogenic mutations, it is an emerging realization that Notch signaling also plays a role in non-mutated cells in the tumor microenvironment. In this review, we discuss how aberrant Notch signaling can affect three types of cells in the tumor stroma—cancer-associated fibroblasts, immune cells and vascular cells—and how this influences their interactions with the tumor cells. Insights into the roles of Notch in cells of the tumor environment and the impact on tumor-stroma interactions will lead to a deeper understanding of Notch signaling in cancer and inspire new strategies for Notch-based tumor therapy.
Keywords	Notch signaling ; cancer ; tumor ; tumor microenvironment ; oncogene ; tumor suppressor gene ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	572
Language	English
Publishing date	2022-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Identification of a Notch transcriptomic signature for breast cancer.

Braune, Eike-Benjamin / Geist, Felix / Tang, Xiaojia / Kalari, Krishna / Boughey, Judy / Wang, Liewei / Leon-Ferre, Roberto A / D'Assoro, Antonino B / Ingle, James N / Goetz, Matthew P / Kreis, Julian / Wang, Kang / Foukakis, Theodoros / Seshire, Anita / Wienke, Dirk / Lendahl, Urban

Breast cancer research : BCR

2024 Volume 26, Issue 1, Page(s) 4

Abstract: Background: Dysregulated Notch signalling contributes to breast cancer development and progression, but validated tools to measure the level of Notch signalling in breast cancer subtypes and in response to systemic therapy are largely lacking. A ... ...

Abstract	Background: Dysregulated Notch signalling contributes to breast cancer development and progression, but validated tools to measure the level of Notch signalling in breast cancer subtypes and in response to systemic therapy are largely lacking. A transcriptomic signature of Notch signalling would be warranted, for example to monitor the effects of future Notch-targeting therapies and to learn whether altered Notch signalling is an off-target effect of current breast cancer therapies. In this report, we have established such a classifier. Methods: To generate the signature, we first identified Notch-regulated genes from six basal-like breast cancer cell lines subjected to elevated or reduced Notch signalling by culturing on immobilized Notch ligand Jagged1 or blockade of Notch by γ-secretase inhibitors, respectively. From this cadre of Notch-regulated genes, we developed candidate transcriptomic signatures that were trained on a breast cancer patient dataset (the TCGA-BRCA cohort) and a broader breast cancer cell line cohort and sought to validate in independent datasets. Results: An optimal 20-gene transcriptomic signature was selected. We validated the signature on two independent patient datasets (METABRIC and Oslo2), and it showed an improved coherence score and tumour specificity compared with previously published signatures. Furthermore, the signature score was particularly high for basal-like breast cancer, indicating an enhanced level of Notch signalling in this subtype. The signature score was increased after neoadjuvant treatment in the PROMIX and BEAUTY patient cohorts, and a lower signature score generally correlated with better clinical outcome. Conclusions: The 20-gene transcriptional signature will be a valuable tool to evaluate the response of future Notch-targeting therapies for breast cancer, to learn about potential effects on Notch signalling from conventional breast cancer therapies and to better stratify patients for therapy considerations.
MeSH term(s)	Humans ; Female ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Gene Expression Profiling ; Transcriptome
Language	English
Publishing date	2024-01-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2015059-3
ISSN	1465-542X ; 1465-5411
ISSN (online)	1465-542X
ISSN	1465-5411
DOI	10.1186/s13058-023-01757-7
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Article: Aurora-A Kinase as a Promising Therapeutic Target in Cancer.

D'Assoro, Antonino B / Haddad, Tufia / Galanis, Evanthia

Frontiers in oncology

2016 Volume 5, Page(s) 295

Abstract: ... Aurora-A, -B, and -C), Aurora-A and Aurora-B are expressed at detectable levels in somatic cells ...

