THE LOCAL AND GLOBAL EXISTENCE OF THE SOLUTIONS OF HYPERBOLIC-PARABOLIC SYSTEM MODELING BIOLOGICAL PHENOMENA

The authors prove the local existence and uniqueness of weak solution of a hyperbolic-parabolic system and establish the global existence of the weak solution for this system for the spatial dimension n = 1.

Metabolomic studies of human gastric cancer:Review

Metabolomics is a field of study in systems biology that involves the identification and quantification of metabolites present in a biological system. Analyzing metabolic differences between unperturbed and perturbed networks, such as cancerous and noncancerous samples, can provide insight into underlying disease pathology, disease prognosis and diagnosis. Despite the large number of review articles concerning metabolomics and its application in cancer research, biomarker and drug discovery, these reviews do not focus on a specific type of cancer. Metabolomics may provide biomarkers useful for identification of early stage gastric cancer, potentially addressing an important clinical need. Here, we present a short review on metabolomics as a tool for biomarker discovery in human gastric cancer, with a primary focus on its use as a predictor of anticancer drug chemosensitivity, diagnosis, prognosis, and metastasis.

下调体外培养头颈部鳞状细胞癌细胞iASPP的表达能抑制细胞增殖、侵袭，增加对紫杉醇的化学敏感性（英文）

Objective Our previous study has revealed that iASPP is elevated in human head and neck squamous cell carcinoma(HNSCC)and iASPP overexpression signifcantly correlates with tumor malignant progression and poor survival of HNSCC.This study investigated the function of iASPP playing in proliferation and invasion of HNSCC in vitro.Methods HNSCC cell line Tu686 transfected with Lentiviral vector-mediated iASPP-specific shRNA and control shRNA were named the shRNA-iASPP group and shRNA-NC group,respectively.The non-infected Tu686 cells were named the CON group.CCK-8 assay,flow cytometry,transwell invasion assay were performed to detect the effects of iASPP inhibition in vitro.Results Our results demonstrated that the proliferation of shRNA-iASPP cells at the time of 72 h(F=32.459,P=0.000),96 h(F=51.407,P=0.000),120 h(F=35.125,P=0.000)post-transfection,was significantly lower than that of shRNANC cells and CON cells.The apoptosis ratio of shRNA-iASPP cells was 9.42%±0.39%(F=299.490,P=0.000),which was significantly higher than that of CON cells(2.80%±0.42%)and shRNA-NC cells(3.18%±0.28%).The percentage of shRNA-iASPP cells in G0/G1 phase was 74.65%±1.09%(F=388.901,P=0.000),which was strikingly increased,compared with that of CON cells(55.19%±1.02%)and shRNA-NC cells(54.62%±0.88%).The number of invading cells was 56±4 in the shRNA-iASPP group(F=84.965,P=0.000),which decreased significantly,compared with the CON group(111±3)and the shRNA-NC group(105±8).The survival rate of shRNA-iASPP cells administrated with paclitaxel was highly decreased,compared with CON cells and shRNA-NC cells(F=634.841,P=0.000).Conclusion These results suggest iASPP may play an important role in progression and aggressive behavior of HNSCC and may be an efficient chemotherapeutic target for the treatment of HNSCC.

Is there still a role for cytotoxic chemotherapy after targeted therapy and immunotherapy in metastatic melanoma? A case report and literature review

Metastatic melanoma has long been considered to have a very poor prognosis and to be chemo-resistant. However, a subgroup of patients with metastatic melanoma presents remarkable responses to chemotherapeutic agents, even in the absence of a response to modern targeted therapies and immunotherapies; accordingly, determining predictive biomarkers of the response to chemotherapies for metastatic melanoma remains a priority to guide treatment in these patients. We report a case study of a patient with B-Raf proto-oncogene serine/threonine kinase-mutated metastatic melanoma harbouring many genetic mutations. The patient did not respond to prior targeted therapies or immunotherapies but experienced a dramatic objective radiological and clinical response to subsequent dacarbazine-based chemotherapy. In the era of targeted therapies and immunotherapies for metastatic melanoma, cytotoxic chemotherapies may still represent an interesting therapeutic weapon in a well-deined subgroup of patients presenting with speciic genetic and molecular features.

Low hypoxia inducible factor-1α(HIF-1α)expression in testicular germ cell tumors--a major reason for enhanced chemosensitivity?

