In conclusion, these findings substantiate the notion that breast cancer progression is often associated with alterations in expressions of ER, PgR, and HER-2/neu.
Subsequent stratified analyses also revealed that associations between BC risk and rs217727 genotypes were more profound in patients with estrogen receptor-positive, human epidermal growth factor receptor 2 (HER2)-negative, and hormone receptor-positive-HER2-negative molecular subtypes (all passed the threshold for Bonferroni correction, <i>P</i><0.005).
The majority of patients had T1 (52%), N0 (61%) grade 2 (58%) ER positive (87%), HER2 negative (84%) breast cancer and were PM at diagnosis of breast cancer (93%).
The aim of this case-control based prospective study was to determine the distribution of HER-2 genotype and its association with risk factors of breast cancer in the population of women in Slovak republic.
CONCLUSION These analyses suggest that the HER2 valine allele might be associated with increased risk of breast cancer, especially in young women and in women with a family history of the disease.
A significantly increased breast cancer risk was associated with the Proline allele [odds ratio 1.84 (95 % CI: 1.22-2.77), risk ratio 1.34 (95 % CI: 1.11-1.63), p value 0.003], HER2/neu status (p = 0.01) and distant metastasis (p = 0.05).
In addition, CA, CA/AA genotype, and A allele of rs3761548 were related to larger tumor size, and the A allele was also correlated with a positive status of Her-2 in BC patients.
We examined the expression of β III-tubulin, thymidylate synthase, breast cancer susceptibility gene 1 and ribonucleotide reductase M1 (RRM1); identified mutations in epidermal growth factor receptor (EGFR), KRAS, BRAF and HER2; and detected ALK, ROS1 and RET rearrangements.
ER expression in normal terminal duct lobular epithelium of postmenopausal women with breast cancer was significantly associated with estrogen and triple (estrogen, progesterone receptors, and HER2) negative phenotypes.
Overall, implementing the revised 2018 HER2 guidelines is predicted to change the HER2 results of 10.7% of breast cancers, mainly by reclassifying previously equivocal to negative results.
Replication in larger studies using estrogen receptor (ER)-negative or triple-negative (i.e., ER-, progesterone receptor-, and HER2-negative) cases could therefore be helpful to confirm the association of this locus with breast cancer risk.
This study shows that the HER2 codon 655 G-allele was associated with a larger reduction in plasma HDL-C levels in breast cancer patients under tamoxifen therapy.
We conclude that array comparative genomic hybridization is an accurate and objective DNA-based alternative for clinical evaluation of HER2 gene copy number, and that polysomy 17 is a rare event in breast cancer.
In the current study, we explored the use of quantitative real time reverse transcription-PCR (RT-qPCR) as a potential method for the accurate relative quantification of the HER2 gene using formalin fixed paraffin embedded (FFPE) breast cancer biopsy samples.
Breast cancers in BRCA mutation carriers were more likely to be hormone receptor negative, diagnosed at 35 years or before and multiple during the lifetime than tumors in women at increased familial risk, while the distribution of invasive cancers and HER2 positive tumors was similar in the different risk groups.
In this review, we summarize the current knowledge of lapatinib and pose questions which need to be addressed as we further expand our knowledge of the HER-2 subtypes of breast cancer.
In conclusion, using G129R-based fusion proteins to target mammary carcinomas and to tackle multiple hallmarks of cancer at the same time was an effective strategy for treating HER2-postive mammary cancer in this mouse tumor model.
In vitro experiments provided functional evidence to suggest that BRF2 and DSN1 overexpression/amplification, and the HER2I767M mutation may be alterations that compensate for the lack of HER2 amplification in the HER2-negative components of HER2 heterogeneous breast cancers.