Abstract	Mammalian Aurora family of serine/threonine kinases are master regulators of mitotic progression and are frequently overexpressed in human cancers. Among the three members of the Aurora kinase family (Aurora-A, -B, and -C), Aurora-A and Aurora-B are expressed at detectable levels in somatic cells undergoing mitotic cell division. Aberrant Aurora-A kinase activity has been implicated in oncogenic transformation through the development of chromosomal instability and tumor cell heterogeneity. Recent studies also reveal a novel non-mitotic role of Aurora-A activity in promoting tumor progression through activation of epithelial-mesenchymal transition reprograming resulting in the genesis of tumor-initiating cells. Therefore, Aurora-A kinase represents an attractive target for cancer therapeutics, and the development of small molecule inhibitors of Aurora-A oncogenic activity may improve the clinical outcomes of cancer patients. In the present review, we will discuss mitotic and non-mitotic functions of Aurora-A activity in oncogenic transformation and tumor progression. We will also review the current clinical studies, evaluating small molecule inhibitors of Aurora-A activity and their efficacy in the management of cancer patients.
Language	English
Publishing date	2016-01-06
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2015.00295
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Article ; Online: Spectroscopic label-free microscopy of changes in live cell chromatin and biochemical composition in transplantable organoids.

Pettinato, Giuseppe / Coughlan, Mark F / Zhang, Xuejun / Chen, Liming / Khan, Umar / Glyavina, Maria / Sheil, Conor J / Upputuri, Paul K / Zakharov, Yuri N / Vitkin, Edward / D'Assoro, Antonino B / Fisher, Robert A / Itzkan, Irving / Zhang, Lei / Qiu, Le / Perelman, Lev T

Science advances

2021 Volume 7, Issue 34

Abstract: Organoids formed from human induced pluripotent stem cells (hiPSCs) could be a limitless source of functional tissue for transplantations in many organs. Unfortunately, fine-tuning differentiation protocols to form large quantities of hiPSC organoids in ... ...

Abstract	Organoids formed from human induced pluripotent stem cells (hiPSCs) could be a limitless source of functional tissue for transplantations in many organs. Unfortunately, fine-tuning differentiation protocols to form large quantities of hiPSC organoids in a controlled, scalable, and reproducible manner is quite difficult and often takes a very long time. Recently, we introduced a new approach of rapid organoid formation from dissociated hiPSCs and endothelial cells using microfabricated cell-repellent microwell arrays. This approach, when combined with real-time label-free Raman spectroscopy of biochemical composition changes and confocal light scattering spectroscopic microscopy of chromatin transition, allows for monitoring live differentiating organoids without the need to sacrifice a sample, substantially shortening the time of protocol fine-tuning. We used this approach to both culture and monitor homogeneous liver organoids that have the main functional features of the human liver and which could be used for cell transplantation liver therapy in humans.
MeSH term(s)	Cell Differentiation ; Chromatin ; Endothelial Cells ; Humans ; Induced Pluripotent Stem Cells ; Microscopy ; Organoids
Chemical Substances	Chromatin
Language	English
Publishing date	2021-08-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abj2800
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Article ; Online: Evaluation of Alisertib Alone or Combined With Fulvestrant in Patients With Endocrine-Resistant Advanced Breast Cancer: The Phase 2 TBCRC041 Randomized Clinical Trial.

JAMA oncology

2023 Volume 9, Issue 6, Page(s) 815–824

Abstract: Importance: Aurora A kinase (AURKA) activation, related in part to AURKA amplification and variants, is associated with downregulation of estrogen receptor (ER) α expression, endocrine resistance, and implicated in cyclin-dependent kinase 4/6 inhibitor ( ...

