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Ding Ma

Publications and source records attributed to Ding Ma.

At least 37 records · Page 2Linked to original sources
PubMed2006

[Expression of Ezrin and E-cadherin in invasive ductal breast cancer and their correlations to lymphatic metastasis].

BACKGROUND & OBJECTIVE: Ezrin, a cytoskeleton linker protein, is actively involved in regulating the growth and metastasis of cancer cells. This study was performed to detect the expression of Ezrin and E-cadherin in primary invasive ductal breast cancer in order to evaluate their possible roles in lymphatic metastasis. METHODS: The expression of Ezrin and E-cadherin in 60 specimens of primary invasive ductal breast cancer (23 with metastasis, 37 without metastasis) was detected by SP immunohistochemistry. RESULTS: The abnormal expression rates of Ezrin and E-cadherin were significantly higher in the cases with metastasis than in the cases without metastasis (73.91% vs. 51.35%, P=0.039; 65.22% vs. 40.54%, P<0.001). The abnormal expression of Ezrin was positively correlated to that of E-cadherin (r=0.898, P=0.038). CONCLUSION: Ezrin and E-cadherin are closely related to invasion and metastasis of ductal breast cancer, suggesting that they are important tumor markers in predicting lymphatic metastasis of invasive ductal breast cancer.

Adult↗
PubMed2006

[Expression and clinical significance of Pin1 and Cyclin D1 in cervical cancer cell lines and cervical epithelial tissues].

BACKGROUND & OBJECTIVE: Peptidyl-prolyl cis/trans isomerase Pin1 is prevalently overexpressed in human cancers. Up-regulation of Pin1 elevates the expression of Cyclin D1, and plays an important role in tumorigenesis and tumor progression. This study was to investigate the expression and clinical significance of Pin1 and Cyclin D1 in cervical cancer cell lines and cervical epithelial tissues. METHODS: The expression of Pin1 and Cyclin D1 in cervical cancer cell lines HeLa, SiHa, C33a and Caski were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Their expression in 88 samples of cervical tissues, including 10 samples of normal cervix, 21 samples of cervical intraepithelial neoplasia (CIN), and 57 samples of invasive cervical cancer, were detected by immunohistochemistry. RESULTS: The mRNA and protein levels of Pin1 were significantly higher in HeLa, SiHa, C33a, and Caski cells than in normal cervical epithelial tissues (P<0.05). The expression of Pin1 increased progressively along with the disease process from normal cervix to CIN, and to invasive cervical cancer (0%, 47.62%, 64.91%, P<0.05). Pin1 expression had no relation to disease stage (FIGO), pathologic grade, and pelvic lymph node metastasis status (P>0.05). The positive rate of Pin1 was significantly higher in cervical adenocarcinoma than in cervical squamous cell carcinoma (100% vs. 60.0%, P<0.05). In cervical cancer tissues, the overexpression of Pin1 was positively correlated to that of Cyclin D1 (P<0.05). CONCLUSIONS: Pin1 is overexpressed in HeLa, SiHa, C33a and Caski cell lines as well as in cervical cancer tissues. The overexpression of Pin1 is closely related to Cyclin D1 expression in cervical cancer. The aberrant expression of Pin1 and Cyclin D1 might contribute to tumorigenesis of cervical cancer.

Adenocarcinoma↗
PubMed2006

The effect of RhoA on human umbilical vein endothelial cell migration and angiogenesis in vitro.

The mechanisms that control the morphologic organization of endothelial cells (ECs) into new blood vessels are not well understood. Recent studies revealed that the small G proteins of the Rho family are key regulators of cell migration, involving reorganization of the actin cytoskeleton, cell migration and the regulation of gene transcription. We hypothesized that RhoA GTPase, a member of the Rho family, may play an important role in EC organization during angiogenesis, the process of new vessel formation in pre-existing tissues. To test this hypothesis, we investigated the effects of RhoA on human umbilical vein endothelial (HUVE) cell migration and angiogenesis in vitro, by stably transfecting HUVE cells with sense RhoA expression plasmid through the Lipofect-2000 system. Wound assay in vitro and 3-dimensional cell culture were used to detect the migration and angiogenesis capacity of HUVE cells. The morphological changes of transfected cells were revealed under confocal and phase contrast microscopy. Our results demonstrated that the increased expression of RhoA in HUVE cells significantly enhanced the morphogenetic changes and cytoskeletal reorganization of the transfected cells, and also enhanced cell migration and angiogenic capacity in vitro, suggesting that RhoA plays an important role in the process of HUVE cell migration and angiogenesis in vitro.

