Recent studies indicated nm23-H1 played a role in cancer progression. Therefore, we investigated clinical significance of nm23-H1 expression in oral squamous cell carcinoma (OSCC). In total, 86 OSCC specimens were immunohistochemically stained with nm23-H1-specific monoclonal antibodies. Immunohistochemical staining of nm23-H1 was confirmed by immunoblotting. The relations between nm23-H1 expression and clinicopathologic variables were evaluated by w 2 analysis. As increased size of primary tumour could escalate metastatic potential and the data of patients at the late T stage might confound statistical analyses, we thus paid special attention to 54 patients at the early T stage of OSCC. Statistical difference of survival was compared by a log-rank test. Immunohistochemically, nm23-H1 expression was detected in 48.8% (42 out of 86) of tumorous specimens. It positively correlated with larger primary tumour size (P ¼ 0.03) and inversely with cigarette-smoking habit (P ¼ 0.042). In patients at the early T stage, decreased nm23 expression was associated with increased incidence of lymph node metastasis (P ¼ 0.004) and indicated poor survival (P ¼ 0.014). Tumour nm23-H1 expression is a prognostic factor for predicting better survival in OSCC patients at the early T stage, which may reflect antimetastatic potential of nm23. Therefore, modulation of nm23-H1 expression in cancer cells can provide a novel possibility of improving therapeutic strategy at this stage. In addition, our results further indicated cigarette smoking could aggravate the extent of nm23-H1 expression and possibly disease progression of OSCC patients.
Recently, the serum level of interleukin (IL)-6 has been shown to correlate with disease progression and prognosis of cancer patients. However, the available information about the source and the pathophysiological regulation of IL-6 in cancer cells is limited. Thus, in this study, we tried to identify the source and the clinical roles of serum IL-6 in patients with oesophageal squamous cell carcinoma (ESCC), and then further to characterize the biological regulation of IL-6 in ESCC cell lines. Sera and tissue specimens from 80 consecutive patients with ESCC were collected between 1993 and 1997. Additionally, three ESCC cell lines were used for in vitro study. The concentration of serum IL-6 was measured by enzyme-linked immunosorbent assay (ELISA), and correlated the survival time with measured IL-6 level. Expressions of IL-6, IL-6Rα (IL-6 receptor alpha) and gp130 in pathological sections and cell lines were characterized by immunological staining. Detection of IL-6 mRNA was determined by in situ hybridization (ISH) and reverse transcription-polymerase chain reaction (RT-PCR). Up-regulation of IL-6 by n-sodium butyrate (n-BT) was studied in ESCC cell lines. The levels of serum IL-6 in patients with ESCC were significantly higher than those in the healthy controls. Serum levels of IL-6 were also shown to correlate with disease progression and survival. However, sCD8 levels and lymphocyte counts in the peripheral blood were not parallel to the changed pattern of serum IL-6. In pathological sections and ESCC cell lines, message of IL-6 was identified by ISH in cancer cells. Expression of IL-6 mRNA was further confirmed with RT-PCR in ESCC cell lines. Although IL-6 was detected in some ESCC cell lines, IL-6 gene expression and protein production could be induced or enhanced by n-BT treatment in all three cell lines. The serum levels of IL-6 are frequently elevated at diagnosis of ESCC, and are associated with poor prognosis. IL-6 that could be produced by cancer cells is up-regulated by n-BT. © 1999 Cancer Research Campaign
The role of new cytotoxic agents like gemcitabine has not yet been proven in the neoadjuvant settings. We designed a phase II study to test the feasibility of using gemcitabine and cisplatin before local treatment for stage III non-small cell lung cancer patients. Patients received three cycles of induction chemotherapy of gemcitabine (1000 mg m 72 , days 1, 8, 15) and cisplatin (90 mg m 72 , day 15) every 4 weeks before evaluation for operability. Operable patients underwent radical resection. Inoperable patients and patients who had incomplete resection received concurrent chemoradiotherapy with daily low dose cisplatin. All patients who did not progress after local treatment received three more cycles of adjuvant chemotherapy of gemcitabine and cisplatin. Fifty-two patients received induction treatment. Two patients had complete response and 31 patients had partial response (response rate 63.5%) after induction chemotherapy. Thirty-six patients (69%) were operable. Eighteen patients (35%) had their tumours completely resected. Two patients had pathological complete response. Median overall survival was 19.1 months, projected 1-year survival was 66% and 2-year survival was 34%. Three cycles of gemcitabine and cisplatin is effective and can be used as induction treatment before surgery for locally advanced non-small cell lung cancer patients.
BACKGROUND.Microsatellite studies in histologic types B3 and C thymic neoplasia detected gains on chromosome 17q, which contains the Her‐2/neu and its juxtaposed topoisomerase 2α (T2α) genes. The study aimed to evaluate their impact on tumor biology and survival of advanced thymic neoplasia patients.METHODS.From 1991 to 2005, 36 consecutive stage IV thymic carcinoma patients were treated, 18 men and 18 women, aged 11 to 84 years. There were 22 thymic carcinoma, 13 type B3, and 1 type B2 thymoma. Patients received treatment consisting of surgical resection, combination chemotherapy with the CAP (cyclophosphamide, Adriamycin, cisplatin) regimen, or radiation therapy potentiated by high‐dose weekly 5‐fluorouracil infusion. Permutations of these 3 treatment modalities were prescribed as necessary.RESULTS.T2α gene amplification was detected in 4 of 14 thymic carcinoma and 1 of 15 type B3 thymoma. Three thymic carcinoma patients had Her‐2/neu coamplification and these 3 patients had rapidly growing tumor and extensive disease at initial diagnosis. CAP was prescribed in 28 patients and 20 patients responded (response rate, 71.4%, 95% confidence interval [CI]: 52.8% to 85%); all responders overexpressed (≥10% nuclei positive) the T2α protein, whereas 4 nonresponders had very low expression. T2α overexpression predicts CAP response, and its absence predicts resistance (P = .001). Overall survival was significantly prolonged if the tumor was resectable (P = .001), of type B3 histology (P = .0039), and had no Her‐2 gene amplification (P = .0081).CONCLUSION.T2α and Her‐2/neu genes play a pivotal role in the tumor biology, CAP response, and survival of advanced thymic neoplasia patients. Cancer 2007;109:502–509. © 2006 American Cancer Society.
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