The molecular basis for enhanced chemosensitivity of testicular germ cell tumors （GCT） has been an area of great interest, as it could potentially give us therapeutic leads in other resistant malignancies. Thus far, however, the increased sensitivity of C＆T has been variously attributed to multiple factors -- an inability to detoxify cisplatin, a lack of export pumps, an inability to repair the DNA damage, an intact apoptotic cascade and lack of p53 mutation; but a unifying underlying etiology leading to the aforementioned processes and having a translational implication has so far been elusive. Herein, we offer evidence to support a potential significant role for the previously demonstrated low hypoxia inducible factor-la （HIF-la） expression in mediating the general exquisite chemosensitivity of testicular GCT, through the aforementioned processes. This molecular mechanism based hypothesis could have a significant translational implication in platinum refractory GCT as well as other platinum resistant malignancies.

Inhibition of Girdin enhances chemosensitivity of colorectal cancer cells to oxaliplatin

AIM: To investigate the effect of Girdin knockdown on the chemosensitivity of colorectal cancer cells to oxaliplatin and the possible mechanisms involved.METHODS: Four siRNAs targeting Girdin were transfected into the chemoresistant colorectal cancer cell line DLD1. Real-time polymerase chain reaction(PCR) was employed to assess Girdin mRNA expression and the most effective siRNA was chosen for conversion into shRNA. Then, DLD1 cells were infected with lentiviruses expressing the Girdin shRNA and a scramble control, respectively, and Girdin mRNA and protein expression levels were assessed by real-time PCR and Western blotting. Furthermore, microarray experiments were used to assess global gene expression profile after Girdin suppression in DLD1 cells. Finally, the cytotoxic effect of simultaneous treatment with oxaliplatin and adriamycin(an inhibitor of a significantly downregulated gene after Girdin suppression in DLD1 cells) was examined by MTT assay.RESULTS: The most effective siRNA suppressed Girdinexpression with an inhibition efficiency of 57%. Compared with the scramble control, DLD1 cells infected with the Girdin shRNA displayed decreased Girdin mRNA and protein levels(P < 0.05), and Girdin knockdown significantly enhanced chemosensitivity to oxaliplatin in colorectal cancer cells(P < 0.05). Microarray data revealed that 381 and 162 genes were upregulated and downregulated in response to Girdin reduction, respectively, with ratios > 1.2 or < 0.8(P < 0.01). Interestingly, TOP2B(DNA topoisomerase 2-β) was downregulated(ratio = 0.78, P = 0.0001) and oxaliplatin/adriamycin combination resulted in increased cell death compared with treatments with individual agents(P < 0.05).CONCLUSION: Girdin knockdown enhances chemosensitivity of colorectal cancer cells to oxaliplatin via TOP2B down-regulation. These findings provide a promising approach to overcome the chemoresistance of colorectal cancer cells.

VHH212 nanobody targeting the hypoxia-inducible factor 1α suppresses angiogenesis and potentiates gemcitabine therapy in pancreatic cancer in vivo

Objective:We aimed to develop a novel anti-HIF-1αintrabody to decrease gemcitabine resistance in pancreatic cancer patients.Methods:Surface plasmon resonance and glutathione S-transferase pull-down assays were conducted to identify the binding affinity and specificity of anti-HIF-1αVHH212[a single-domain antibody(nanobody)].Molecular dynamics simulation was used to determine the protein-protein interactions between hypoxia-inducible factor-1α(HIF-1α)and VHH212.The real-time polymerase chain reaction(PCR)and Western blot analyses were performed to identify the expressions of HIF-1αand VEGF-A in pancreatic ductal adenocarcinoma cell lines.The efficiency of the VHH212 nanobody in inhibiting the HIF-1 signaling pathway was measured using a dual-luciferase reporter assay.Finally,a PANC-1 xenograft model was developed to evaluate the anti-tumor efficiency of combined treatment.Immunohistochemistry analysis was conducted to detect the expressions of HIF-1αand VEGF-A in tumor tissues.Results:VHH212 was stably expressed in tumor cells with low cytotoxicity,high affinity,specific subcellular localization,and neutralization of HIF-1αin the cytoplasm or nucleus.The binding affinity between VHH212 and the HIF-1αPAS-B domain was 42.7 n M.Intrabody competitive inhibition of the HIF-1αheterodimer with an aryl hydrocarbon receptor nuclear translocator was used to inhibit the HIF-1/VEGF pathway in vitro.Compared with single agent gemcitabine,co-treatment with gemcitabine and a VHH212-encoding adenovirus significantly suppressed tumor growth in the xenograft model with 80.44%tumor inhibition.Conclusions:We developed an anti-HIF-1αnanobody and showed the function of VHH212 in a preclinical murine model of PANC-1 pancreatic cancer.The combination of VHH212 and gemcitabine significantly inhibited tumor development.These results suggested that combined use of anti-HIF-1αnanobodies with first-line treatment may in the future be an effective treatment for pancreatic cancer.

