Andrew M. Lowy

UC San Diego Health System

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Co-Authors

Jay Patel

University of California, San Diego

121

Evangeline Mose

University of California, San Diego

120

Jonathan Weitz

University of California, San Diego

119

Tatiana Hurtado de Mendoza

University of California, San Diego

118

Siming Sun

University of California, San Diego

Hervé Tiriac

University of California, San Diego

Pablo Tamayo

University of California, San Diego

Michael Bouvet

University of California, San Diego

Timothy V. Pham

University of California, San Diego

Shweta Joshi

University of California, San Diego

Cooperative Institutions

University of California, San Diego

460

The University of Texas MD Anderson Cancer Center

144

Moores Cancer Center

136

UC San Diego Health System

115

University of Cincinnati

110

Harvard University

107

University of Cincinnati Medical Center

Johns Hopkins University

University of California, San Francisco

Sanford Burnham Prebys Medical Discovery Institute

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Supplementary Data from Syk inhibition reprograms tumor-associated macrophages and overcomes gemcitabine-induced immunosuppression in pancreatic ductal adenocarcinoma

Deepak Rohila In Hwan Park Timothy V. Pham Jonathan Weitz Tatiana Hurtado de Mendoza

Supplementary methods and Legends to supplementary figures

Immunosuppression

Pancreatic carcinoma

10.1158/0008-5472.27028201.v1

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Citations (0)

Pancreatic Adenocarcinoma, Version 2.2017, NCCN Clinical Practice Guidelines in Oncology

Journal of the National Comprehensive Cancer Network (2017)

Margaret A. Tempero Mokenge P. Malafa Mahmoud M. Al-Hawary Horacio J. Asbun Andrew Bain

Ductal adenocarcinoma and its variants account for most pancreatic malignancies. High-quality multiphase imaging can help to preoperatively distinguish between patients eligible for resection with curative intent and those with unresectable disease. Systemic therapy is used in the neoadjuvant or adjuvant pancreatic cancer setting, as well as in the management of locally advanced unresectable and metastatic disease. Clinical trials are critical for making progress in treatment of pancreatic cancer. The NCCN Guidelines for Pancreatic Adenocarcinoma focus on diagnosis and treatment with systemic therapy, radiation therapy, and surgical resection.

Systemic therapy

Neoadjuvant Therapy

10.6004/jnccn.2017.0131

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Citations (914)

SURGICAL MANAGEMENT OF HEREDITARY PANCREATIC CANCER

Medical Clinics of North America (2000)

Bradley R. Davis Andrew M. Lowy

10.1016/s0025-7125(05)70256-x

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Citations (16)

Data from Integrin α4β1 Signaling Is Required for Lymphangiogenesis and Tumor Metastasis

Barbara Garmy‐Susini Christie J. Avraamides Michael C. Schmid Philippe Foubert Lesley G. Ellies

<div>AbstractRecent studies have shown that lymphangiogenesis or the growth of lymphatic vessels at the periphery of tumors promotes tumor metastasis to lymph nodes. We show here that the fibronectin-binding integrin α4β1 and its ligand fibronectin are novel functional markers of proliferative lymphatic endothelium. Tumors and lymphangiogenic growth factors, such as vascular endothelial growth factor-C (VEGF-C) and VEGF-A, induce lymphatic vessel expression of integrin α4β1. Integrin α4β1 then promotes growth factor and tumor-induced lymphangiogenesis, as genetic loss of integrin α4β1 expression in Tie2Cre+ α4loxp/loxp mice or genetic loss of α4 signaling in α4Y991A knock-in mice blocks growth factor and tumor-induced lymphangiogenesis, as well as tumor metastasis to lymph nodes. In addition, antagonists of integrin α4β1 suppress lymphangiogenesis and tumor metastasis. Our studies show that integrin α4β1 and the signals it transduces regulate the adhesion, migration, invasion, and survival of proliferating lymphatic endothelial cells. As suppression of α4β1 expression, signal transduction, or function in tumor lymphatic endothelium not only inhibits tumor lymphangiogenesis but also prevents metastatic disease, these results show that integrin α4β1–mediated tumor lymphangiogenesis promotes metastasis and is a useful target for the suppression of metastatic disease. Cancer Res; 70(8); 3042–51. ©2010 AACR.</div>

