AACR 101st Annual Meeting 2010: Plenary Sessions

Chairperson: Frank McCormick, UCSF Helen Diller Family Comprehensive Cancer Center, San Francisco, CA

Overcoming drug resistance: Lessons from prostate cancer
Charles L. Sawyers, Memorial Sloan-Kettering Cancer Center, New York, NY

• Androgen receptor (AR) transcriptional activity is crucial for the growth and survival of both hormone-sensitive and castration-resistant prostate cancer. Sawyers and colleagues show that AR transcriptional activity is blocked by histone deacetylase inhibitors in castration-resistant prostate cancer models, suggesting their use in the treatment of this lethal stage of the disease. View a summary of their recent research and a free link to their relevant article in Cancer Research.

The Breast International Group (BIG): Building on an accelerated path to tailored adjuvant cancer therapy
Martine J. Piccart-Gebhart, Institut Jules Bordet, Brussels, Belgium

• Piccart-Gebhart and colleagues define modules based on gene expression data and use these modules to predict clinical outcome in the main breast cancer molecular subtypes. View a summary of their recent research and a free link to their relevant article in Clinical Cancer Research.

Targeting the PI3K pathway in the therapy of breast cancer
José Baselga, Vall d'Hebron University Hospital, Barcelona, Spain

• Genetic alterations of the PI3K pathway are frequently present in human cancers. Baselga and colleagues report that NVP-BEZ235, a next-generation dual inhibitor of PI3K and the downstream mammalian target of rapamycin, shows anti-proliferative and anti-tumor activity in cancer cells containing both wild-type PI3K and the commonly mutated form p110α. View a summary of their recent research and a free link to their relevant article in Clinical Cancer Research.

Synthetic lethal approaches to the development of new therapeutic approaches to cancer
Alan Ashworth, Institute of Cancer Research, London, United Kingdom

Chairperson: Arul M. Chinnaiyan, University of Michigan, Ann Arbor, MI

Introduction and overview: The impact of genomics on cancer - The time has come
Arul M. Chinnaiyan

The sequence of all 185,000 coding exons in each of 100 human tumors: What has it taught us?
Bert Vogelstein, Johns Hopkins University, Baltimore, MD

• Vogelstein and colleagues describe a computational method to identify and prioritize missense mutations most likely to generate functional changes that enhance tumor cell proliferation. View a summary of their recent research and a free link to their relevant article in Cancer Research.

Patient and research perspectives for molecular profiling in breast cancer
Laura J. van't Veer, UCSF Helen Diller Family Comprehensive Cancer Center, San Francisco, CA

• van ’t Veer and colleagues report that PIK3CA mutations can be used as a biomarker for increased risk for local recurrence as well as a determinant to minimize overtreatment in those patients with low risk of recurrence. View a summary of their recent research and a free link to their relevant article in Clinical Cancer Research.

From cancer genomics to personalized oncology
Levi A. Garraway, Dana-Farber Cancer Institute, Boston, MA

Genome-wide association studies in cancer: What have we found and what's next?
Stephen J. Chanock, National Cancer Institute, Bethesda, MD

Chairperson: Joan S. Brugge, Harvard Medical School, Boston, MA

Introduction and overview
Joan S. Brugge

Mechanisms that control tumor cell anchorage
Joan S. Brugge

• Brugge and colleagues identify ribosomal S6 kinase as a critical component of FGFR1 signaling in lobular carcinoma and potential therapeutic target in FGFR1-expressing tumors. View a summary of their recent research and a free link to their relevant article in Cancer Research.

Some cancers follow a stem cell model, while other cancers have common tumorigenic cells with little hierarchical organization
Sean J. Morrison, University of Michigan, Ann Arbor, MI

Inflammation and cancer: Repolarizing the immune microenvironment as a therapeutic anticancer strategy
Lisa M. Coussens, UCSF Helen Diller Family Comprehensive Cancer Center, San Francisco, CA

Cancer complexity: Insights from genetic network analysis of tumor susceptibility
Allan Balmain, UCSF Helen Diller Family Comprehensive Cancer Center, San Francisco, CA

Chairperson: Danny R. Welch, University of Alabama, Birmingham, AL

Introduction and overview: Metastasis, genetics, epigenetics, and microenvironmental influences
Danny R. Welch

Microenvironments of carcinoma cell dissemination and metastasis: Insights derived in vivo
John S. Condeelis, Albert Einstein College of Medicine, Bronx, NY

• In recent studies, Condeelis and colleagues report that human breast tumor cell invasion in an animal model depends on colony-stimulating factor-1 ligand and its receptor in both an autocrine signaling loop with only tumor cells as well as paracrine signaling with macrophages. In part based on these data, the authors then introduce a tumor microenvironment of metastasis (TMEM), defined by the presence of invasive carcinoma cell, macrophage, and endothelial cell, and show that TMEM density in human breast tissue samples can predict the development of distant metastases. View a summary of Dr. Condeelis' recent research and free links to his relevant articles in AACR journals.

Experimental studies of tumor metastasis and clinical implications
Ann F. Chambers, London Regional Cancer Center, London, ON, Canada

• Chambers and colleagues report on a magnetic resonance imaging technique that quantifies the majority of the metastatic cell population, including both growing metastases and solitary cells. View a summary of their recent research and a free link to their relevant article in Cancer Research.

Clinical trials of metastasis inhibitors: How will they work?
George W. Sledge, Indiana University Cancer Center, Indianapolis, IN

The EMT stem cells and metastatic progression
Robert A. Weinberg, MIT Whitehead Institute for Biomedical Research, Cambridge, MA

• Weinberg and colleagues show that loss of E-cadherin does not enable metastasis via its role in cell-cell adhesion as generally thought. Rather, loss of E-cadherin promotes metastasis through the induction of multiple transcription factors and resulting functional changes. View a summary of their recent research and a free link to their relevant article in Cancer Research.