Alexandra G. Lopez‐Aguiar

Emory University

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Shishir K. Maithel

Emory University

George A. Poultsides

Stanford University

Kamran Idrees

Vanderbilt University Medical Center

Ryan C. Fields

Washington University in St. Louis

Flavio G. Rocha

Oregon Health & Science University

Megan Beems

University of Michigan–Ann Arbor

Paula Marincola Smith

Vanderbilt University Medical Center

Mary Dillhoff

The Ohio State University

Eleftherios Makris

Stanford University

Eliza W. Beal

The Barbara Ann Karmanos Cancer Institute

Cooperative Institutions

European Neuroendocrine Tumor Society

126

Emory University

The Ohio State University Wexner Medical Center

The Ohio State University

The University of Texas MD Anderson Cancer Center

University of Wisconsin–Madison

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

Washington University in St. Louis

Northwestern University

Stanford University

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Supplementary Figure 5 from Evidence for the Ubiquitin Protease UBP43 as an Antineoplastic Target

Yongli Guo Fadzai Chinyengetere Andrey V. Dolinko Alexandra G. Lopez‐Aguiar Yun Lu

<p>PDF file, 166K, Repression of UBP43 mRNA inhibits in vivo and in vitro growth of ED1 lung cancer cells.</p>

10.1158/1535-7163.22498662.v1

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Citations (0)

Redefining the Ki-67 Index Stratification for Low-Grade Pancreatic Neuroendocrine Tumors: Improving Its Prognostic Value for Recurrence of Disease

Annals of Surgical Oncology (2017)

Alexandra G. Lopez‐Aguiar Cecilia G. Ethun Lauren M. Postlewait Kristen Zhelnin Alyssa M. Krasinskas

Lymphovascular invasion

Surgical oncology

Ki-67

Group B

10.1245/s10434-017-6140-8

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Citations (19)

Lymphotropic Sarcomas (Epithelioid Sarcoma and Clear Cell Sarcoma)

Alexandra G. Lopez‐Aguiar Kenneth Cardona

Lymphotropic sarcomas encompass a rare subset of soft tissue sarcoma histotypes known for their distinct ability to metastasize to locoregional lymph nodes. Epithelioid and clear cell sarcomas are the predominant lymphotropic subtypes and the focus of this review. The utility of lymph node assessment, whether clinical, radiographic, and/or surgical, in patients with these sarcomas is presented. The role of sentinel lymph node biopsy as well as completion lymphadenectomy in patients with these lymphotropic sarcoma histotypes is discussed. Surgery remains the only potential curative option for these tumors, and advancement in histology-specific chemotherapeutic regimens and biologic therapy options is necessary. This review contains 6 tables and 50 references. Key words: clear cell sarcoma, completion lymphadenectomy, epithelioid sarcoma, EWS-ATF1, limb-sparing surgery, lymph node metastasis, sentinel lymph node biopsy, soft tissue sarcoma

Clear-cell sarcoma

Epithelioid sarcoma

Lymphadenectomy

10.2310/7800.16116

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Surgeon Perspectives on the Management of Aborted Cancer Surgery: Results of a Society of Surgical Oncology Member Survey

Annals of Surgical Oncology (2023)

Alexandra G. Lopez‐Aguiar Angela Sarna Sharla Wells‐DiGregorio Emily Huang Peter J. Kneuertz

Surgical oncology

Occult

10.1245/s10434-023-14804-6

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Citations (2)

The Oncologic Impact of Postoperative Complications Following Resection of Truncal and Extremity Soft Tissue Sarcomas

Annals of Surgical Oncology (2017)

Justine S. Broecker Cecilia G. Ethun David K. Monson Alexandra G. Lopez‐Aguiar Nina Le

Neurovascular bundle

Surgical oncology

Univariate analysis

10.1245/s10434-017-6034-9

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Citations (17)

Issue Information ‐ TOC

Journal of Surgical Oncology (2018)

Mohammad Y. Zaidi Alexandra G. Lopez‐Aguiar George A. Poultsides Mary Dillhoff Flavio G. Rocha

Using a mul -ins tu onal database, this study found that for pa ents with func onal neuroendocrine tumors, the failure to achieve symptom improvement a er the resec on is associated with earlier disease recurrence even when accoun ng for histological type, the presence of gene c syndromes, R1 resec on margin, and lymph node involvement.