Abstract	Importance: Aurora A kinase (AURKA) activation, related in part to AURKA amplification and variants, is associated with downregulation of estrogen receptor (ER) α expression, endocrine resistance, and implicated in cyclin-dependent kinase 4/6 inhibitor (CDK 4/6i) resistance. Alisertib, a selective AURKA inhibitor, upregulates ERα and restores endocrine sensitivity in preclinical metastatic breast cancer (MBC) models. The safety and preliminary efficacy of alisertib was demonstrated in early-phase trials; however, its activity in CDK 4/6i-resistant MBC is unknown. Objective: To assess the effect of adding fulvestrant to alisertib on objective tumor response rates (ORRs) in endocrine-resistant MBC. Design, setting, and participants: This phase 2 randomized clinical trial was conducted through the Translational Breast Cancer Research Consortium, which enrolled participants from July 2017 to November 2019. Postmenopausal women with endocrine-resistant, ERBB2 (formerly HER2)-negative MBC who were previously treated with fulvestrant were eligible. Stratification factors included prior treatment with CDK 4/6i, baseline metastatic tumor ERα level measurement (<10%, ≥10%), and primary or secondary endocrine resistance. Among 114 preregistered patients, 96 (84.2%) registered and 91 (79.8%) were evaluable for the primary end point. Data analysis began after January 10, 2022. Interventions: Alisertib, 50 mg, oral, daily on days 1 to 3, 8 to 10, and 15 to 17 of a 28-day cycle (arm 1) or alisertib same dose/schedule with standard-dose fulvestrant (arm 2). Main outcomes and measures: Improvement in ORR in arm 2 of at least 20% greater than arm 1 when the expected ORR for arm 1 was 20%. Results: All 91 evaluable patients (mean [SD] age, 58.5 [11.3] years; 1 American Indian/Alaskan Native [1.1%], 2 Asian [2.2%], 6 Black/African American [6.6%], 5 Hispanic [5.5%], and 79 [86.8%] White individuals; arm 1, 46 [50.5%]; arm 2, 45 [49.5%]) had received prior treatment with CDK 4/6i. The ORR was 19.6%; (90% CI, 10.6%-31.7%) for arm 1 and 20.0% (90% CI, 10.9%-32.3%) for arm 2. In arm 1, the 24-week clinical benefit rate and median progression-free survival time were 41.3% (90% CI, 29.0%-54.5%) and 5.6 months (95% CI, 3.9-10.0), respectively, and in arm 2 they were 28.9% (90% CI, 18.0%-42.0%) and 5.4 months (95% CI, 3.9-7.8), respectively. The most common grade 3 or higher adverse events attributed to alisertib were neutropenia (41.8%) and anemia (13.2%). Reasons for discontinuing treatment were disease progression (arm 1, 38 [82.6%]; arm 2, 31 [68.9%]) and toxic effects or refusal (arm 1, 5 [10.9%]; arm 2, 12 [26.7%]). Conclusions and relevance: This randomized clinical trial found that adding fulvestrant to treatment with alisertib did not increase ORR or PFS; however, promising clinical activity was observed with alisertib monotherapy among patients with endocrine-resistant and CDK 4/6i-resistant MBC. The overall safety profile was tolerable. Trial registration: ClinicalTrials.gov Identifier: NCT02860000.
MeSH term(s)	Humans ; Female ; Middle Aged ; Fulvestrant ; Breast Neoplasms/pathology ; Estrogen Receptor alpha ; Aurora Kinase A/therapeutic use ; Receptor, ErbB-2/metabolism ; Receptors, Estrogen/metabolism ; Antineoplastic Combined Chemotherapy Protocols/adverse effects
Chemical Substances	Fulvestrant (22X328QOC4) ; Estrogen Receptor alpha ; MLN 8237 ; Aurora Kinase A (EC 2.7.11.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; Receptors, Estrogen
Language	English
Publishing date	2023-03-06
Publishing country	United States
Document type	Randomized Controlled Trial ; Clinical Trial, Phase II ; Journal Article ; Research Support, N.I.H., Extramural
ISSN	2374-2445
ISSN (online)	2374-2445
DOI	10.1001/jamaoncol.2022.7949
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Article ; Online: Aurora-A kinase oncogenic signaling mediates TGF-β-induced triple-negative breast cancer plasticity and chemoresistance.

Oncogene

2021 Volume 40, Issue 14, Page(s) 2509–2523

Abstract: Triple-negative breast cancer (TNBCs) account for 15-20% of all breast cancers and represent the most aggressive subtype of this malignancy. Early tumor relapse and progression are linked to the enrichment of a sub-fraction of cancer cells, termed breast ...

