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Tumor dormancy is not only a biologic character in malignant tumor cells but also the key cause of failure to the treatment, metastasis, and recurrence of tumors. In this article, the evidence of tumor dormancy in patients, the evolution of the definition of tumor dormancy, the establishment of the animal mode of tumor dormancy, and the molecular mechanism of tumor dormancy were reviewed. Recent progress on novel antitumor drugs through inducing tumor dormancy was summarized.

Background & Objective: Recently, studies showed nm23, E-cadherin, and Catenins play important roles in cellular signal transduction, which enhance complexity of their functions in tumor metastasis and can partly explain the diversity of the results from different studies. This study was to investigate correlations of expressions of nm23, E-cadherin, and beta-Catenin in non-small cell lung cancer (NSCLC) to metastasis and prognosis, and their interrelations., Methods: Expressions of nm23, E-cadherin, and beta-Catenin in 112 specimens of NSCLC and 30 specimens of benign pulmonary lesion were detected by SP immunohistochemistry., Results: The expressions of nm23, E-cadherin and beta-Catenin were significantly weaker in NSCLC tissues than in adjacent non-cancerous tissues, and benign pulmonary tissues (53.0% vs. 64.8%, and 76.9%, P < 0.01; 53.1% vs. 79.7%, and 83.5%, P < 0.01; and 47.2% vs. 80.6%, and 85.6%, P < 0.01), significantly weaker in NSCLC tissues with lymph node metastasis than in those without metastasis (48.0% vs. 65.0%, P < 0.01; 47.3% vs. 60.5%, P < 0.01; and 41.8% vs. 60.3%, P < 0.01), and significantly weaker in NSCLC tissues of stage III-IV than in those of stage I-II (44.8% vs. 67.2%, P < 0.01; 46.6% vs. 64.3%, P < 0.01; 38.1% vs. 63.1%, P < 0.01). The 5-year survival rates of patients with weak expressions of nm23, E-cadherin, and beta-Catenin were significantly lower than those of patients with strong expressions (3.6% vs. 39.3%, P < 0.01; 6.8% vs. 35.8%, P < 0.01; and 3.8% vs. 37.3%, P < 0.01)., Conclusions: Down-regulations of nm23, E-cadherin, and beta-catenin closely relate to metastasis of NSCLC. Detection of nm23, E-cadherin, and beta-Catenin might be helpful to predict prognosis of NSCLC patients.

Background & Objective: nm23-H1, a tumor metastasis suppressive gene, can reverse tumor metastasis phenotype. But the molecular mechanism of nm23-H1 in inhibiting or reversing metastasis of lung cancer is unclear. This study was to explore the molecular mechanism of nm23-H1 in reversing metastasis phenotype of lung cancer., Methods: nm23-H1 gene and pLXSN were separately transfected into human lung cancer cell line L9981. Proliferation of L9981, L9981-pLXSN, and L9981-nm23-H1 cells was detected by MTT assay, cell invasive ability was detected by modified Boyden chamber. Tumorigenesis and experimental lung metastasis were determined in vivo. mRNA and protein levels of beta-catenin, E-Cadherin, CD44S, CD44V6, matrix metalloproteinase-2 (MMP-2), tissue inhibitor of metalloproteinase-1 (TIMP-1), and vascular endothelial growth factor (VEGF) were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot., Results: (1)Cell proliferation, clone formation, and invasive ability were significantly lower in L9981-nm23-H1 cells than in L9981 cells [(19.5+/-2.9)% vs. 100%, 10.3+/-0.7 vs. 21.7+/-1.3, 31.0+/-3.0 vs. 151.0+/-6.3, P<0.01]. (2) The inhibitory rate of tumorigenesis of nude mice was significantly higher in L8891-nm23-H1 group than in L9981 group (85.6% vs. 0%, P<0.001)u the lung metastatic rate was significantly lower in L9981-nm23-H1 group than in L9981 group (0% vs. 100%, P<0.001). (3)nm23-H1 up-regulated mRNA and protein levels of beta-catenin, E-Cadherin, and TIMP-1, and down-regulated levels of MMP-2, CD44V6, and VEGF (P<0.01). (4) nm23-H1 up-regulated mRNA level of CD44s, protein level of CD44s didn't change (P>0.05)., Conclusion: nm23-H1 gene can reverse malignant and metastatic phenotype of L9981 cells through regulating the expressions of lung cancer metastasis-related genes.