Lymphangiogenesis

10.1158/0008-5472.c.6501734

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Data from KRas Induces a Src/PEAK1/ErbB2 Kinase Amplification Loop That Drives Metastatic Growth and Therapy Resistance in Pancreatic Cancer

Jonathan A. Kelber Theresa Reno Sharmeela Kaushal Cristina Metildi Tracy J. Wright

<div>AbstractEarly biomarkers and effective therapeutic strategies are desperately needed to treat pancreatic ductal adenocarcinoma (PDAC), which has a dismal 5-year patient survival rate. Here, we report that the novel tyrosine kinase PEAK1 is upregulated in human malignancies, including human PDACs and pancreatic intraepithelial neoplasia (PanIN). Oncogenic KRas induced a PEAK1-dependent kinase amplification loop between Src, PEAK1, and ErbB2 to drive PDAC tumor growth and metastasis in vivo. Surprisingly, blockade of ErbB2 expression increased Src-dependent PEAK1 expression, PEAK1-dependent Src activation, and tumor growth in vivo, suggesting a mechanism for the observed resistance of patients with PDACs to therapeutic intervention. Importantly, PEAK1 inactivation sensitized PDAC cells to trastuzumab and gemcitabine therapy. Our findings, therefore, suggest that PEAK1 is a novel biomarker, critical signaling hub, and new therapeutic target in PDACs. Cancer Res; 72(10); 2554–64. ©2012 AACR.</div>

10.1158/0008-5472.c.6503010

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Supplemental Figure 3 from Tumor Radiosensitization by Monomethyl Auristatin E: Mechanism of Action and Targeted Delivery

Lisa Buckel Elamprakash N. Savariar Jessica L. Crisp Karra A. Jones Angel M. Hicks

HCT-116 tumor xenografts have b3 integrin expression.

Mechanism of Action

10.1158/0008-5472.22407374

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Predictors of nonresection following neoadjuvant therapy for resectable PDAC: Analysis of SWOG S1505

HPB (2023)

Jordan M. Cloyd Sarah Colby Katherine A. Guthrie Andrew M. Lowy G. Chiorean

Neoadjuvant Therapy

Distal pancreatectomy

10.1016/j.hpb.2023.05.187

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Optimal Differentially Private Learning with Public Data

arXiv (Cornell University) (2023)

Andrew M. Lowy Zeman Li Tianjian Huang Meisam Razaviyayn

Differential privacy (DP) ensures that training a machine learning model does not leak private data. In practice, we may have access to auxiliary public data that is free of privacy concerns. In this work, we assume access to a given amount of public data and settle the following fundamental open questions: 1. What is the optimal (worst-case) error of a DP model trained over a private data set while having access to side public data? 2. How can we harness public data to improve DP model training in practice? We consider these questions in both the local and central models of pure and approximate DP. To answer the first question, we prove tight (up to log factors) lower and upper bounds that characterize the optimal error rates of three fundamental problems: mean estimation, empirical risk minimization, and stochastic convex optimization. We show that the optimal error rates can be attained (up to log factors) by either discarding private data and training a public model, or treating public data like it is private and using an optimal DP algorithm. To address the second question, we develop novel algorithms that are "even more optimal" (i.e. better constants) than the asymptotically optimal approaches described above. For local DP mean estimation, our algorithm is \ul{optimal including constants}. Empirically, our algorithms show benefits over the state-of-the-art.

10.48550/arxiv.2306.15056

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Supplementary Table 5 from Racial, Ethnic, and Sex-based Disparities among High-risk Individuals Undergoing Pancreatic Cancer Surveillance

Bryson W. Katona Kelsey Klute Randall E. Brand Jessica N. Everett James J. Farrell

Supplementary Table 5: Consent and biosample collection rates amongst HRIs stratified by age

Table (database)

10.1158/1940-6207.23274804.v1

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Supplementary Figure from An Ex Vivo Organotypic Culture Platform for Functional Interrogation of Human Appendiceal Cancer Reveals a Prominent and Heterogenous Immunological Landscape

Jonathan Weitz Tatiana Hurtado de Mendoza Hervé Tiriac James Lee Siming Sun

Supplementary Figure from An Ex Vivo Organotypic Culture Platform for Functional Interrogation of Human Appendiceal Cancer Reveals a Prominent and Heterogenous Immunological Landscape

Ex vivo

Interrogation

10.1158/1078-0432.22488890.v1

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