A study of the expression of p53 in posttransfection cells with rAdp53 gene and inhibitory activity in vitro

Objective： To investigate the inhibitory effect and IC50, （rAdp53） in colorectal cancer cells in vitro and to guide （50% inhibiting concentration） of the recombinant adenoviral p53 gene clinical practice. Methods： We evaluated the efficiency （IC50）of the rAdp53 and six kinds of anti-cancer drugs（5-fluorouracil, tegafur, mitomycin c, cisplatin, oxaliplatin, paclitaxel） in human colorectal cancer cell line-174 through the cell culture and MTT chemosensitivity assay to make sure the anti-cancer capability of rAdp53. Expression of p53 protein in transfection cells of colorectal cancer line-174 with rAdp53 was evaluated by immunohistochemical staining. Results： The rAdp53 is a dose-and time-dependent anti-cancer drug, its IC50 is 5.73×10^11 VP/ml, but its effect was not obvious when compared with other anti-cancer drugs. In control group, the immunohistochemistry stain was negative. However, rAd-p53 of five different concentrations were all positive in infected colorectal cancer cells with rAd-p53 and the earliest positive result would present 24 hours after infection. Conclusion： The rAdp53 has good anti-cancer efficacy is colorectal cancer cell line-174 in vitro. But its anti-cancer efficacy was less than those of the classical chemical medicine mitomycin c, 5-fluorouracil and cisplatin etc., when it was used alone.

Isolation and Characterization of Radiation-resistant Lung Cancer D6-R Cell Line

Objective To isolate an isogenic radioresistant cancer cell line after fractioned X-ray radiation and characterize the resistant cells. Methods D6 cells were exposed to repeated X-ray irradiation, and after a total dose of 5200 cGy in 8 fractions, a radioresistant monoclone D6-R was obtained. The radiosensitivity and drug sensitivity of the novel radioresistant D6-R cells, together with their parent D6 cells, were measured using clonogenic assay and MTT assay respectively. Cell cycle distribution was analyzed by flow cytometry. Fluorescence microscopy and flow cytometry were applied for apoptosis detection Comet assay was used for the detection of DNA damage and repair. Results D6-R cells showed higher and broader initial shoulder （D0=2.08 Gy, Dq=1.64 Gy, N=2.20） than the parent D6 cells （D0=1.84 Gy, Dq=0.34 Gy, N=1.20）. They were 1.65-fold more radioresistant than D6 cells in terms of SF2 （63% vs 38%） and were more resistant to ADM （3.15-fold） and 5-FU （3.86-fold） as compared with the latter. It was found that D6-R cells had higher fractions of cells in S phase （53.4% vs 37.8%） and lower fractions of cells in G1 （44.1% vs 57.2%） and G2-M phase （2.5% vs 5%）. There was no difference in radiation-induced apoptosis between D6-R and D6 cells. D6-R cells showed less initial DNA damage and increased capacity in DNA repair after irradiation, as compared with the parent cells. Conclusions D6-R cells have been isolated by exposing the parental D6 cells to repeated irradiation. The difference in cell cycle pattern together with the induction and repair of DNA damage might, at least partially, explain the mechanism of the radioresistance.