Abstract	Triple-negative breast cancer (TNBCs) account for 15-20% of all breast cancers and represent the most aggressive subtype of this malignancy. Early tumor relapse and progression are linked to the enrichment of a sub-fraction of cancer cells, termed breast tumor-initiating cells (BTICs), that undergo epithelial to mesenchymal transition (EMT) and typically exhibit a basal-like CD44
MeSH term(s)	Aurora Kinase A/metabolism ; Breast Neoplasms/genetics ; Breast Neoplasms/mortality ; Cell Plasticity/genetics ; Female ; Humans ; Signal Transduction ; Survival Analysis
Chemical Substances	Aurora Kinase A (EC 2.7.11.1)
Language	English
Publishing date	2021-03-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-021-01711-x
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Zs.A 2218: Show issues

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Article ; Online: Aurora-A overexpression is linked to development of aggressive teratomas derived from human iPS cells.

Ohmine, Seiga / Salisbury, Jeffrey L / Ingle, James / Pettinato, Giuseppe / Haddox, Candace L / Haddad, Tufia / Galanis, Evanthia / Ikeda, Yasuhiro / D'assoro, Antonino B

Oncology reports

2018 Volume 39, Issue 4, Page(s) 1725–1730

Abstract: The discovery of human induced pluripotent stem cells (hiPSCs) is a promising advancement in the field of regenerative and personalized medicine. Expression of SOX2, KLF4, OCT4 and MYC transcription factors induces the nuclear reprogramming of somatic ... ...

Abstract	The discovery of human induced pluripotent stem cells (hiPSCs) is a promising advancement in the field of regenerative and personalized medicine. Expression of SOX2, KLF4, OCT4 and MYC transcription factors induces the nuclear reprogramming of somatic cells into hiPSCs that share striking similarities with human embryonic stem cells (hESCs). However, several studies have demonstrated that hESCs and hiPSCs could lead to teratoma formation in vivo, thus limiting their current clinical applications. Aberrant cell cycle regulation of hESCs is linked to centrosome amplification, which may account, for their enhanced chromosomal instability (CIN), and thus increase their tumorigenicity. Significantly, the tumor suppressor p53 plays a key role as a 'guardian of reprogramming', safeguarding genomic integrity during hiPSC reprogramming. Nevertheless, the molecular mechanisms leading to development of CIN during reprogramming and increased tumorigenic potential of hiPSCs remains to be fully elucidated. In the present study, we analyzed CIN in hiPSCs derived from keratinocytes and established that chromosomal and mitotic aberrations were linked to centrosome amplification, Aurora-A overexpression, abrogation of p53-mediated G1/S cell cycle checkpoint and loss of Rb tumor-suppressor function. When hiPSCs were transplanted into the kidney capsules of immunocompromised mice, they developed high-grade teratomas characterized by the presence of cells that exhibited non-uniform shapes and sizes, high nuclear pleomorphism and centrosome amplification. Significantly, ex vivo cells derived from teratomas exhibited high self-renewal capacity that was linked to Aurora-A kinase activity and gave rise to lung metastasis when injected into the tail vein of immunocompromised mice. Collectively, these findings demonstrated a high risk for malignancy of hiPSCs that exhibit Aurora-A overexpression, loss of Rb function, centrosome amplification and CIN. Based on these findings, we proposed that Aurora-A-targeted therapy could represent a promising prophylactic therapeutic strategy to decrease the likelihood of CIN and development of aggressive teratomas derived from hiPSCs.
MeSH term(s)	Animals ; Aurora Kinase A/genetics ; Carcinogenesis/genetics ; Cell Differentiation/genetics ; Centrosome/metabolism ; Chromosomal Instability/genetics ; Gene Expression Regulation, Neoplastic ; Human Embryonic Stem Cells/transplantation ; Humans ; Induced Pluripotent Stem Cells/transplantation ; Keratinocytes/metabolism ; Keratinocytes/pathology ; Kruppel-Like Factor 4 ; Mice ; Teratoma/genetics ; Teratoma/pathology ; Teratoma/therapy
Chemical Substances	KLF4 protein, human ; Klf4 protein, mouse ; Kruppel-Like Factor 4 ; Aurora Kinase A (EC 2.7.11.1)
Language	English
Publishing date	2018-01-31
Publishing country	Greece
Document type	Journal Article
ZDB-ID	1222484-4
ISSN	1791-2431 ; 1021-335X
ISSN (online)	1791-2431
ISSN	1021-335X
DOI	10.3892/or.2018.6239
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Article ; Online: Molecular targeting of the Aurora-A/SMAD5 oncogenic axis restores chemosensitivity in human breast cancer cells.

