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Article ; Online: Editor's Note: Combining EGFR and mTOR Blockade for the Treatment of Epithelioid Sarcoma.

Xie, Xianbiao / Ghadimi, Markus P H / Young, Eric D / Belousov, Roman / Zhu, Quan-Sheng / Liu, Juehui / Lopez, Gonzalo / Colombo, Chiara / Peng, Tingsheng / Reynoso, David / Hornick, Jason L / Lazar, Alexander J / Lev, Dina

Clinical cancer research : an official journal of the American Association for Cancer Research

2024 Volume 30, Issue 4, Page(s) 921

Language	English
Publishing date	2024-02-16
Publishing country	United States
Document type	Published Erratum
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-23-3969
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Article ; Online: Managing elderly soft tissue sarcoma patients-should age drive treatment?

Lev, Dina / Pollock, Raphael E

Annals of surgical oncology

2010 Volume 17, Issue 7, Page(s) 1725–1726

MeSH term(s)	Age Factors ; Aged ; Humans ; Sarcoma/diagnosis ; Sarcoma/surgery
Language	English
Publishing date	2010-07
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	1200469-8
ISSN	1534-4681 ; 1068-9265
ISSN (online)	1534-4681
ISSN	1068-9265
DOI	10.1245/s10434-010-1035-y
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Zs.A 4042: Show issues

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Article ; Online: Editor's Note: Inhibition of Platelet-derived Growth Factor-mediated Proliferation of Osteosarcoma Cells by the Novel Tyrosine Kinase Inhibitor STI571.

McGary, Eric C / Weber, Kristy / Mills, Lisa / Doucet, Michelle / Lewis, Valerie / Lev, Dina Chelouche / Fidler, Isaiah J / Bar-Eli, Menashe

Clinical cancer research : an official journal of the American Association for Cancer Research

2019 Volume 25, Issue 10, Page(s) 3196

Language	English
Publishing date	2019-05-13
Publishing country	United States
Document type	Journal Article ; Expression of Concern
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-19-1101
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Article ; Online: β-catenin S45F mutation results in apoptotic resistance.

Braggio, Danielle / Zewdu, Abeba / Londhe, Priya / Yu, Peter / Lopez, Gonzalo / Batte, Kara / Koller, David / Costas Casal de Faria, Fernanda / Casadei, Lucia / Strohecker, Anne M / Lev, Dina / Pollock, Raphael E

Oncogene

2020 Volume 39, Issue 34, Page(s) 5589–5600

Abstract: Wnt/β-catenin signaling is one of the key cascades regulating embryogenesis and tissue homeostasis; it has also been intimately associated with carcinogenesis. This pathway is deregulated in several tumors, including colorectal cancer, breast cancer, and ...

Abstract	Wnt/β-catenin signaling is one of the key cascades regulating embryogenesis and tissue homeostasis; it has also been intimately associated with carcinogenesis. This pathway is deregulated in several tumors, including colorectal cancer, breast cancer, and desmoid tumors. It has been shown that CTNNB1 exon 3 mutations are associated with an aggressive phenotype in several of these tumor types and may be associated with therapeutic tolerance. Desmoid tumors typically have a stable genome with β-catenin mutations as a main feature, making these tumors an ideal model to study the changes associated with different types of β-catenin mutations. Here, we show that the apoptosis mechanism is deregulated in β-catenin S45F mutants, resulting in decreased induction of apoptosis in these cells. Our findings also demonstrate that RUNX3 plays a pivotal role in the inhibition of apoptosis found in the β-catenin S45F mutants. Restoration of RUNX3 overcomes this inhibition in the S45F mutants, highlighting it as a potential therapeutic target for malignancies harboring this specific CTNNB1 mutation. While the regulatory effect of RUNX3 in β-catenin is already known, our results suggest the possibility of a feedback loop involving these two genes, with the CTNNB1 S45F mutation downregulating expression of RUNX3, thus providing additional possible novel therapeutic targets for tumors having deregulated Wnt/β-catenin signaling induced by this mutation.
MeSH term(s)	Abdominal Neoplasms/genetics ; Abdominal Neoplasms/metabolism ; Abdominal Neoplasms/pathology ; Adenomatous Polyposis Coli/genetics ; Adenomatous Polyposis Coli/metabolism ; Adenomatous Polyposis Coli/pathology ; Apoptosis/genetics ; Cell Line, Tumor ; Core Binding Factor Alpha 3 Subunit/genetics ; Core Binding Factor Alpha 3 Subunit/metabolism ; Down-Regulation ; Fibromatosis, Aggressive/genetics ; Fibromatosis, Aggressive/metabolism ; Fibromatosis, Aggressive/pathology ; Gene Expression Profiling/methods ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Humans ; Mutation, Missense ; Wnt Signaling Pathway/genetics ; beta Catenin/genetics ; beta Catenin/metabolism
Chemical Substances	Core Binding Factor Alpha 3 Subunit ; beta Catenin
Language	English
Publishing date	2020-07-10
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/s41388-020-1382-5
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Zs.A 2218: Show issues

