BackgroundAccording to the very limited cancer registry, incidence and mortality rates for female breast cancer in China are regarded to be increasing especially in the metropolitan areas. Representative data on the breast cancer profile of Chinese women and its time trend over years are relatively rare. The aims of the current study are to illustrate the breast cancer profile of Chinese women in time span and to explore the current treatment approaches to female breast cancer.MethodsThis was a hospital-based nation-wide and multi-center retrospective study of female primary breast cancer cases. China was divided into 7 regions according to the geographic distribution; from each region, one tertiary hospital was selected. With the exception of January and February, one month was randomly selected to represent each year from year 1999 to 2008 at every hospital. All inpatient cases within the selected month were reviewed and related information was collected based on the designed case report form (CRF). The Cancer Hospital/Institute, Chinese Academy of Medical Sciences (CICAMS) was the leading hospital in this study.ResultsFour-thousand two-hundred and eleven cases were randomly selected from the total pool of 45,200 patients and were included in the analysis. The mean age at diagnosis was 48.7 years (s.d. = 10.5 yrs) and breast cancer peaked in age group 40-49 yrs (38.6%). The most common subtype was infiltrating ductal carcinoma (86.5%). Clinical stage I & II accounted for 60.6% of 4,211 patients. Three-thousand five-hundred and thirty-four cases had estrogen receptor (ER) and progestin receptor (PR) tests, among them, 47.9% were positive for both. Two-thousand eight-hundred and forty-nine cases had human epidermal growth factor receptor 2(HER-2) tests, 25.8% of them were HER-2 positive. Among all treatment options, surgery (96.9% (4,078/4,211)) was predominant, followed by chemotherapy (81.4% (3,428/4,211). Much less patients underwent radiotherapy (22.6% (952/4,211)) and endocrine therapy (38.0% (1,599/4,211)).ConclusionsThe younger age of breast cancer onset among Chinese women and more advanced tumor stages pose a great challenge. Adjuvant therapy, especially radiotherapy and endocrine therapy are of great unmet needs.

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([Ca 2ϩ ] i ) in cardiomyocytes and to have positive inotropic effects on the heart (1, 2). In addition to their importance in the acute regulation of cardiac function, their significance has increased further as the transcriptional pathways that lead to cardiac hypertrophy have been elucidated. Although initially compensatory, prolonged hypertrophy is often associated with decompensation, dilated cardiomyopathy, arrhythmia, fibrotic disease, and heart failure (3).The importance of agonists that activate PLC to cardiac hypertrophy is now well established (4). One well studied mouse model of cardiac hypertrophy involves the overexpression of a constitutively active form of a G protein subunit, G␣ q , which leads to chronic activation of PLC and the continuous production of IP 3 and diacylglycerol (5). In addition, overexpression in the heart of the PLC-activating angiotensin II (Ang II) type I receptor also leads to hypertrophy (6, 7). More clinically relevant, hypertrophied hearts induced by volume overload are commonly characterized by high levels of IP 3 -generating agonists such as Ang II (8).There are multiple signaling pathways downstream of PLC leading to cardiac hypertrophy. One involves diacylglycerol, protein kinase C, small guanine nucleotide-binding proteins (9), the MEK1-ERK1/2 branch of the mitogen-activated protein kinase pathway (10), and the transcription factor GATA4 (11, 12). Two others involve IP 3 and elevated levels of [Ca 2ϩ ] i . One of these is dependent on Ca 2ϩ /calmodulin-dependent calmodulin kinase and the transcription factor MEF2 (13), and the other is mediated by the Ca 2ϩ /calmodulin-activated protein phosphatase calcineurin and the transcription factor NFAT3 (14). The latter signaling pathway was first defined in lymphocytes (15) and is fundamental to an array of biological responses in a variety of cell types (16,17). A rise in [Ca 2ϩ ] i triggered by ligands generating IP 3 leads to the activation of the phosphatase activity of calcineurin, the dephosphorylation of NFAT family members, and their translocation to the nucleus to initiate transcription. Rapid export of NFAT from the nucleus when [Ca 2ϩ ] i levels drop prevents brief [Ca 2ϩ ] i pulses from initiating transcription of NFATdependent genes (15,16).A critical, unresolved issue for cardiac hypertrophy is the mechanism leading from IP 3 -mediated stimuli to elevated [Ca 2ϩ ] i . In most cell types, the initial increase in [Ca 2ϩ ] i in response to IP 3 -generating agonists is due to the release of Ca 2ϩ from the endoplasmic reticulum (ER

2؉ -sensitive nuclear translocation of a chimeric protein bearing the nuclear localization signal of a nuclear factor of activated T-cells transcription factor. The attenuation of CCE by hyperglycemia was prevented by azaserine, an inhibitor of hexosamine biosynthesis, and partially by inhibitors of oxidative stress. This complements previous work showing that increasing hexosamine metabolites in neonatal cardiomyocytes also inhibited CCE. The inhibition of CCE by hyperglycemia thus provides a likely explanation for the transition to diabetic cardiomyopathy as well as to the protection afforded to injury after ischemia/reperfusion in diabetic models. Diabetes