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Old 05-18-2014, 02:18 PM   #1
'lizbeth
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Post Regulation of C-terminal and N-terminal fragments of HER2 by mRNA.

Regulation of C-terminal and N-terminal fragments of HER2 by mRNA.



Abstract No:
e11593
Publication-only abstracts (abstract number preceded by an "e"), published in conjunction with the 2014 ASCO Annual Meeting but not presented at the Meeting, can be found online only.

Author(s): Daishu Miura, Masami Kadowaki, Nobuko Tamura, Hidetaka Kawabata, Takeshi Fujii; Toranomon Hospital, Tokyo, Japan; Department of Breast and Endocrine Surgery, Toranomon Hospital, Tokyo, Japan; Tokyo Medical and Dental University, Tokyo, Japan; Department of Pathology, Toranomon Hospital, Tokyo, Japan
Abstract Disclosures

Abstract:

Background: A subgroup of HER2-positive breast cancers express a series of C-terminal fragments of HER2 (H2CT) collectively known as HER2 CTFs or p95HER2. H2CT cancers have worse prognosis and are resistant to the treatment with trastuzumab. While the existence of a novel N-terminal fragment of HER2 (H2NTF), characterized to be devoid of the tyrosine kinase domain but it readily interacts with full-length HER2 (H2FL) and other HER families was recently described. H2NT is frequently expressed in breast cancer samples and acts as a dominant negative, attenuating the signaling triggered by full-length HER receptors. We wish to determine whether H2FL, H2CT, and H2NT are regulated by the transcription of mRNA using clinical samples and also determine the clinical characterizations of these cancers. Methods: Among early breast cancers with HER2 over-expressed who received neo-adjuvant chemotherapy (FEC/EC followed by weekly paclitaxel and trastuzumab), 20 samples of pre-treatment biopsy specimen available were selected (10 ER+ve. and 10 ER–ve. samples). We performed in situ hybridization of mRNA using the QuantiGene viewRNA (Affymetrix) that has unique probe designing and branched DNA to amplify the signal to detect mRNA in FFPE tissue samples. We used 2 kinds of probes for human erbb2 (NM_004448). Targeted sequence of one probe is from 1nt to 2068nt (NTF, red) and another is from 2069nt to the end (CTF, blue). We used these probes to identify the truncated region of HER2 and defined H2NT as having red dominant, H2CT as having blue dominant, and H2FL as almost similar number of red and blue signals. Results: Among 20 cases, pathological CR (pCR) was found in 6 and distant recurrence in 3 cases. Both red (N-terminal) and blue (C-terminal) were found in all 20 samples. Twelve samples were in H2FL, 4 in H2NT, and 4 in H2CT. All 4 in H2CT were ER negative and 3 out of 4 had pCR. Two out of 3 who had distant recurrence were in H2NT. Conclusions: We found the short fragments of HER2 mRNA in HER2 over-expressed breast cancer samples by in situ hybridization and also one of the possibilities that different subtype of H2CT and H2NT from H2FL were generated by mRNA transcription. As similar results of previous description, none of the H2CT was ER positive.
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