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Article ; Online: Autophagy blockade enhances HDAC inhibitors' pro-apoptotic effects: potential implications for the treatment of a therapeutic-resistant malignancy.

Lopez, Gonzalo / Torres, Keila / Lev, Dina

Autophagy

2011 Volume 7, Issue 4, Page(s) 440–441

Abstract: Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive, highly metastatic, poor prognosis tumors for which effective therapeutic strategies are currently lacking. We summarize recent work focusing on preclinical evaluation of histone ... ...

Abstract	Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive, highly metastatic, poor prognosis tumors for which effective therapeutic strategies are currently lacking. We summarize recent work focusing on preclinical evaluation of histone deacetylase inhibitors (HDACis) for the treatment of MPNST. HDACis are a novel drug class with anti-cancer therapeutic promise. Using human MPNST cell lines and xenograft models we found that a MPNST subset is highly sensitive to HDACis, whereas a fraction is relatively resistant. HDACis were found to induce autophagy in all MPNST cells in vitro and in vivo; in "sensitive" MPNST cells autophagy occurs in concert with apoptosis, whereas unopposed autophagy develops in "resistant" cells. Genetic and chemical autophagy blockade significantly enhances HDACi-induced apoptotic cell death in both resistant and sensitive cells. Combined chloroquine and HDACi treatment abrogates growth of human MPNST xenografts and lung metastases. The potential role of autophagy in cancer therapeutic response remains controversial; however, our study supports HDACi-induced autophagy as a MPNST survival mechanism. These data also imply that the consequences of drug-induced autophagy may be compound-type, tumor-type, or even molecular context-dependent, suggesting a complex crosstalk between autophagy and apoptosis. Clinical trials evaluating HDACis with autophagy blockade for therapy of MPNST therefore merit consideration.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Apoptosis ; Autophagy ; Chloroquine/pharmacology ; Gene Expression Regulation, Neoplastic ; Histone Deacetylase Inhibitors/metabolism ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Lung Neoplasms/drug therapy ; Mice ; Models, Biological ; Neoplasm Metastasis ; Neoplasm Transplantation ; Nerve Sheath Neoplasms/drug therapy ; Nerve Sheath Neoplasms/metabolism
Chemical Substances	Antineoplastic Agents ; Histone Deacetylase Inhibitors ; Chloroquine (886U3H6UFF)
Language	English
Publishing date	2011-04-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.4161/auto.7.4.14680
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Zs.A 6741: Show issues

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Article ; Online: Experimental models of undifferentiated pleomorphic sarcoma and malignant peripheral nerve sheath tumor.

Laboratory investigation; a journal of technical methods and pathology

2022 Volume 102, Issue 6, Page(s) 658–666

Abstract: Undifferentiated pleomorphic sarcoma (UPS) and malignant peripheral nerve sheath tumor (MPNST) are aggressive soft tissue sarcomas that do not respond well to current treatment modalities. The limited availability of UPS and MPNST cell lines makes it ... ...