Drug resistance gene expression and chemotherapy sensitivity detection in Chinese women with different molecular subtypes of breast cancer

Objective:The aim of the study was to identify specific chemosensitivity drugs for various molecular subtypes of breast tumors in Chinese women,by detecting the expression of drug resistance genes and by using the drug sensitivity test on different molecular subtypes of breast cancers.Methods:The expression of drug resistance genes including Topo Ⅱ,GST-π,P-gp,LRP,and CD133 were detected with immunohistochemistry in a tissue microarray.Drug sensitivity tests included those for paclitaxel,epirubicin,carboplatin,vinorelbine,and fluorouracil and were conducted on primary cancer tissue cells and cell lines,including the T47 D,BT-474,and MDA-MB-231 cells and human breast cancer xenografts in nude mice.Results:The different drug resistant genes Topo Ⅱ,GST-π,P-gp,and LRP were differentially expressed among different molecular subtypes of breast cancers(P<0.05).Positive expression of CD133 was highest in basal-like breast cancer(P<0.05).Kaplan-Meier survival analysis showed that positive expressions of Topo Ⅱ and CD133 both correlated with shorter disease-free survival(DFS)(P<0.05)and overall survival(P<0.05),and positive expression of LRP correlated only with shorter DFS(P<0.05).BT-474 showed chemosensitivity to paclitaxel and epirubicin,while MDA-MB-231 showed chemosensitivities to paclitaxel,epirubicin,carboplatin,and fluorouracil(T/C≤50%).The basal-like and HER2+breast cancer primary cells showed chemosensitivities to paclitaxel and epirubicin with significant differences compared with luminal breast cancer primary cells(P<0.05).Conclusions:The differential expression of drug resistance genes and the differential chemosensitivities of drugs in different molecular subtype of breast cancers suggested that individual treatment should be given for each type of breast cancer.

MicroRNA-708 inhibits the proliferation and chemoresistance of pancreatic cancer cells

Pancreatic cancer is one of the most aggressive malignancies with poor prognosis and high mortality.Recent studies showed that microRNAs are dysregulated and involved in the initiation and progression of pancreatic cancer.In this study,we found that miR-708 was significantly downregulated in pancreatic cancer tissues and cell lines.Lentivirus-mediated overexpression of miR-708 could significantly inhibit the proliferation and invasion,while enhanced chemosensitivity to gemcitabine in both Panc-1 and SW1990 cells.Luciferase reporter assay showed that miR-708 bound the 3’-untranslated region of survivin and suppressed the expression of survivin in pancreatic cancer cells.In pancreatic cancer tissues,survivin protein was highly expressed and negatively correlated with miR-708 expression.Furthermore,the restoration of survivin expression could partially antagonize proliferation inhibition and apoptosis induction by miR-708 in pancreatic cancer cells.The Panc-1 cells with overexpression of miR-708 also showed decreased proliferation capability in nude mouse model compared with parental cells.In conclusion,our results suggest that miR-708 inhibits pancreatic cancer and could be a novel potential candidate to treat pancreatic cancer.

Sensitizing effects of aradio－ and chemo－sensitizer，metronidazol amino acidum natrium（CMNa）

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Differential expression of pancreatic protein and chemosensing receptor m RNAs in NKCC1-null intestine

AIM: To investigate the intestinal functions of the NKCC1 Na^+-K^+-2Cl cotransporter(SLC12a2 gene), differential m RNA expression changes in NKCC1-null intestine were analyzed.METHODS: Microarray analysis of m RNA from intestines of adult wild-type mice and gene-targeted NKCC1-null mice(n = 6 of each genotype) was performed to identify patterns of differential gene expression changes. Differential expression patterns were further examined by Gene Ontology analysis using the online Gorilla program, and expression changes of selected genes were verified using northern blot analysis and quantitative real time-polymerase chain reaction. Histological staining and immunofluorescence were performed to identify cell types in which upregulated pancreatic digestive enzymes were expressed.RESULTS: Genes typically associated with pancreatic function were upregulated. These included lipase, amylase, elastase, and serine proteases indicative of pancreatic exocrine function, as well as insulin and regenerating islet genes, representative of endocrine function. Northern blot analysis and immunohistochemistry showed that differential expression of exocrine pancreas m RNAs was specific to the duodenum and localized to a subset of goblet cells. In addition, a major pattern of changes involving differential expression of olfactory receptors that function in chemical sensing, as well as other chemosensing G-protein coupled receptors, was observed. These changes in chemosensory receptor expression may be related to the failure of intestinal function and dependency on parenteral nutrition observed in humans with SLC12a2 mutations. CONCLUSION: The results suggest that loss of NKCC1 affects not only secretion, but also goblet cell function and chemosensing of intestinal contents via G-protein coupled chemosensory receptors.