Actins↗
PubMed2006

[Inhibitory effects of tetraethylammonium on proliferation and voltage-gated potassium channels in human cervical carcinoma cell line SiHa].

BACKGROUND & OBJECTIVE: Various potassium channels are known to be involved in proliferation of many malignant cell lines. This study was to explore the role of voltage-gated potassium channels in proliferation of human cervical carcinoma cells through observing the effects of tetraethylammonium (TEA) on proliferation and outward potassium currents in human cervical carcinoma cell line SiHa. METHODS: SiHa cells were treated with TEA. The effect of TEA on proliferation of SiHa cells was assessed by MTT assay. Cell apoptosis and cell cycle were detected by flow cytometry with Hoechst 33258 staining. The outward potassium currents were recorded by patch clamp technique. RESULTS: TEA inhibited the proliferation of SiHa cells in dose-and time-dependent manners, and induced cell apoptosis. The cell cycle was arrested at G0/G1 phase after treatment with TEA. Exposure of SiHa cells to 10 mmol/L TEA reduced the peak outward potassium currents significantly from (260+/-12) pA to (58+/-6) pA (P<0.01). CONCLUSIONS: Voltage-gated potassium channels play an important role in regulating proliferation of cervical carcinoma SiHa cells. Blocking voltage-gated potassium channels could inhibit proliferation of SiHa cells.

Apoptosis↗
PubMed2006

[Inverse correlation between Snail and E-cadherin expression in carcinoma cell lines and invasive ability in vitro].

OBJECTIVE: Malignant transformation of epithelial cell frequently coincides with loss of E-cadherin. Here we study the expression of Snail and E-cadherin and correlate their expression with cell differentiation and in vitro invasion. METHODS: The expression and localization of Snail and E-cadherin were studied by Northern blot and laser confocal microscopy in two normal cell lines (MDCK, NIH 3T3) and six carcinoma cell lines (A431, MCF-7, MDA-MB-453, HepG2, MDA-MB-435s, MDA-MB-231). Boyden chamber assay was done to detect the invasive ability of cells in vitro. RESULTS: Snail mRNA and protein were detected in fibroblasts NIH 3T3 and poorly differentiated carcinoma cell lines HepG2, MDA-MB-435s and MDA-MB-231. On the contrary, E-cadherin mRNA and protein were detected in normal epithelial cell line MDCK and well differentiated carcinoma cell lines A431 and MDA-MB-453. In MCF-7 cells, Snail and E-cadherin expressions were revealed both at mRNA and protein levels. The cells with higher expression of Snail had stronger ability of invasion than those with lower expression of Snail. CONCLUSION: There is an inverse correlation between Snail and E-cadherin expressions and their expressions are correlated with cell differentiation and tumor invasiveness.

3T3 Cells↗
PubMed2006

[Short hairpin RNA silences Pin1 and affects proliferation and apoptosis in HeLa cell line].

OBJECTIVE: To study the effect of short hairpin RNA (shRNA) on the expression of Pin1 mRNA and protein and its influence on the proliferation and apoptosis in HeLa cell lines. METHODS: The recombinant plasmid pSIREN-Pin1 expressing Pin1-targeted shRNA was constructed and then transfected into cervical cancer cell lines by lipofectamine (HeLa/p-shRNA), the control vector pSIREN-Con (HeLa/p-Con) and culture media (HeLa) as control, respectively. The Pin1 mRNA and protein expression were detected by RT-PCR and immunoblotting. The proliferation of cells after transfection was detected by methyl thiazolyl tetrazolium (MTT) and colony formation in soft agar. Flow cytometry (FCM) was used to test the apoptosis of cells marked with fluorescein isothiocyanate (FITC)-annexin V. RESULTS: After transfected with pSIREN-Pin1 for 48 h, the expression of Pin1 mRNA and protein in HeLa cells were 0.19 +/- 0.05 and 0.33 +/- 0.14 respectively. Compared with HeLa/p-Con cells (0.84 +/- 0.16, 0.79 +/- 0.17) and HeLa cells (0.89 +/- 0.11, 0.81 +/- 0.15), the difference was significant respectively (P < 0.05). The proliferation was suppressed significantly in HeLa/p-shRNA cells. The colony ratios are as follows: HeLa/p-shRNA, (12 +/- 3)%; HeLa/p-Con, (20 +/- 5)%; HeLa, (24 +/- 4)% (P < 0.05). The apoptosis ratio was (24.3 +/- 5.7)% in HeLa/p-shRNA cells. It was significantly higher than that in HeLa/p-Con cells (5.0 +/- 1.4)% and HeLa cells (1.8 +/- 0.4)% (P < 0.05). CONCLUSIONS: RNA interference through Pin1-targeted shRNA can effectively inhibit the expression of target gene, and might be potentially useful in gene therapy of Pin1 related cervical cancers. Silencing Pin1 gene can suppress the proliferation and promote the apoptosis in HeLa cells.

