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Reasons for Hope: Canadian Breast Cancer Research Conference, Le Concorde Hotel, Quebec City, Quebec, Canada, 3–5 May 2001

DOI: 10.1186/bcr331

Keywords: breast cancer, epigenetics, genetics, microenvironment

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Abstract:

The Canadian Breast Cancer Research Initiative (CBCRI) sponsored its second 'Reasons For Hope' Conference, 3–5 May 2001, in Quebec City. This gathering brought together researchers, clinicians, healthcare providers and advocates to present and discuss some of the latest findings in breast cancer research, diagnosis and treatment. The multidisciplinary objective of the meeting's organizers was clearly illustrated by the initial reports from the CBCRI's recently instituted 'Streams of Excellence' program, which has brought together teams of researchers from across Canada to tackle large scale projects in a thorough and comprehensive manner. For example, Tim Whelan (McMaster University, Hamilton, Ontario, Canada) and Irene Andrulis (Lunenfeld Institute, Toronto, Ontario, Canada) outlined their group's conceptual framework for accelerating the discovery of clinically relevant molecular changes in breast cancer and rapidly translating these findings into novel treatment paradigms. Michael Pollak (Jewish General Hospital, Montreal, Quebec, Canada) and his group are taking a similar approach as it specifically relates to insulin-like growth factors in breast cancer development and progression. Both of these programs, and other CBCRI-funded ventures, have strong basic research components. The following is a sampling of the basic research highlights from this meeting.In a plenary session entitled 'Genetic Approaches to Understanding the Conversion of Normal to Malignant Cells', Phil Leder (Harvard Medical School, Boston, MA, USA) and Mina Bissell (Berkeley National Laboratory, Berkeley, CA, USA) presented data and persuasive arguments for the importance of genetic and epigenetic change, respectively, in breast tumorigenesis. Leder's laboratory pioneered the use of transgenic mice to identify the functional consequences of combinatorial oncogene overexpression in the mammary gland. This group has more recently used single oncogenes as genetic 'initiators' followed by mouse ma

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