Increased leucine-rich repeats and immunoglobulin- like domains 1 expression enhances chemosensitivity in glioma

Leucine-rich repeats and immunoglobulin-like domains 1 （LRIG1） is an anti-oncogene. LRIG1 is correlated with Bcl-2 in ependymomas. Decreased Bcl-2 and manganese superoxide dismutase expression can improve the chemosensitivity of glioma. In the present study, a tissue microarray of human brain astrocytomas was constructed. To investigate the relationship of LRIG1 with Bcl-2 and manganese superoxide dismutase, LRIG1, Bcl-2 and manganese superoxide dismutase expression in our tissue microarray was determined using immunohistochemistry. In addition, we constructed the LRIG1-U251 cell line, and its responses to doxorubicin and temozolomide were detected using the MTT assay. Results showed that LRIG1 expression was significantly negatively correlated with Bcl-2 and manganese superoxide dismutase expression in glioma. Also, proliferation of LRIG1-U251 cells exposed to doxorubicin or temozolomide was significantly inhibited, i.e. in the LRIG1-U251 cell line, the chemosensitivity to doxorubicin and temozolomide was increased. This indicates that increased LRIG1 expression produces a chemosensitivity in glioma.

The Aryl Hydrocarbon Receptor: A Target for Breast Cancer Therapy

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that regulates a battery of genes in response to exposure to a broad class of environmental poly aromatic hydrocarbons (PAH). AhR is historically characterized for its role in mediating the toxicity and adaptive responses to these chemicals, however mounting evidence has established a role for it in ligand-independent physiological processes and pathological conditions, including cancer. The AhR is overexpressed and constitutively activated in advanced breast cancer cases and was shown to drive the progression of breast cancer. In this article we will review the current state of knowledge on the possible role of AhR in breast cancer and how it will be exploited in targeting AhR for breast cancer therapy.

Loss of heterozygosity for loci on chromosome arms 1p and 10q in oligoden-droglial tumors: relationship to outcome and chemosensitivity

Oligodendroglial tumors frequently have deletions ofchromosomal loci on lp and l9q.Loas of heterozygosity(LOH)of chromosome 10 may be a negative prognostic factor.We reviewed 23 patients with oligodendroglial tumors,toevaluate the frequency of lp and 10q LOH and correlate with clinical outcome.Three loci(DlS402,DlSl 172,MCT118)on lp and 2 loci(Dl0S520 and D10S521)on 10q were analyzed for LOH using PCR techniques.

Study on the influence of curcumin on chemosensitivity of nephroblastoma cells

Objective:To study the influence of curcumin on chemosensitivity of nephroblastoma cells.Methods:Human nephroblastoma cells line SK-NEP-1 was transplanted to the nude mice subcutaneously to establish the implantation tumor model of human nephroblastoma cells.A total of 30 tumor-bearing mice were divided into three groups of ten randomly.The routine chemotherapy group was given vincristine(0.05 mg/mL·0.2 mL/d) and actinomycin D(15 ng/mL·0.2 mL/d) combined chemotherapy regime.The curcumin chemotherapy group was given the same combined chemotherapy regimens and curcumin(30 mg/kg/d) by intraperitoneal injection.The control group was given normal saline(NS) of the same volume by intraperitoneal injection.Continuous administration would be kept for 4 weeks and 3 days a week.The volumetric changes of every group were recorded.The serum of every group in different time was collected and the VEGF content was detected by ELISA.All mice were cercrificed and the tumor tissues were stripped and weighed after 4 weeks’ treatment.The tumor inhibition rate was calculated.The cell proliferation activity and apoptosis rate were detected by MTT and flow cytometry method.All data were statistically analyzed by SPSS 19.0.Results:The tumor volume,serum VEGF content,tumor inhibition rate,cell proliferation activity and apoptosis rate of routine chemotherapy group and curcumin chemotherapy group had significant differences comparing with the control group(P<0.05) after 4-week’s treatment.The cancer growth of curcumin chemotherapy group was obviously decreased and even tended to shrink comparing with routine chemotherapy group(χ2=15.732,P=0.007).The cell proliferation activity was significantly reduced and the apoptosis rate was significantly higher,(χ~2=9.427,P=0.012)which showing the effect of chemotherapy was enhanced.Conclusions:The chemosensitivity of nephroblastoma cells could be improved by curcumin,then the effect of preoperative adjuvant chemotherapy scheme would be enhanced,the growth of nephroblastoma cells would be inhibited and the surgical risk of nephroblastoma would be reduced.

