Title |
Silencing of HSulf-2 expression in MCF10DCIS.com cells attenuate ductal carcinoma in situ progression to invasive ductal carcinoma in vivo
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Published in |
Breast Cancer Research, March 2012
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DOI | 10.1186/bcr3140 |
Pubmed ID | |
Authors |
Ashwani Khurana, Hiedi McKean, Hyunseok Kim, Sung-Hoon Kim, Jacie Mcguire, Lewis R Roberts, Matthew P Goetz, Viji Shridhar |
Abstract |
Ductal carcinoma in situ (DCIS) of the breast is a heterogeneous group of proliferative cellular lesions that have the potential to become invasive. Very little is known about the molecular alterations involved in the progression from DCIS to invasive ductal carcinoma (IDC). Heparan endosulfatase (HSulf-2) edits sulfate moieties on heparan sulfate proteoglycans (HSPGs) and has been implicated in modulating heparin binding growth factor signaling, angiogenesis and tumorigenesis. However, the role of HSulf-2 in breast cancer progression is poorly understood. MCF10DCIS.com cells (referred as MCF10DCIS) express HSulf-2 and form comedo type DCIS and progress to IDC when transplanted in immune-deficient mice and, therefore, is an ideal model to study breast cancer progression. We evaluated the role of HSulf-2 in progression from DCIS to IDC using mouse fat pad mammary xenografts. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
---|---|---|
Australia | 1 | 5% |
Unknown | 19 | 95% |
Demographic breakdown
Readers by professional status | Count | As % |
---|---|---|
Student > Ph. D. Student | 10 | 50% |
Researcher | 3 | 15% |
Other | 2 | 10% |
Student > Master | 1 | 5% |
Student > Doctoral Student | 1 | 5% |
Other | 0 | 0% |
Unknown | 3 | 15% |
Readers by discipline | Count | As % |
---|---|---|
Agricultural and Biological Sciences | 7 | 35% |
Biochemistry, Genetics and Molecular Biology | 3 | 15% |
Medicine and Dentistry | 3 | 15% |
Chemistry | 2 | 10% |
Engineering | 2 | 10% |
Other | 0 | 0% |
Unknown | 3 | 15% |