Opyrchal, Mateusz / Gil, Malgorzata / Salisbury, Jeffrey L / Goetz, Mathew P / Suman, Vera / Degnim, Amy / McCubrey, James / Haddad, Tufia / Iankov, Ianko / Kurokawa, Chenye B / Shumacher, Nicole / Ingle, James N / Galanis, Evanthia / D'Assoro, Antonino B

Oncotarget

2017 Volume 8, Issue 53, Page(s) 91803–91816

Abstract: Although the majority of breast cancers initially respond to the cytotoxic effects of chemotherapeutic agents, most breast cancer patients experience tumor relapse and ultimately die because of drug resistance. Breast cancer cells undergoing epithelial ... ...

Abstract	Although the majority of breast cancers initially respond to the cytotoxic effects of chemotherapeutic agents, most breast cancer patients experience tumor relapse and ultimately die because of drug resistance. Breast cancer cells undergoing epithelial to mesenchymal transition (EMT) acquire a CD44
Language	English
Publishing date	2017-09-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.20610
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Article ; Online: Pleiotropic effects of p300-mediated acetylation on p68 and p72 RNA helicase.

Mooney, Steven M / Goel, Apollina / D'Assoro, Antonino B / Salisbury, Jeffrey L / Janknecht, Ralf

The Journal of biological chemistry

2010 Volume 285, Issue 40, Page(s) 30443–30452

Abstract: Here, we demonstrate that p68 (DDX5) and p72 (DDX17), two homologous RNA helicases and transcriptional cofactors, are substrates for the acetyltransferase p300 in vitro and in vivo. Mutation of acetylation sites affected the binding of p68/p72 to histone ...

Abstract	Here, we demonstrate that p68 (DDX5) and p72 (DDX17), two homologous RNA helicases and transcriptional cofactors, are substrates for the acetyltransferase p300 in vitro and in vivo. Mutation of acetylation sites affected the binding of p68/p72 to histone deacetylases, but not to p300 or estrogen receptor. Acetylation additionally increased the stability of p68 and p72 RNA helicase and stimulated their ability to coactivate the estrogen receptor, thereby potentially contributing to its aberrant activation in breast tumors. Also, acetylation of p72, but not of p68 RNA helicase, enhanced p53-dependent activation of the MDM2 promoter, pointing at another mechanism of how p72 acetylation may facilitate carcinogenesis by boosting the negative p53-MDM2 feedback loop. Furthermore, blocking p72 acetylation caused cell cycle arrest and apoptosis, revealing an essential role for p72 acetylation. In conclusion, our report has identified for the first time that acetylation modulates RNA helicases and provides multiple mechanisms how acetylation of p68 and p72 may affect normal and tumor cells.
MeSH term(s)	Acetylation ; Apoptosis/physiology ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Cell Cycle/physiology ; DEAD-box RNA Helicases/genetics ; DEAD-box RNA Helicases/metabolism ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Female ; HeLa Cells ; Humans ; Proto-Oncogene Proteins c-mdm2/genetics ; Proto-Oncogene Proteins c-mdm2/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; p300-CBP Transcription Factors/genetics ; p300-CBP Transcription Factors/metabolism
Chemical Substances	Estrogen Receptor alpha ; TP53 protein, human ; Tumor Suppressor Protein p53 ; p300-CBP Transcription Factors (EC 2.3.1.48) ; p300-CBP-associated factor (EC 2.3.1.48) ; MDM2 protein, human (EC 2.3.2.27) ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27) ; DDX17 protein, human (EC 3.6.1.-) ; Ddx5 protein, human (EC 3.6.1.-) ; DEAD-box RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2010-07-27
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M110.143792
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