Abstract	Undifferentiated pleomorphic sarcoma (UPS) and malignant peripheral nerve sheath tumor (MPNST) are aggressive soft tissue sarcomas that do not respond well to current treatment modalities. The limited availability of UPS and MPNST cell lines makes it challenging to identify potential therapeutic targets in a laboratory setting. Understanding the urgent need for improved treatments for these tumors and the limited cellular models available, we generated additional cell lines to study these rare cancers. Patient-derived tumors were used to establish 4 new UPS models, including one radiation-associated UPS-UPS271.1, UPS511, UPS0103, and RIS620, one unclassified spindle cell sarcoma-USC060.1, and 3 new models of MPNST-MPNST007, MPNST3813E, and MPNST4970. This study examined the utility of the new cell lines as sarcoma models by assessing their tumorigenic potential and mutation status for known sarcoma-related genes. All the cell lines formed colonies and migrated in vitro. The in vivo tumorigenic potential of the cell lines and corresponding xenografts was determined by subcutaneous injection or xenograft re-passaging into immunocompromised mice. USC060.1 and UPS511 cells formed tumors in mice upon subcutaneous injection. UPS0103 and RIS620 tumor implants formed tumors in vivo, as did MPNST007 and MPNST3813E tumor implants. Targeted sequencing analysis of a panel of genes frequently mutated in sarcomas identified TP53, RB1, and ATRX mutations in a subset of the cell lines. These new cellular models provide the scientific community with powerful tools for detailed studies of tumorigenesis and for investigating novel therapies for UPS and MPNST.
MeSH term(s)	Animals ; Humans ; Mice ; Models, Theoretical ; Mutation ; Neurofibrosarcoma/genetics ; Sarcoma/genetics ; Sarcoma/pathology ; Soft Tissue Neoplasms/genetics
Language	English
Publishing date	2022-02-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80178-1
ISSN	1530-0307 ; 0023-6837
ISSN (online)	1530-0307
ISSN	0023-6837
DOI	10.1038/s41374-022-00734-6
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Ud II Zs.164: Show issues

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Article ; Online: Desmoid tumor: from surgical extirpation to molecular dissection.

Lazar, Alexander J F / Hajibashi, Shohrae / Lev, Dina

Current opinion in oncology

2009 Volume 21, Issue 4, Page(s) 352–359

Abstract: Purpose of review: Desmoid tumors are associated with a variable and unpredictable clinical course. Surgery is the therapeutic mainstay, but there has been much discussion of late regarding its proper application. Little is known regarding the molecular ...

Abstract	Purpose of review: Desmoid tumors are associated with a variable and unpredictable clinical course. Surgery is the therapeutic mainstay, but there has been much discussion of late regarding its proper application. Little is known regarding the molecular determinates of desmoid tumor behavior. Some recent work has focused on the role of beta-catenin in desmoid tumor biology. Recent findings: Given the variable clinical course of desmoid tumors, the interpretation of factors classically associated with recurrence such as microscopic status of margins appears more nuanced that previously thought. The application of multidisciplinary assessment with multimodality treatment, including surgery, radiation and systemic therapies may underlie these changes and now form the basis of care for this tumor. The precise CTNNB1 mutation present appears to be strongly predictive of recurrence after initial resection in one large, retrospective, multivariate analysis. Summary: Establishing the population benefiting most from various treatment modalities and combinations is critical for progress in this disease. Assessment and treatment of individual patients in a multidisciplinary setting is critical to achieve the most favorable outcome. Additional study of the molecular determinates of desmoid behavior is needed to guide therapeutic selection.
MeSH term(s)	Combined Modality Therapy ; Fibromatosis, Aggressive/genetics ; Fibromatosis, Aggressive/metabolism ; Fibromatosis, Aggressive/pathology ; Fibromatosis, Aggressive/therapy ; Humans ; Mesenchymoma/genetics ; Mesenchymoma/metabolism ; Mesenchymoma/pathology ; Mesenchymoma/therapy ; Wnt Proteins/metabolism ; beta Catenin/genetics ; beta Catenin/metabolism
Chemical Substances	CTNNB1 protein, human ; Wnt Proteins ; beta Catenin
Language	English
Publishing date	2009-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1049384-0
ISSN	1531-703X ; 1040-8746
ISSN (online)	1531-703X
ISSN	1040-8746
DOI	10.1097/CCO.0b013e32832c9502
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Article: Editor's Note: Genomic and Molecular Characterization of Malignant Peripheral Nerve Sheath Tumor Identifies the IGF1R Pathway as a Primary Target for Treatment.