Apoptosis↗
PubMed2006

Pin1 contributes to cervical tumorigenesis by regulating cyclin D1 expression.

The prolyl isomerase Pin1, which specifically catalyzes conformational changes in certain proline-directed phosphorylation sites, is thought to be a critical catalyst for multiple oncogenic pathways. However, little is known about the role of Pin1 in human cervical cancer. Our previous study showed that Pin1 was overexpressed in cervical cancer tissues as well as cell lines. In this study, whether Pin1 is involved in cervical oncogenesis by regulating cyclin D1 was explored and the potential of Pin1-targeted gene silencing in inhibiting cellular growth and tumorigenicity in cervical cancer was investigated. A Pin1-directed shRNA and a sense Pin1 plasmid were constructed, and then the effects of the shRNA and the sense plasmid on HeLa cells were evaluated. The results showed that Pin1 directly regulated cyclin D1 levels. In addition, silencing Pin1 with RNAi significantly reduced cancer cell proliferation, colony formation, and strongly enhanced the apoptosis of HeLa cells. It is suggested that Pin1 may contribute to cervical tumorigenesis by regulating cyclin D1 expression and Pin1 may serve as a promising molecular target for diagnostics and therapeutics in cervical cancer.

Apoptosis↗
PubMed2006

Regulation of DNA methylation on the expression of the FHIT gene contributes to cervical carcinoma cell tumorigenesis.

The purpose of this study was to determine the effect of the FHIT gene on tumorigenesis of cervical cancer. RT-PCR and MTT were used to detect the expression of FHIT and cell proliferation respectively. Flow cytometry was used to test cell cycle and cell apoptosis. The expression of FHIT was not induced at all four cervical cancer cells treated with demethylating agent 5-aza-2'-deoxycytidine (5-Aza-CdR). However, a constant level of FHIT expression was detected in the human umbilical vein endothelial cell before and after 5-aza-dC treatment. The proliferation of all four cervical cancer cells was inhibited evidently when treated with 5-aza-dC and the inhibiting rate of cell growth along with the increasing concentration of 5-aza-dC. There was no obvious inhibiting effect on the growth of the human umbilical vein endothelial cell treated with 5-aza-dC. An increasing G1 phase and high apoptosis rate were detected in all four cervical cancer cells. However, a negligible change was seen in the human umbilical vein endothelial cell. These results suggest that aberrant methylation of the FHIT gene might be a key mechanism for silenced FHIT gene, which could be reactivated and whose tumor suppressing function could be restored by demethylating agent treatment.

Acid Anhydride Hydrolases↗
PubMed2006

[Relationship between VEGF-C expression and nasopharyngeal carcinoma proliferation and metastasis].

OBJECTIVE: To detect the expression of VEGF-C in nasopharyngeal carcinoma (NPC) and explore its relationship with proliferation and metastasis of NPC. METHODS: Biopsy specimens of 62 NPC patients were divided into 2 equal portions, one for immunohistochemical staining with VEGF-C polyclonal antibody by streptavidin peroxidase method, another for flow cytometry with Ki67 antibody to analyze the proliferation of tumors. The patients were followed up periodically, and then their 3-year survival and the cause of death were statistically analyzed. RESULTS: Of the 62 patients, the percentage of VEGF-C positive cells in the tumors ranged from 0 - 82%, 17 (27.4%) were negative, 13 (21.0%) weak positive, 18 (29.0%) moderate positive and 14 (22.6%) strong positive. Ki67 positive tumor cells ranged from 0 - 52%, 40 cases (64.5%) showed low expression which include 15 cases of negative, 22 (35.5%) showed high expression. There was a direct relationship between the expression of VEGF-C and Ki67 (r = 0.323, P < 0.05). The 3-year survival rate of 62 patients was 66.1%. The expression of VEGF-C in the patients with positive lymph node was much higher than that with negative lymph node (P < 0.01). Among the 8 patients with distant metastasis, their VEGF-C expression was strong positive while among the 21 disease free survival patients, their VEGF-C expression was (-) or (+) account for 80.9%. An inverse correlation was found between the VEGF-C expression and prognosis of NPC patients, but the difference has no statistical significance (r = -0.219, P > 0.05). CONCLUSION: High expression of VEGF-C is related with proliferation and metastasis of NPC cells. It is not an independent prognostic factor, but a predictive marker of disease-free survival of NPC patients.