10.1002/jso.25341

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Pathologic and Prognostic Implications of Incidental versus Nonincidental Gallbladder Cancer: A 10-Institution Study from the United States Extrahepatic Biliary Malignancy Consortium

The American Surgeon (2017)

Cecilia G. Ethun Nina Le Alexandra G. Lopez‐Aguiar Timothy M. Pawlik George A. Poultsides

Most gallbladder cancers (GBCs) are discovered incidentally after routine cholecystectomy. The influence of timing of diagnosis on disease stage, treatment, and prognosis is not known. Patients with GBC who underwent resection at 10 institutions from 2000 to 2015 were included. Patients diagnosed incidentally (IGBC) and nonincidentally (non-IGBC) were compared. Primary outcome was overall survival (OS). Of 445 patients with GBC, 266 (60%) were IGBC and 179 (40%) were non-IGBC. Compared with IGBC, non-IGBC patients were more likely to have R2 resections (43% vs 19%; P < 0.001), advanced T-stage (T3/T4: 70% vs 40%; P < 0.001), high-grade tumors (50% vs 31%; P < 0.001), lymphovascular invasion (64% vs 45%; P = 0.01), and positive lymph nodes (60% vs 43%; P = 0.009). Receipt of adjuvant chemotherapy was similar between groups (49% vs 49%). Non-IGBC was associated with worse median OS compared with IGBC (17 vs 32 months; P < 0.001), which persisted among stage III patients (12 vs 29 months; P < 0.001), but not stages I, II, or IV. Despite accounting for other adverse pathologic factors (grade, T-stage, lymphovascular invasion, margin, lymph node), adjuvant chemotherapy was associated with improved OS only in stage III IGBC, but not in non-IGBC. Compared with incidental discovery, non-IGBC is associated with reduced OS, which is most evident in stage III disease. Despite being well matched for other adverse pathologic factors, adjuvant chemotherapy was associated with improved survival only in stage III patients with incidentally discovered cancer. This underscores the importance of timing of diagnosis in GBC and suggests that these two groups may represent a distinct biology of disease, and the same treatment paradigm may not be appropriate.

Lymphovascular invasion

Gallbladder Cancer

Adjuvant Therapy

10.1177/000313481708300721

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Citations (64)

Abstract 1655: The ubiquitin protease UBP43 is a target for lung cancer therapy and prevention

Cancer Research (2011)

Yongli Guo Fadzai Chinyengetere Andrey V. Dolinko Alexandra G. Lopez‐Aguiar Fabrizio Galimberti

Abstract Lung cancer is the leading cause of cancer mortality for women and men in the United States. Given this, there is a need to find new targets to combat lung cancer. This study explores the E1-like ubiquitin-activating enzyme (UBE1L) that associates with the interferon-stimulated gene 15 (ISG15), which complexes with cyclin D1 and other specific proteins. The ubiquitin protease UBP43 removes ISG15 from conjugated proteins. The UBE1L-ISG15-UBP43 pathway was previously proposed to inhibit lung carcinogenesis by repressing cyclin D1 expression. Our prior work is extended here by reporting that UBP43 is enzymatically active in cells. Also, gain of UBP43 expression specifically stabilizes cyclin D1 while UBP43 knock-down destabilizes cyclin D1, but not cyclin E or other D-type cyclins. This occurs by regulating ISG15 complexes with cyclin D1. UBP43 effects on cyclin D1 were not antagonized by cycloheximide treatment. Whether the deconjugase UBP43 was a lung cancer target was independently addressed through engineered gain and loss of UBP43 expression in lung cancer cells. UBP43 knock-down triggered apoptosis in these cells. In contrast, UBP43 over-expression promoted lung cancer cell growth by inhibiting apoptosis. That cyclin D1 plays a key role in conferring these effects was shown by engineered loss of UBP43 along with forced cyclin D1 expression. Cyclin D1 antagonized effects of loss of UBP43. Engineered UBP43 knock-down in lung cancer cells significantly increased apoptosis (P < 0.05), reduced growth (P < 0.05) and inhibited lung cancer formation (P < 0.05) in FVB mice injected via tail veins with syngeneic lung cancer cells. In marked contrast, forced UBP43 over-expression in lung cancer cells antagonized the effects of interferon, cisplatin and all-trans-retinoic acid, indicating that UBP43 can regulate response to anti-neoplastic agents. To ascertain the clinical impact of this pathway, a paired normal-malignant human lung tissue array from 74 cases was examined for immunohistochemical expression profiles of UBP43 and cyclin D1 proteins. Notably, UBP43 was significantly increased in the malignant as compared to the adjacent normal lung tissues (P = 0.04 for adenocarcinoma and P = 0.02 for squamous cell carcinoma). Intriguingly, a direct relationship was found between UBP43 and cyclin D1, validating clinical relevance. Thus, UBP43 knock-down appears to exert its anti-neoplastic effects by destabilizing cyclin D1. Taken together, these findings establish that the deconjugase UBP43 is a tractable target for lung cancer therapy and prevention. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1655. doi:10.1158/1538-7445.AM2011-1655

Cyclin D

Cyclin B

Cyclin E

ISG15

Cyclin E1

10.1158/1538-7445.am2011-1655

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Transplantation versus resection for hilar cholangiocarcinoma: an argument for shifting treatment paradigms for resectable disease

HPB (2017)

Cecilia G. Ethun Alexandra G. Lopez‐Aguiar Debra Anderson Andrew Adams Ryan C. Fields

10.1016/j.hpb.2017.02.015