Yang, Jilong / Ylipää, Antti / Sun, Yan / Zheng, Hong / Chen, Kexin / Nykter, Matti / Trent, Jonathan / Ratner, Nancy / Lev, Dina C / Zhang, Wei

Clinical cancer research : an official journal of the American Association for Cancer Research

2019 Volume 25, Issue 10, Page(s) 3195

Language	English
Publishing date	2019-05-12
Publishing country	United States
Document type	Journal Article ; Expression of Concern
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-19-1144
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Article ; Online: MDM2

Casadei, Lucia / Calore, Federica / Braggio, Danielle A / Zewdu, Abeba / Deshmukh, Ameya A / Fadda, Paolo / Lopez, Gonzalo / Wabitsch, Martin / Song, Chi / Leight, Jennifer L / Grignol, Valerie P / Lev, Dina / Croce, Carlo M / Pollock, Raphael E

Cancer research

2019 Volume 79, Issue 19, Page(s) 4911–4922

Abstract: Dedifferentiated liposarcoma (DDLPS) is frequently diagnosed late, and patients typically respond poorly to treatments. DDLPS is molecularly characterized by wild-type p53 and amplification of ... ...

Abstract	Dedifferentiated liposarcoma (DDLPS) is frequently diagnosed late, and patients typically respond poorly to treatments. DDLPS is molecularly characterized by wild-type p53 and amplification of the
MeSH term(s)	Adipocytes/metabolism ; Extracellular Vesicles/metabolism ; Humans ; Liposarcoma/metabolism ; Liposarcoma/pathology ; Proto-Oncogene Proteins c-mdm2/metabolism ; Stem Cells/metabolism ; Tumor Microenvironment/physiology
Chemical Substances	MDM2 protein, human (EC 2.3.2.27) ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27)
Language	English
Publishing date	2019-08-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-19-0203
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Article ; Online: Autophagy inhibition overcomes sorafenib resistance in S45F-mutated desmoid tumors.

Braggio, Danielle / Koller, David / Jin, Feng / Siva, Nanda / Zewdu, Abeba / Lopez, Gonzalo / Batte, Kara / Casadei, Lucia / Welliver, Meng / Strohecker, Anne M / Lev, Dina / Pollock, Raphael E

Cancer

2019 Volume 125, Issue 15, Page(s) 2693–2703

Abstract: Background: Desmoid tumors (DTs) are rare and understudied fibroblastic lesions that are frequently recurrent and locally invasive. DT patients often experience chronic pain, organ dysfunction, decrease in quality of life, and even death.: Methods: ... ...

Abstract	Background: Desmoid tumors (DTs) are rare and understudied fibroblastic lesions that are frequently recurrent and locally invasive. DT patients often experience chronic pain, organ dysfunction, decrease in quality of life, and even death. Methods: Sorafenib has emerged as a promising therapeutic strategy, which has led to the first randomized phase 3 clinical trial devoted to DTs. Concurrently, we conducted a comprehensive analysis of sorafenib efficacy in a large panel of desmoid cell strains to probe for response mechanism. Results: We found distinctive groups of higher- and lower-responder cells. Clustering the lower-responder group, we observed that CTNNB1 mutation was determinant of outcome. Our results revealed that a lower dose of sorafenib was able to inhibit cell viability, migration, and invasion of wild-type and T41A-mutated DTs. Apoptosis induction was observed in those cells after treatment with sorafenib. On the other hand, the lower dose of sorafenib was not able to inhibit cell viability, migration, or invasion or to induce apoptosis in the S45F-mutated DTs. The investigation of autophagy showed the dependency of S45F-mutated DTs on this pathway as a part of cell survival mechanism. Significantly, when autophagy was inhibited genetically or pharmacologically in the S45F mutant cell strains, sensitivity to sorafenib was restored. Conclusions: Our findings suggest that the response to sorafenib differs when comparing S45F-mutated DTs and T41A-mutated or wild-type DTs. Furthermore, the combination of hydroxychloroquine and sorafenib enhances the antiproliferative and proapoptotic effects in S45F-mutated DT cells, suggesting that profiling β-catenin status could guide clinical management of desmoid patients who are considering sorafenib treatment.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Autophagy/drug effects ; Female ; Fibromatosis, Aggressive/drug therapy ; Humans ; Male ; Sorafenib/pharmacology ; Sorafenib/therapeutic use
Chemical Substances	Antineoplastic Agents ; Sorafenib (9ZOQ3TZI87)
Language	English
Publishing date	2019-04-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1429-1
ISSN	1097-0142 ; 0008-543X ; 1934-662X
ISSN (online)	1097-0142
ISSN	0008-543X ; 1934-662X
DOI	10.1002/cncr.32120
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