Adult↗
PubMed2005

Location, acid strength, and mobility of the acidic protons in Keggin 12-H3PW12O40: a combined solid-state NMR spectroscopy and DFT quantum chemical calculation study.

Solid-state 13C NMR experiments and quantum chemical Density Functional Theory (DFT) calculations of acetone adsorption were used to study the location of protons in anhydrous 12-tungstophosphoric acid (HPW), the mobility of the isolated and hydrated acidic protons, and the acid strength heterogeneity of the anhydrous hydroxyl groups. This study presents the first direct NMR experimental evidence that there are two types of isolated protons with different acid strengths in the anhydrous Keggin HPW. Rotational Echo DOuble Resonance (REDOR) NMR experiments combined with quantum chemical DFT calculations demonstrated that acidic protons in anhydrous HPW are localized on both bridging (Oc) and terminal (Od) atoms of the Keggin unit. The CP/MAS NMR experiments revealed that the isolated acidic protons are immobile, but hydrated acidic protons are highly mobile at room temperature. The isotropic chemical shift of the adsorbed acetone suggested that the acid strength of the H(H2O)n+ species in partially hydrated HPW is comparable to that of a zeolite, while the acidity of an isolated proton is much stronger than that of a zeolite. Isolated protons on the bridging oxygen atoms of anhydrous HPW are nearly superacidic.

Journal Article↗
PubMed2005

Novel oncolytic adenovirus selectively targets tumor-associated polo-like kinase 1 and tumor cell viability.

PURPOSE: Polo-like kinase 1 (plk1) is a serine/threonine protein kinase essential for multiple mitotic processes. Previous observations have validated plk1 as a promising therapeutic target. Despite being conceptually attractive, the potency and specificity of current plk1-based therapies remain limited. We sought to develop a novel plk1-targeting strategy by constructing an oncolytic adenovirus to selectively silence plk1 in tumor cells. EXPERIMENTAL DESIGN: Two artificial features were engineered into one wild-type adenovirus type 5 (wt-Adv5) genome to generate a new oncolytic adenovirus (M1). First, M1 contains a 27-bp deletion in E1A region, which confers potent, oncolytic efficacy. Second, M1 is armed with a fragment of antisense plk1 cDNA that substitutes the E3 region encoding 6.7K and gp19K. In this design, tumor-selective replication of M1 would activate the native adenovirus E3 promoters to express the antisense plk1 cDNA preferentially in tumor cells and silence tumor-associated plk1 protein. RESULTS: By virtue of combining oncolysis with plk1 targeting, M1 exhibited potent antitumoral efficacy in vitro and in vivo. Systemic administration of M1 plus cisplatin induced complete tumor regression in 80% of orthotopic hepatic carcinoma model mice that were otherwise resistant to cisplatin and disseminated metastases. CONCLUSIONS: Coupling plk1 targeting with oncolysis had shown superior antitumor efficacy. Present findings would benefit the development of novel oncolytic adenoviruses generally applicable to a wide range of molecule-based therapeutics.

Adenoviridae↗
PubMed2005

Effects of human papillomavirus type 16 E7 protein on the growth of cervical carcinoma cells and immuno-escape through the TGF-beta1 signaling pathway.