SOMATOSTATIN MAY ENHANCE CYTOTOXIC EFFECT OF DOXORUBICIN ON GALLBLADDER CANCER CELLS

Objective: To explore the change of chemosensitivity of gallbladder cancer cells pre-treated with somatostatin. Methods: Twenty-four hours after somatostatin treatment, gradient concentrated Doxorubicin was added and growth curve of gallbladder cancer cells was investigated to measure IC50, i.e., concentration of Doxorubicin at 50% cell viability. Results: Somatostatin ccould induce gallbladder cancer cell growth arrest in S phase. Inhibition of growth of cancer cell line was detected by Doxorubicin concentration- dependently (P<0.05). IC50 value was significantly lower by combined-treating with somatostatin and Doxorubicin compared with by Doxorubicin alone (P<0.05). Conclusion: Somatostatin could increase the cytotoxic effect of Doxorubicin on gallbladder cancer cell by modulating its cell cycle.

γ-生育三烯酚可能用做新型胃癌化疗增敏剂(英文)

Gamma-tocotrienol,a member of vitamin E superfamily has attracted great attention of late for its anti-proliferative and anti-carcinogenic potential against different cancers.For example,our group had previously reported that anti-proliferative and chemosensitizing effects ofγ-tocotrienol are associated with its ability to suppress activation of signal transducers and activator of transcription 3(STAT3),apro-inflammatory transcription factor that plays a pivotal role in the survival,proliferation,angiogenesis and chemoresistance of hepatocellular carcinoma.However,the potential of gamma-tocotrienol to overcome chemoresistance in gastric cancer,which is one of the deadliest cancers in Asia-pacific region,has never been explored before.Hence,we analyzed the efficacy of gamma-tocotrienol in combination with capecitabine to modulate tumor growth and survival in gastric cancer cell lines and xenograft mouse model.Cell proliferation and apoptosis assays indicated that gamma-tocotrienol potentiated capecitabine induced programmed cell death in various gastric cancer cell lines.Gamma-tocotrienol also inhibited expression of Bcl-2,Bcl-xL,cyclin-D1,COX-2,ICAM-1,VEGF,CXCR4,MMP-9 proteins,induced PARP cleavage and inhibited constitutive and capecitabine-induced NF-κB activation in gastric cancer cells.In vivo studies using xenograft model of human gastric cancer demonstrated that gamma-tocotrienol alone suppressed tumor growth and this effect was further potentiated in conjunction with capecitabine.Also the markers of proliferation index Ki-67 and the micro vessel density CD31 were significantly downregulated in tumor tissues by the combination of capecitabine and gamma-tocotrienol.As compared to the vehicle control,gamma-tocotrienol further suppressed the NF-κB activation and expression of cyclin D1,COX-2,ICAM-1,MMP-9 and survivin in tumor tissues obtained from treatment groups.Overall our results suggest for the first time that gamma-tocotrienol can potentiate the effects of capecitabine through modulation of multiple markers of proliferation,invasion,angiogenesis and metastasis in gastric cancer.

STUDY ON RELATIONSHIP BETWEEN CHEMOSENSITIVITY OFBREAST CANCER AND EXPRESSION OF p73α AND p53

Objective： To investigate the relationship between the expression of p73α and p53 versus the chemosensitivity in breast cancer cells. Methods： Twelve surgical samples of breast cancer diagnosed by pathology were used. The cancer sample cells were separately cultured in the incubator at 37℃, 5% CO2 in vitro. The relative inhibition rate of cancer cells by 4 kinds of anticancer drugs, which were EPI, MMC, 5-Fu and DDP, were assayed by MTT method. Immunocytochemistry was used to detect the expression of p73α and p53 in the cancer cells. Results： The positive expression of p73α was found in 5/12 （41.67%）, and p53 positive expression rate was 50.0% （6/12）. The relative inhibition rate of MMC, EPI, 5-Fu and DDP were significantly higher in the p73α positive cancer cells than in the p73α negative cancer cells. A positive correlation was found between expression of p73α and chemosensitivity for all the four anticancer drugs. Condusion： The expression of p73α is related with the chemosensitivity of the breast cancer cells, and it may become one of the markers for judging the effect of chemotherapy in clinic.