B-cell lymphoma 2 (BCL2) family is the most important regulator of apoptosis, and -938C>A single nucleotide polymorphism (SNP) of <i>BCL2</i> gene promoter has been demonstrated to influence breast cancer susceptibility.
To gain insight into the molecular mechanisms involved in human prolactin receptor antagonist (hPRL-G129R)-induced apoptosis, we used real-time reverse transcription-polymerase chain reaction to measure bax and bcl-2 gene expression in 11 human breast cancer cell lines following treatment with hPRL and hPRL-G129R.
The topics include (i) repair mechanisms of heavy ion-induced DNA damage, (ii) superior effects of heavy ions on radioresistant tumor cells (intratumor quiescent cell population, TP53-mutated and BCL2-overexpressing tumors), (iii) novel capacity of heavy ions in suppressing cancer metastasis and neoangiogenesis, and (iv) potential of heavy ions to induce secondary (especially breast) cancer.
In conclusion, our study suggests a role of genetic variation in BIRC5, BCL2 and CLU as progression and prognostic markers for BC, supporting previous studies based on the expression of the genes.
Angiopoietin-2, an angiogenic regulator, promotes initial growth and survival of breast cancer metastases to the lung through the integrin-linked kinase (ILK)-AKT-B cell lymphoma 2 (Bcl-2) pathway.
Tea phytoconstituents are known to modulate myriad molecular events which include prominent regulators of intracellular signaling, such as phosphatidylinositide 3-kinase/protein kinase B/nuclear factor-κB, epidermal growth factor receptor, vascular endothelial growth factor, B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein in the development and progression of breast carcinoma.
More recently, Bcl-2 has been recognized as an important prognostic factor in breast cancer, although controversies persist with respect to the significance of its expression.
Borrelidin has limited anti-cancer effects in bcl-2 overexpressing breast cancer and leukemia cells and reveals toxicity in non-malignant breast epithelial cells.
There was significant co-expression of TFF3 with AKT1 (p = 0.0365), BCl2 (p = 0.0152), and NF Kappa-B (p = 0.0243) in breast carcinoma cases with residual carcinoma following neoadjuvant therapy which support the role of TFF3 in chemoresistance.
Breast cancer in women aged less than 35 years also had higher histologic grade and higher frequency of bcl-2-negative tumor than that found in the 36- to 50-year age group.
The reduction of Bak may play important roles in malignant development of breast cancer to acquire estrogen independency, counteracting the reduced Bcl-2.
Because anti-apoptotic BCL-2 family proteins can affect the threshold for induction of apoptosis and thus limit the effectiveness of the chemotherapeutic payload, we examined whether inhibition of BCL-2/X<sub>L</sub> would enhance the efficacy of T-DM1 in five HER2-expressing patient-derived breast cancer xenograft models.
The study results indicate that Bcl-2 and S-phase analysis of fine-needle samples of breast carcinomas provide a convenient tool for the assessment of these tumors.
This study focuses on the effect of nicotine on the expressions of the α7 nicotinic receptor gene and Bax and Bcl-2 proteins in mammary gland epithelial-7 (MCF-7) breast cancer cells and its relationship to drug resistance.
Bcl-2, c-Myc and c-Jun does not only take part in cell death, but also in cell division in breast carcinoma cells in which the regulation of cell division and cell death are strictly connected.