OBJECTIVE: E7 is regarded as one of the main oncoproteins of high-risk human papillomaviruses (HPVs). It may affect the transforming growth factor beta 1 (TGF-beta1) signaling pathway. In this study, the relationship between HPV-16 infection and the functions of three critical factors of the TGF-beta1/Smads pathway was explored to assess the possible role of E7 in the development of cervical cancer. METHODS: The expression of E7, TGF-beta1, TbetaR-II and Smad4 was detected by immunohistochemistry in paraffin-embedded cervical samples, and by RT-PCR and Western blotting in cervical cancer cell lines. The effect of TGF-beta1 on the growth of cervical cancer cells were tested by methyl thiazolyl tetrazolium (MTT), and the effects of HPV-16 E7 protein on normal and malignant cervical cells were investigated by flow cytometry. RESULTS: During the progression from benign to malignant lesions, the expression levels of TGF-beta1 and Smad4 increased significantly in cervical carcinoma tissues. The expression of TGF-beta1 was positively correlated with E7 expression. In vitro experiments showed that TGF-beta1 could not inhibit the proliferation of several cervical carcinoma cell lines in long-term regulation, but could inhibit immunologic reactions of peripheral blood mononuclear cells (PBMCs). Blocking E7 expression could lower the expression level of TGF-beta1 and induce cells to enter apoptosis. CONCLUSIONS: Our data indicate that HPV-16 E7 protein plays an important role during the development of cervical cancer by immuno-inhibition and stimulation of tumor cell proliferation through the TGF-beta1/Smads signaling pathway.

Cell Growth Processes↗
PubMed2005

Reversing chemoresistance in cisplatin-resistant human ovarian cancer cells: a role of c-Jun NH2-terminal kinase 1.

To investigate the role of activation of c-Jun NH2-terminal kinase 1 (JNK1) in mediating cisplatin-induced apoptosis and the possibility of induction of JNK activity in triggering relation to DNA damage and drug resistance. We investigated the difference of cisplatin-induced activation of JNK pathway and H2O2 alteration between cisplatin-sensitive human ovarian carcinoma cell line A2780 and its resistant variant A2780/DDP. JNK, p-JNK protein, and extracellular H2O2 levels were determined in both A2780 and A2780/DDP cells which were transfected with dominant negative allele of JNK and recombinant JNK1 separately. Both A2780 and A2780/DDP were treated with CDDP, the JNK pathway was activated and a prolonged JNK activation was maintained for at least 12 h in A2780, and only a transient activation (3 h) was detected in A2780/DDP in response to cisplatin treatment. Inhibition of JNK activity by transfection with a dominant negative allele of JNK blocked CDDP-induced apoptosis significantly in A2780 cells. Selective stimulation of the JNK pathway by lipofectamine-mediated delivery of recombinant JNK1 led to activation of c-Jun and decrease of extracellular H2O2, as well as apoptosis sensitization to CDDP in A2780/DDP cells. We concluded that JNK pathway might play an important role in mediating cisplatin-induced apoptosis in A2780 cells, and the duration of JNK activation might be critical in determining whether cells survive or undergo apoptosis. The resistance to CDDP can be reversed through activating c-Jun and decreasing extracellular generation of H2O2 by pcDNA3(FLAG)-JNK1-wt transfection in A2780/DDP cells.

Antineoplastic Agents↗
PubMed2005

A comparison of four screening methods for cervical neoplasia.

OBJECTIVE: To evaluate the sensitivity and accuracy of 4 screening methods for cervical neoplasia. METHODS: Cervical samples from 450 women were evaluated for human papillomavirus DNA with a second-generation hybridization assay. Visual inspection, colposcopy, and liquid-based cytology were also performed for 273 of these women. The sensitivity, specificity, efficiency, positive predictive value (PPV), negative predictive value (NPV), Youden index, and kappa value of the different screening methods were compared. RESULTS: Liquid-based cytology was superior in specificity (98.63%) and PPV (92.86%) to visual inspection and colposcopy, while human papillomavirus DNA testing was superior in sensitivity (88.89%) and NPV (97.10%) to visual inspection and colposcopy. The best concordance with histologic findings was achieved by using both liquid-based cytology and viral DNA hybridization. CONCLUSION: Visual inspection and colposcopy should not be used when screening for early stage cervical lesions. The DNA hybridization assay is the best choice in primary screening, if available. Screening should begin at the age of 20 years.

Adult↗
PubMed2005

Role of hTERT in apoptosis of cervical cancer induced by histone deacetylase inhibitor.

