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Tetsuya Toge

Publications and source records attributed to Tetsuya Toge.

At least 73 records · Page 4Linked to original sources
PubMed2002

Current status of the molecular mechanisms of anticancer drug-induced apoptosis. The contribution of molecular-level analysis to cancer chemotherapy.

Apoptosis is an important phenomenon in cytotoxicity induced by anticancer drugs. Here, we review the current status of the molecular mechanisms of anticancer drug-induced apoptosis in order to assess the contribution of molecular-level analysis to cancer chemotherapy. It is apparent that the molecular mechanisms by which anticancer drugs induce apoptosis are mediated by death receptor-dependent and -independent pathways, which are related to the release of cytochrome c through voltage-dependent anion channels in the mitochondrial inner membrane. The release of cytochrome c is the central gate in turning on/off apoptosis, and is regulated by the interaction of proapoptotic proteins, including Bid, Bax and Bak, and antiapoptotic proteins including Bcl-2 and Bcl-X(L), and a specific class of inhibitors of apoptosis proteins (IAPs) including Akt, survivin, and heat-shock proteins. The caspase cascade is activated by the release of cytochrome c, which is initiated by the formation of apoptosomes consisting of procaspase-9, Apaf-1 and cytochrome c in the presence of dATP, and results in the activation of caspase-9 and caspase-3, thereby leading to apoptosis. Drug sensitivity can be enhanced by the introduction of proapoptotic genes and the inhibition of antiapoptotic proteins. The latter process is mediated by antisense oligonucleotides and is associated with apoptosis. The signal transduction pathways that are triggered by the central gate in mitochondria play a critical role in anticancer drug-induced apoptosis. The modulation of signal transduction pathways targeting the proteins involved in these signal transduction pathways using antisense IAPs, and growth factor antibodies may be a good strategy for enhancing therapeutic efficacy of anticancer drugs in cancer chemotherapy.

Antineoplastic Agents↗
PubMed2002

Utility of technetium-99m methoxyisobutyl isonitrile uptake analysis for prediction of the response to chemotherapy in advanced and relapsed breast cancer.

BACKGROUND: Technetium-99m methoxyisobutyl isonitrile (Tc-SESTAMIBI) is a substrate of P-glycoprotein and multidrug-resistance associated protein in drug-resistant cells. To assess the clinical effectiveness of Tc-SESTAMIBI for predicting the chemotherapy response to treatment with anthracyclines and vinca alkaloids, we retrospectively evaluated the relationship between the accumulation of Tc-SESTAMIBI and the tumor response. METHODS: Thirteen patients, including 12 advanced cases and 1 relapsed case, were investigated, all of whom had been treated with anthracyclines or a vinca alkaloid regimen. The accumulation of Tc-SESTAMIBI was compared at 10 min and 2 h after Tc-SESTAMIBI administration. The relationship between the accumulation of Tc-SESTAMIBI and the tumor response following treatment with anthracyclines and vinca alkaloids was assessed. RESULTS: Eight of 13 patients responded to treatment with anthracyclines and vinca alkaloids, whereas 5 patients did not respond to treatment. At 10 min, 6 (75.0% ) of the 8 responding patients had a high accumulation of Tc-SESTAMIBI, whereas 4 (80.0% ) of the 5 non-responding patients had a low accumulation of Tc-SESTAMIBI. The overall predictive value was 76.9%. The relationship was not statistically significant (Fisher's test). The difference in the decrease of accumulation of Tc-SESTAMIBI between 10 min and 2 h was not associated with tumor response to treatment in 6 of the responding patients with high accumulation. Two false negative cases and one false positive case were observed, suggesting the presence of another factor contributing to drug sensitivity in tumor response, such as apoptosis-related genes. CONCLUSIONS: Assessment of the initial accumulation of Tc-SESTAMIBI can be a predictive marker of tumor response to treatment with anthracyclines and vinca alkaloids in patients with advanced and relapsed breast cancer. Further studies are required to explore other factors involved in the tumor response to treatment with anthracyclines and vinca alkaloids.

Adult↗
PubMed2002

Cavernous hemangioma of the rib.

A 59-year-old man with an enlarged left chest wall mass that had been followed up for 3 years underwent surgical resection. The mass was pathologically diagnosed as cavernous hemangioma of the rib. This is the fourth case of this rare disease to be reported. However, it suggests that hemangioma of the rib should be considered in the differential diagnosis of rib tumors, especially in asymptomatic patients.

