The Aurora kinase family of serine/threonine kinases plays an important role in chromosome alignment,segregation and cytokinesis during mitosis.Overexpression of Aurora kinases has been observed in a variety of human solid tumors and hematological malignancies.Aberrant expression of Aurora kinase can interrupt the function of the checkpoint in mitosis,lead to instability of genetic substance and induce tumorigenesis.

The acetylation status of histories regulates access of transcription factors to DNA and influences levels of gene expression.Histone deacetylase(HDAC)activity diminishes acctylation of histones,causing compaction of the DNA-histone complex.This compaction blocks gene transcription and inhibits cell differentiation.HDAC inhibitom decompact the DNA-histone complex and promote cell growth arrest,differentiation,and apoptosis of tumor cells.Meantime,HDAC inhibition also affects acetylation status and function of non-histone proteins.HDAC inhibitors not only possess significant anti-tumor effects with single use,but also has great significance in combined therapy with other drugs.

CD44 has been the subject of extensive research because of its role in cancer and many physiological processes.Through binding to different ligands,CD44 can initiate a series of cascade.CD44 not only can promote tumorigenic and tumor metastasis,but also can suppress tumor growth and progression.In-depth study of CD44 and its role in signal pathway may provide a new path for cancer treatment.

Cancer immunotherapy is a new approach to cancer treatment. Dendritic cells, the most potent antigen-presenting cells found in humans, have attracted a lot of researches. However, dendritic cells are insufficient to cross-present self-antigens in-vivo. To improve the dendritic cells' antigen-presenting capabilities and the anti-tumor effect, in vitro preparation of dendritic cell vaccine and combination with pro-apoptotic treatments such as chemotherapy are being used.

Autophagy is an evolutionarily conserved lysosomal pathway for the degradation of cytoplasmic proteins,macromolecules,and organelles.Now,autophagic cell death is considered as programmed cell death type Ⅱ.In multiple studies,inhibition of autophagy will result in contrasting outcomes-survival or death.Thus,whether autophagy in cancer cells causes death or protects cells is controversial.Taken together,the manipulation of autophagy may lead to development of new cancer therapies.This article focuses on recent progresses of autophagy research related to human cancers therapy.

Runt-related transcription factor 2 (Runx2) is a nuclear transcription factor of PEBP2/CBF superfamilies,and can regulate matrix metalloproteinase (MMP),osteopontin (OPN) and bone sialoprotein (BSP) which are associated with the metastasis of tumors including breast cancer and prostate cancer.In these cancers,the expression of Runx2 is highly up-regulated,which is closely correlated with the cell transformation and tumor progress.Lots of studies have demonstrated that the function of Runx2 is involved in several signal pathways activation,which can promote the early metastasis of malignant tumors.Therefore,the treatment targeting to Runx2 may be a new clinically choice to block the metastasis of tumors in the future.

Epithelial-mesenchymal transition cause primary carcinoma cells to acquire mesenchymal features and re-epithelialize to form a secondary mass at a metastatic site. Such plasticity has implications in the progression of breast carcinoma to metastasis, and will likely influence cancer's response to therapy. The transcriptional and epigenetic regulation that underlie the development of breast cancer and result in characteristic changes in cell behavior can be monitored using an array of marker proteins, providing the potential for emergent prognostic and therapeutic targeting.

Drug resistance in tumor treatment is an important factor that affects disease outcome.A lot of researches show that survivin can inhibit tumor cell apoptosis,regulate cell cycle,promote angiogenesis and tumor metastasis.The interactions among survivin,genes and proteins can influence the drug resistance of tumor cells.

Objective To investigate the clinicopathological characteristics and prognosis of lung metastases from breast cancer.Methods The clinical data of 119 breast cancer patients treated at our institution from January 2000 to January 2007 were retrospectively reviewed.Results Among 119 patients with lung metastasis,35.3％ was hormone receptor (HR) +/human epithelial growth factor receptor (HER2)-,17.6％ was HR +/HER2 +,21.8％ was HR-/HER2 + and 25.2％ was trriple negative breast cancer (TNBC).The rate of grade Ⅲ in triple negative breast cancer was higher than the other subtypes(P =0.016).The median overall survival was 60 months (9-141 months),the median time to lung metastases was 29 months (3-99 months),and the median survival after lung metastasis was 33 months (range,6-98 months).The 1-,2-,3-and 5-year survival rate was 72.9％,54.1％,35.1％ and 14.4％.Conclusions TNBC,number of lung metastases,time to lung metastases less than 24 months,and a history of systemic chemotherapy were important factors for prognosis of patients with lung metastases.

Objective To evaluate the effects of Met inhibitor XL-880 on radiosensitivity of breast cancer cells MDA-MB-231.Methods MDA-MB-231 cell lines were assigned to the following treatment groups:control group,radiation group,XL-880 group and combination group.Cell apoptosis,cell cycle distributions and tumorigenicity were investigated by flow cytometry or clonogenic assay.The expression of apoptosis and cell cycle related proteins (p21,Cyclin B1,Bcl-2,Caspase-3 and PARP),and phosphorylation levels of c-Met were measured by Western blot.Results XL-880 combined with radiation significantly decreased the proliferation activity of MDA-MB-231 cells (P ＜ 0.05).Flow cytometry results showed that the rate of G2/M cell were increased with XL-880 (P ＜ 0.05),and the rate were (17.3 ±1.3) ％,(20.0 ± 4.0) ％,(28.5 ± 3.1) ％,(57.0 ± 3.3) ％,respectively.Annexin V/PI double-staining assay showed that XL-880 obviously induced the apoptosis of MDA-MB-231 cells after radiation (P ＜ 0.05),of which the apoptotic rates were (7.3 ±0.9)％,(14.1 ±0.6)％,(35.5 ±4.4)％,(48.2±5.3)％,respectively.XL-880 downregulated the expressions of Cyclin B1 and anti-apoptosis protein Bcl-2,while promoted the expression of apoptosis related protein cleaved Caspase-3 and PARP.Conclusions XL-880 enhance the radiosensitivity of breast cancer cell MDA-MB-231 by inhibiting Met pathway.