Human telomerase reverse transcriptase (hTERT) is the catalytic subunit of telomerase holoenzyme as well as the rate-limiting component of the telomerase enzyme complex. However, the role of the hTERT in apoptosis induced by histone deacetylase inhibitor has only been marginally addressed. For the first time, our study demonstrated that trichostatin A (TSA) briefly activated the proliferation of cervical cancer cell lines, HeLa and SiHa, within 12 h, but then inhibited cell growth after that time point. In response to TSA, hTERT expression, telomerase activity, and telomere length also underwent similar changes during the same time frame. Furthermore, the data in our study showed that cells transfected with dominant negative hTERT were more likely to undergo apoptosis induced by TSA than cells transfected with wild-type hTERT. The cyclin/cdk inhibitor p21waf1 was down-regulated by hTERT without changing the expression of p53. Results from this study suggest that the hTERT might be a primary target of TSA and the anti-apoptosis effect of hTERT might be carried out through a p21waf1-dependent and p53-independent pathway.

Apoptosis↗
PubMed2005

[A multicenter randomized clinical trial of weekly paclitaxel and carboplatin vs three weeks paclitaxel and carboplatin as first line chemotherapy in epithelial ovarian cancer].

OBJECTIVE: To compare the efficacy of combination regiments of taxol given weekly plus carboplatin and taxol given every three weeks plus carboplatin. To observe the toxicity of the two regiments. To observe the two-year survival rate in the two groups. METHODS: Total 125 eligible patients in 13 centers of CGOG were entered into the two arms of this randomized clinical trial, of whom 51 were entered into weekly taxol group and 74 entered into 3 weeks taxol group. RESULTS: 81.6% (102/125) of patients had satisfactory decreasing of CA125 level after optimal cytoreductive surgery and chemotherapy. 86.3% (44/51) of patients is in weekly group and 78.4% (58/74) of patients in three weeks group (P > 0.05). Relapse frequency is 29.7% in every three weeks group and 19.6% in weekly group (P > 0.05). Median interval to relapse is 15.7 months in every three weeks group and 13.6 months in weekly group (P > 0.05). One-year survival rate is 95.2% in every three weeks and 93.9% in weekly group (P > 0.05). Two-year survival rate is 78.7% in every three weeks and 85.3% in weekly group (P > 0.05). Grade III and IV myelosuooression is 45.9% in three weeks group and, 27.5% in weekly group (P < 0.05). CONCLUSION: (1) The two regiments had equal efficacy. (2) Myelosuppression was less frequency in the weekly group than in every three weeks group. (3) Weekly taxol therapy has mild toxicity and is more suitable for the old and feeble patients. Weekly taxol therapy can be conveniently administered in outpatients department.

Adult↗
PubMed2005

[Clinical effects of combination chemotherapy with irinotecan hydrochloride and cisplatin on cervical cancer: study of 46 patients].

OBJECTIVE: To evaluate the efficacy and toxicity of the combination chemotherapy of irinotecan hydrochloride plus cisplatin on cervical cancer. METHODS: Forty-six patients with cervical cancer, 43 with squamous cell carcinoma, 2 adenocarcinoma, and 1 small cell carcinoma, 41 being treated initially and 5 being recurrent cases of which 2 had undergone radiotherapy plus chemotherapy, 2 radical hysterectomy plus pelvic radiotherapy after operation, and 1 radical hysterectomy plus chemotherapy, aged 38 (22-61), were treated with irinotecan hydrochloride, 60 mg/m(2) in 250 ml normal saline administered on days 1, 8, and 15 by intravenous infusion over 60 min, plus cisplatin, 60 mg/m(2) in 500 ml 5% glucose given on day 1. This regimen was repeated every 28 days. Effectiveness evaluation was conducted after 1-2 courses for the initially treated patients and after 2-6 courses for the recurrent patients. RESULTS: Totally 79 courses of treatment were given to the 41 patients. After 1-2 courses 4 (9.8%) of the 41 stage Ib2-IIIb initially treated patients achieved complete remission, 30 (73.2%) achieved partial remission, and 7 (17.1%) remained at stationary phase with a overall effective rate of 82.9%. Of the 29 IIb and IIIb stage advanced patients who failed to receive operation originally 20 patients (69%) succeeded to be treated by radical hysterectomy after 1 to 2 courses when the tumorless space between the uterine and the pelvic wall > or = 3 cm with an operatibility rate of 69%. Of the 5 recurrent patients 1 case achieved complete remission, 2 partial remission, and 2 remained stable; none progression of disease was observed after 4-6 courses. The main toxic response and side effect included myelosuppression and diarrhea. CONCLUSION: Effective neoadjuvant chemotherapy on cervical cancer, combination therapy of irinotecan hydrochloride and cisplatin win opportunity for treatment and improves their life quality with tolerable side effects.

Adenocarcinoma↗