Bone Neoplasms↗
PubMed2002

The effect of adjuvant 5'-deoxy-5-fluorouridine in early stage breast cancer patients: results from a multicenter randomized controlled trial.

To assess the efficacy of 5'-DFUR, an intermediate of capecitabine, for adjuvant treatment of early breast cancer, we conducted an open-labeled multi-center randomized controlled trial to compare postoperative 5'-DFUR treatment with surgery alone. We enrolled 1217 primary breast cancer patients and randomly assigned them into two treatment groups; one received six-month postoperative 5'-DFUR treatment by consecutive or intermittent administration, and the other surgery alone. Follow-up surveys were conducted once a year for all subjects simultaneously and examined their outcome/presence or absence of the cancer recurrence. The central study committee reviewed all follow-up data and judged the recurrence data to be used for the analysis. Eight-year follow-up data showed no significant differences in relapse-free and overall survival between the two groups, and 5'-DFUR treatment regimen showed an extremely high tolerance. Possible explanations are discussed for the finding of no significant survival difference between adjuvant 6-month 5'-DFUR monotherapy and surgery alone in early breast cancer.

Adult↗
PubMed2002

Mechanism(s) of antitumor action in protracted infusion of low dose 5-fluorouracil and cisplatin in gastric carcinoma.

The therapeutic efficacy of low dose administration of 5-fluorouracil (5-FU) and cisplatin (CDDP) (low dose FP) has been reported in patients with advanced and recurrent gastric carcinoma. Mechanism(s) by which low dose FP exerts antitumor effect is not entirely clear. We investigated mechanism(s) of the therapeutic efficacy in combination with 5-FU and CDDP in terms of signal transduction pathways leading to apoptosis. Using two human gastric carcinoma cell lines, MKN28 and MKN45, antitumor effect in combination treatment with 5-FU and CDDP was assessed by MTT 5-day assay. The significant antitumor effect was determined with more than 50% growth inhibition compared to control cells. Enhancement of antitumor effect in the combination treatment was analyzed using isobologram. Apoptotic cell death was assessed by DNA ladder formation assay, and expression of apoptosis-related genes was detected by Western blotting. Concentration of free platinum and 5-FU was measured by high-pressure liquid chromatography (HPLC), and dihydropyrimidine dehydrogenase (DPD) activity and total folate levels were assessed by enzyme immunoassays. Antitumor effect in single treatment with 5-FU was not observed significantly with the concentration from 1 to 5 microM in vitro. In contrast, antitumor effect in combination treatment with 5-FU and CDDP showed a synergism with the concentration of CDDP from 1.5 to 3 microM. Single treatment with CDDP also did not show significant antitumor effect with the concentration from 1.5 to 3 microM. The enhancement in the synergistic effect by CDDP was dose-dependent. Any free platinum treated with low dose CDDP was not detected into gastric carcinoma cells, however, treatment with CDDP induced a receptor signaling pathway, that is mediated by Fas but not DR4. It may directly activate caspase 3 leading to apoptosis. Although the receptor signaling pathway in apoptosis was not observed by 5-FU, Bax-induced cytochrome c and caspase 3 was also observed in a receptor-independent pathway by 5-FU and CDDP. Total folate levels by cotreatment with CDDP was increased to 1.5-fold compared to 5-FU alone, whereas DPD activity and 5-FU concentration were not changed by cotreatment of CDDP in vivo. The enhancement of antitumor effect by low dose FP can be explained as follows: i) low dose treatment with CDDP induces apoptotic cell death through a receptor signaling pathway even in absence of free platinum into cells; ii) increased folate level by CDDP and a non-receptor signaling pathways by 5-FU contribute to apoptotic cell death in gastric carcinoma.

Antineoplastic Agents↗
PubMed2002

[Interim report of JFMC study no. 23--phase III randomized clinical trial on the effectiveness of low-dose cisplatin plus 5-FU as a postoperative adjuvant chemotherapy for advanced gastric cancer].