Background & Objective: H101 is an E1B-55 kDa gene-deleted replication-selective adenovirus, which showed a significant antitumor activity. This study was to compare effects and toxicities of intratumoral H101 injection combined with cisplatin plus 5-fluorouracil (PF) regimen or adriamycin plus 5-fluorouracil (AF) regimen versus PF or AF regimen alone in treating patients with head and neck or esophagus squamous cell cancer., Methods: A total of 160 patients were recruited. PF regimen (cisplatin 20 mg/m(2) ivgtt, qd x 5d; 5-fluorouracil 500 mg/m(2) ivgtt, qd x 5d) was administered to patients have no history of PF chemotherapy,or sensitive to PF chemotherapy,while AF regimen (adriamycin 50 mg/m(2) iv,d1; 5-fluorouracil 500 mg/m(2) ivgtt, qd x 5d) was administered to patients didn't response to PF regimen. All patients were randomized to either receive intratumoral H101 injection (5.0 x 10(11)-1.5 x 10(12) VP/day for 5 consecutive days every 3 weeks) or not. Treatment repeated every 3 weeks,all patients have to receive at least 2 cycles of chemotherapy., Results: Among 123 accordant patients,overall response rate of PF plus H101 group (group A1) was 78.8% (41/52),of PF alone group (group B1) was 39.6% (21/53),of AF plus H101 group (group A2) was 50.0% (7/14),of AF alone group (group B2) was 50.0% (2/4). Differences of response rates between group A1 and group B1,between group A1+A2 and group B1+B2 were significant (P=0.000). Main side effects were fever (45.7%), injection site reaction (28.3%),and influenza-like symptoms (9.8%)., Conclusion: Intratumoral H101 injection showed a distinct efficacy in patients with squamous cell cancer of head and neck or esophagus,and was relatively safe.

Background & Objective: In recent years,great development have been made in cancer therapeutics with replication-competent viruses (oncolytic viruses), E1B deleted adenovirus is one of promising viruses. The current study was designed to evaluate the efficacy and toxicity of intratumoral H101, a E1B-deleted adenovirus, in combination with chemotherapy on patients with cancer., Methods: A total of 50 patients with malignant tumors in multiple centers clinical trial were treated with H101, 0.5ml 5x10(11) viral particle per day for 5 consecutive days every three weeks. Routine chemotherapy was performed at the same time. And the efficacy and toxicity were recorded., Results: Among 46 valuable cases, the overall response rate was 30.4%. The response rate was 28.0% (14/50) among ITT population, including 3 complete response (CR) and 11 partial response (PR). The overall response rate of control lesion was 13.0%, including 1 case of CR and 5 cases of PR. Thus, the response rate in injected lesion is clearly higher than that in control lesion (P< 0.001). Main side effects were injection site pain (26.9%) and fever (30.2%). Grade 1 hepatic dysfunction was found in 4 patients, grade 2 in 1 patients, grade 4 in 1 patients. Grade 4 hematological toxicities were found in 4 patients., Conclusion: The study showed that the combination of genetically modified adenovirus (H101) and chemotherapy possessed some effect for treating the patients with refractory malignant tumors, and the toxicities were lower, well tolerated.

Background and Objective: Cancer chemotherapy can induce thrombocytopenia. It is necessory to develop drugs that can prevent and treat thrombocytopenia. The current study was designed to evaluate the efficacy and toxicity of rhIL-11 in prevention and treatment of chemotherapy-induced thrombocytopenia., Method: A total of 109 cancer patients were involved randomly into AB or BA group and every patient received 2 cycles of chemotherapy. IL-11 was administered subcutaneously(50 micrograms/kg/d), beginning 24 hours after completion of chemotherapy for 14 consecutive days or continuing until platelet count was > 400 x 10(9)/L during cycle A. Patients did not received IL-11 during cycle B. Another 41 cases of cancer patients whose platelet were less than 50 x 10(9)/L after chemotherapy entered into open study group. IL-11 administration was the same as above., Results: Efficacy can be evaluated in 107 cases in controlled study group. Mean platelet count of cycle A was (246.49 +/- 88.64) x 10(9)/L and cycle B was (180.24 +/- 83.34) x 10(9)/L(P = 0.000). Grade III/IV thrombocytopenia in cycle A and cycle B were 7/107(6.5%) and 15/107(14%), respectively (P = 0.04). The minimum platelet counts were (136.46 +/- 74.64) x 10(9)/L and (107.77 +/- 61.33) x 10(9)/L, respectively (P = 0.000). The maximum platelet counts were (381.28 +/- 150.39) x 10(9)/L and (207.44 +/- 113.32) x 10(9)/L, respectively (P = 0.000). For open study group, 32 patients could be evaluated. The platelet count increased from(30.1875 +/- 12.13) x 10(9)/L to (226.25 +/- 163.91) x 10(9)/L after IL-11 administration. Major adverse effects were edema, dizziness, palpitation, etc., Conclusion: rhIL-11 can reduce thrombocytopenia induced by chemotherapy and is a safe and effective drug for treatment of thrombocytopenia.

Background and Objective: Clinical studies showed there was no satisfying treatment of the patients with recurrent advanced ovarian cancer by using chemotherapy of combining platinum, and it is very important for oncologist to seek the second-line drugs to treat the patients with recurrent ovarian cancer. The current study was designed to evaluate the efficacy and toxicity of single agent Topotecan hydrochloride in the patients with recurrent advanced ovarian cancer., Material and Method: A total of 31 patients with recurrent ovarian cancer in a multiple centers clinical trial were treated with Topotecan 1.25 mg/m2 qd, i.v. inf. for 5 consecutive days every three weeks., Result: Among 21 evaluable cases, overall response rate was 33.33%. Among 29 ITT population the response rate was 24.14%, including 3 CR and 4 PR. Main side effects were hematologic toxicities, 31.0% patients and 37.5% courses developed Grade III-IV leukocytopenia, 20.7% patients and 14.3% courses developed Grade III-IV thrombocytopemia. Non-hematologic toxicities were mild., Conclusion: Topotecan is effective for treating the patients with recurrent ovarian cancer who failed with platinum-based regimes.