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HER2-enriched subtype and ERBB2 mRNA as predictors of pathological complete response following trastuzumab and lapatinib without chemotherapy in early-stage HER2-positive breast cancer: A combined analysis of TBCRC006/023 and PAMELA trials
- Source :
- Journal of Clinical Oncology. 36:509-509
- Publication Year :
- 2018
- Publisher :
- American Society of Clinical Oncology (ASCO), 2018.
-
Abstract
- 509Background: HER2-Enriched (HER2-E) intrinsic subtype within HER2-positive breast cancer is characterized by high expression of ERBB2 and related genes. Here we retrospectively evaluated the value of the HER2-E subtype and ERBB2 mRNA expression alone to predict pathological complete response (pCR) in tumor samples from PAMELA and TBCRC 006/023 trials. Methods: All patients had HER2-positive early breast cancer and were treated with neoadjuvant lapatinib and trastuzumab. Patients with hormone receptor-positive tumors were also treated with letrozole or tamoxifen. In PAMELA (NCT01973660), 151 patients were treated for 18 weeks. TBCRC 006 (NCT00548184) treated 66 patients for 12 weeks and TBCRC 023 (NCT00999804) randomized 97 patients to 12 vs. 24 weeks of treatment. pCR was defined as no residual invasive carcinoma in the breast. Baseline intrinsic subtypes and ERBB2 mRNA expression were determined using the nCounter-based PAM50 predictor. ERBB2 expression was dichotomized as low (lowest 1/3) vs high (hig...
- Subjects :
- 0301 basic medicine
Oncology
Cancer Research
medicine.medical_specialty
medicine.medical_treatment
Lapatinib
03 medical and health sciences
0302 clinical medicine
Breast cancer
Trastuzumab
Internal medicine
medicine
Stage (cooking)
skin and connective tissue diseases
neoplasms
Pathological
Chemotherapy
business.industry
Letrozole
medicine.disease
030104 developmental biology
030220 oncology & carcinogenesis
business
Tamoxifen
medicine.drug
Subjects
Details
- ISSN :
- 15277755 and 0732183X
- Volume :
- 36
- Database :
- OpenAIRE
- Journal :
- Journal of Clinical Oncology
- Accession number :
- edsair.doi...........0f6097449f90cc4628c9c8f8714fdc31