The interim analysis of the JFMC study as of May, 2001 covers 190 gastrectomized patients with advanced gastric cancer from 82 institutions between May, 1996 and March, 2000. Patients were randomly assigned to the following two regimens. Group-CD: cisplatin (CDDP) 5 mg/body/day (i.v.) plus 5-FU 300 mg/body/day (cvi) day 1-5, given for 6 weeks, followed by UFT 200 mg (as tegafur) x 2/day for as long as possible. Group-UF: UFT only was administered after surgery as long as possible. The primary endpoint was survival and the secondary endpoint was disease-free survival. The 4-year survival rates were 47.6% in CD and 41.3% in UF, and the hazard ratio of CD versus UF was 0.74 (95% CL: 0.47-1.16, p = 0.189) according to a stratified (with stage) logrank analysis. The 4-year disease-free survival rates were 50.1% in CD and 39.3% in UF, and the hazard ratio of CD versus UF was 0.65 (95% CL: 0.42-1.00, p = 0.049). Cox's regression analysis using time-dependent dummy variables, revealed that the effect on the survival was accentuated within 9 months, that on disease-free survival within 6 months. The quality of life (QOL) of patients for one year after surgery in CD was significantly lower than that of patient in UF, as assessed using a QOL questionnaire. Although the present interim analysis does not statistically confirm the efficacy of the "low-dose CDDP plus 5-FU" regimen, an expectation for better results is suggested if this regimen is administered for a longer period of time. The JFMC Clinical Trial Committee permitted the release of this report on the condition that further study to verify the present study will be conducted.

Adult↗
PubMedDate not supplied

The role of HER-2 oncoprotein in drug-sensitivity in breast cancer (review).

Overexpression of human epidermal growth factor receptor-2 (HER-2) oncoprotein is an important prognostic factor associated with a poor prognosis in breast cancer. Although treatment with trastuzumab, an anti-HER-2 antibody, increases drug-sensitivity in vitro and in vivo, the role of HER-2 oncoprotein in drug-sensitivity is still uncertain. The present work discusses the clinical significance of the HER-2 oncoprotein in drug-sensitivity in breast cancer based on previous clinical and basic results and reviews the current concept of HER-2 oncoprotein in drug-sensitivity. Introduction of HER-2 oncoprotein in vitro induces resistance to several anticancer drugs, including taxanes, cisplatin (CDDP) and 5-fluorouracil (5-FU) in breast cancer cells. The acquisition of drug-resistance by introduction of the HER-2 gene, however, depends on the cell type, because transfection of the HER-2 gene per se does not necessarily induce resistance to the same drugs in all types of breast cancer cells. In clinical studies, patients with HER-2 overexpression responded better to an anthracycline-based regimen than patients with low HER-2 expression, and their overall survival was also superior. In contrast, a correlation between the response to a cyclophosphamide + methotrexate + 5-FU regimen and overexpression of HER-2 is not certain. Taxanes responsiveness in patients with HER-2 oncoprotein overexpression was superior in patients with low HER-2 expression. Treatment with trastuzumab increased drug-sensitivity to anthracyclines, CDDP, and taxanes, but not to 5-FU, in breast cancer cells. Although the mechanism(s) by which trastuzumab enhances drug-sensitivity is not fully understood, modulation of the signal transduction pathways leading to apoptosis, such as down-regulation of the anti-apoptotic protein, Bcl-2, might be an important target to increase drug-sensitivity in breast cancer. HER-2 overexpression can be a good indicator for the selection of aniticancer drugs, especially for anthracycline containing regimens. To modulate HER-2-targeting therapy, the mechanism(s) by which trastuzumab enhances drug-sensitivity requires elucidation at the molecular level, including determination of other factors that influence drug-sensitivity, leading to a more promising treatment for individual patients receiving combination therapy with trastuzumab and anticancer drugs for breast cancer.

Antineoplastic Agents↗
PubMedDate not supplied

Analysis of T cell receptors reactive with squamous cell carcinoma antigen SART-1 presented by the HLA-A24 molecule.

We investigated the induction of cytotoxic T lymphocytes (CTLs) specific for squamous cell carcinoma antigen SART-1 from the peripheral blood mononuclear cells (PBMCs) of an HLA-A24 healthy donor by in vitro stimulation with dendritic cells (DCs) pulsed with the antigenic peptide. Effector cells, designated as cells, exhibited potent cytotoxic activity against target cells in a SART-1-specific and HLA-restricted manner. T cell receptor (TCR) gene usage of the SART-1 PDAK cells analyzed by reverse transcribed-polymerase chain reaction (RT-PCR) and Southern blot analysis showed oligoclonal usage, including TCRVbeta18, which was indicated by blocking assay to be responsible for antigen recognition and killing. Single strand conformation polymorphism (SSCP) analysis revealed clonotypic bands of the TCRVbeta18. The PCR product of the TCRVbeta18 was sequenced and complementarity determining region (CDR) 3 was determined. RT-PCR analysis using this CDR3 sequence as a primer showed, as expected, a positive band of about 30 bp smaller than shown on regular PCR analysis. This clonotypic PCR demonstrated an increasing density of PCR bands in the SART-1 PDAK cells during stimulation with SART-1 peptide plus DCs. It is suggested that clonotypic PCR using the TCR-CDR3 sequence may be useful in assessing the precursor frequency of CTLs reactive with the SART-1 peptide in vivo.

