| pubmed-article:15020226 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15020226 | lifeskim:mentions | umls-concept:C0006142 | lld:lifeskim |
| pubmed-article:15020226 | lifeskim:mentions | umls-concept:C0032580 | lld:lifeskim |
| pubmed-article:15020226 | lifeskim:mentions | umls-concept:C1417490 | lld:lifeskim |
| pubmed-article:15020226 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:15020226 | pubmed:dateCreated | 2004-3-15 | lld:pubmed |
| pubmed-article:15020226 | pubmed:abstractText | The MUC1 tumor antigen is overexpressed on most breast tumors and metastases. It interacts with signaling proteins such as the ErbB kinases and beta-catenin, and is involved in mammary gland oncogenesis and tumor progression. Herein, we report a novel interaction between MUC1 and adenomatous polyposis coli (APC), a tumor suppressor involved in downregulating beta-catenin signaling. Initially identified in colorectal cancer, APC is also downregulated in breast tumors and presumably involved in mammary carcinogenesis. MUC1 and APC co-immunoprecipitate from the ZR-75-1 human breast carcinoma cell line and co-localize in mouse mammary glands and tumors. These studies also indicate that the association of MUC1 and APC may be increased by epidermal growth factor stimulation. Intriguingly, the co-immunoprecipitation of MUC1 and APC increases in human breast tumors and metastases as compared to adjacent normal tissues, indicating that this association may play a role in the formation and progression of breast tumors. | lld:pubmed |
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| pubmed-article:15020226 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15020226 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15020226 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15020226 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15020226 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:15020226 | pubmed:issn | 0006-291X | lld:pubmed |
| pubmed-article:15020226 | pubmed:author | pubmed-author:HanssonGunnar... | lld:pubmed |
| pubmed-article:15020226 | pubmed:author | pubmed-author:SchroederJoyc... | lld:pubmed |
| pubmed-article:15020226 | pubmed:author | pubmed-author:GendlerSandra... | lld:pubmed |
| pubmed-article:15020226 | pubmed:author | pubmed-author:Fernandez-Rod... | lld:pubmed |
| pubmed-article:15020226 | pubmed:author | pubmed-author:HattrupChrist... | lld:pubmed |
| pubmed-article:15020226 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15020226 | pubmed:day | 2 | lld:pubmed |
| pubmed-article:15020226 | pubmed:volume | 316 | lld:pubmed |
| pubmed-article:15020226 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15020226 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15020226 | pubmed:pagination | 364-9 | lld:pubmed |
| pubmed-article:15020226 | pubmed:dateRevised | 2011-9-22 | lld:pubmed |
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| pubmed-article:15020226 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15020226 | pubmed:articleTitle | MUC1 can interact with adenomatous polyposis coli in breast cancer. | lld:pubmed |
| pubmed-article:15020226 | pubmed:affiliation | Tumor Biology Program, Mayo Clinic College of Medicine, Mayo Clinic, Scottsdale, AZ, USA. | lld:pubmed |
| pubmed-article:15020226 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15020226 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15020226 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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