Breast cancer in 30-year-old or younger patients: clinicopathologic characteristics and prognosis.

BACKGROUND: The number of 30-year-old or younger patients with breast cancer is increasing. The aim was to describe the clinicopathological features and prognosis of 30-year-old or younger patients with breast cancer. METHODS: We reviewed the records of 1,406 consecutive patients aged ≤50 years with first diagnosis of invasive breast cancer referred to surgery from March 2001 to March 2009. A total of 105 patients were aged ≤30 years (group I) and 1,301 were aged 31-50 years (group II). RESULTS: Compared with patients of group II, patients of group I had a higher percentage of tumors classified as estrogen receptors (ER) negative (P < 0.001) and progesterone receptors (PR) negative (P = 0.043), with a Ki-67 labeling index ≥20% of the cells (P = 0.011). There was no difference between the two groups for pT and pN, histology, endocrine therapy, and chemotherapy. The 5-year survival of group I was 67.5% as compared with 75.3% for group II (P = 0.003). CONCLUSIONS: Compared with patients aged between 31 and 50 years, patients aged ≤30 years have a greater chance of having an endocrine-unresponsive tumor and a significantly poor prognosis.

A study on the biological function of heat shock factor 1 proteins in breast cancer.

The present study aimed to investigate the effect of HSF1 proteins on cell proliferation, apoptosis and invasion of breast cancer. The Michigan Cancer Foundation-7 (MCF-7) HSF1-knocked down stable cell line (experimental group) and control cell line (control group) were obtained using a lentivirus assay, and the effects of HSF1 knockdown on the proliferation, tumor formation, apoptosis and invasion ability were analyzed, respectively. The effects of HSF1 on downstream signals were analyzed using western blotting. Western blotting results showed that lentivirus successfully established a HSF1 knockdown stable cell line of MCF-7. Compared with the control group, the growth rate of MCF-7 cells in the experimental group was significantly decreased (P<0.05). Flow cytometry showed that the proportion of apoptosis in the control group was significantly lower than that of the experimental group (P<0.05). Notably, the invasion ability of cells in the control group was significantly higher than that in the experimental group (P<0.05). Compared with cells in the control group, the levels of heat shock protein (HSP)70, HSP90, anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and macrophage migration inhibitory factor (MIF) in the experimental group were significantly downregulated, whereas the level of Bax was significantly increased (P<0.05). In conclusion, HSF1 protein, as a transcription factor, regulates the expression levels of HSP70, HSP90, MIF, Bcl-2 and Bax, thus controlling the proliferation, apoptosis and invasion of cells. These findings suggest HSF1 protein as a potential target for the treatment of breast cancer.

A study on the biological function of heat shock factor 1 proteins in breast cancer.

The present study aimed to investigate the effect of HSF1 proteins on cell proliferation, apoptosis and invasion of breast cancer. The Michigan Cancer Foundation-7 (MCF-7) HSF1-knocked down stable cell line (experimental group) and control cell line (control group) were obtained using a lentivirus assay, and the effects of HSF1 knockdown on the proliferation, tumor formation, apoptosis and invasion ability were analyzed, respectively. The effects of HSF1 on downstream signals were analyzed using western blotting. Western blotting results showed that lentivirus successfully established a HSF1 knockdown stable cell line of MCF-7. Compared with the control group, the growth rate of MCF-7 cells in the experimental group was significantly decreased (P<0.05). Flow cytometry showed that the proportion of apoptosis in the control group was significantly lower than that of the experimental group (P<0.05). Notably, the invasion ability of cells in the control group was significantly higher than that in the experimental group (P<0.05). Compared with cells in the control group, the levels of heat shock protein (HSP)70, HSP90, anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and macrophage migration inhibitory factor (MIF) in the experimental group were significantly downregulated, whereas the level of Bax was significantly increased (P<0.05). In conclusion, HSF1 protein, as a transcription factor, regulates the expression levels of HSP70, HSP90, MIF, Bcl-2 and Bax, thus controlling the proliferation, apoptosis and invasion of cells. These findings suggest HSF1 protein as a potential target for the treatment of breast cancer.