Antigens, Neoplasm↗
PubMedDate not supplied

Current status and future perspectives of post-operative adjuvant therapy for gastric carcinoma.

The clinical benefit of post-operative adjuvant immunochemotherapy for survival of patients with gastric carcinoma is unclear, although a number of prospective randomized controlled studies have been conducted. The current status and future perspectives of post-operative adjuvant chemotherapy in gastric carcinoma have been evaluated in terms of survival benefit. The results of randomized clinical studies vary in accordance with the regimen and sample size. A meta-analysis, however, indicated a survival benefit in patients treated with post-operative adjuvant chemotherapy including mitomycin, anthracyclines, cyclophosphamide, alkylating agents and 5-fluorouracil (odds ratio: 0.8 to approximately 0.82, 95% CI<1.0). The survival benefit was observed in patients with stage II and stage III gastric carcinoma, but not those with stage I. Further, the survival benefit in node-positive and high histological grade subgroups was superior to that in node-negative and low histological grade subgroups. Although combination therapy with mitomycin, 5-fluorouracil and non-specific immunomodulators, such as PSK and OK-432, appeared to improve overall survival without immunomodulators, the survival effect of immunomodulators is still not clear. There are several possible reasons why the survival benefit of adjuvant chemotherapy or immunochemotherapy is small and marginal compared to surgery alone: (i) low efficacy of the chemotherapy regimen; (ii) small sample size; and (iii) differences in chemosensitivity of treated patients based on genetic background. The determination of subgroups responsive to chemotherapy and the development of a rationale-based and molecular-targeted chemotherapy are required to clearly demonstrate whether there is a survival benefit of post-operative adjuvant chemotherapy in gastric carcinoma.

Chemotherapy, Adjuvant↗
PubMedDate not supplied

Adjuvant therapy for colorectal carcinoma.

Adjuvant therapy for colorectal carcinoma has been developed over the last two decades. We have reviewed the history of adjuvant chemotherapy for colorectal carcinoma in the United States, Europe and Japan with regard to the rationale of the chemotherapy regimen and the survival benefit for the establishment of a standard regimen. Treatment with 5-fluorouracil (5-FU) and leucovorin (LV) for postoperative adjuvant chemotherapy had an overall survival benefit, compared with surgery alone, in randomized controlled trials in the United States and Europe for Dukes' C colon carcinoma. In contrast, the survival benefit of adjuvant chemotherapy for Dukes' B colon carcinoma and for rectal carcinoma has not yet been established. In Japan, randomized controlled trials have examined combination treatment with mitomycin (MMC) and oral fluoropyrimidines for colorectal carcinoma compared with surgery alone. A meta-analysis indicated that combination treatment with MMC and oral fluoropyrimidines had a survival benefit for colorectal carcinoma. The survival benefit of combination treatment with irinotecan (CPT-11) + 5-FU + LV or uracil + tegaful (UFT) + LV (Orzel) for adjuvant chemotherapy are currently being compared with 5-FU + LV. Meta-analysis revealed a survival benefit at 2-years in the prevention of liver metastasis following intraportal or intraarterial infusion of 5-FU. The survival benefit of preoperative radiotherapy was superior to postoperative radiotherapy for advanced rectal carcinoma in association with the prevention of local recurrence. Clinical trial data suggest that the current standard regimen of adjuvant chemotherapy is a combination of 5-FU and LV for Dukes' C colon carcinoma and that radiotherapy for local control of rectal carcinoma has a survival benefit.

Antineoplastic Combined Chemotherapy Protocols↗
PubMedDate not supplied

Feasibility and therapeutic efficacy of weekly 1-h low-dose paclitaxel infusion for relapsed breast cancer.

The therapeutic efficacy of weekly paclitaxel infusion for relapsed breast cancer patients is not known. We assessed safety, feasibility, and therapeutic efficacy in a pilot study of weekly 1-h low-dose paclitaxel infusion for relapsed breast cancer in an outpatient clinic. Eighteen patients with relapsed breast cancer who had received prior chemotherapy regimens, including anthracyclines, mitomycin, and 5-fluorouracil beyond a second line of treatment were enrolled into the study. The dose of paclitaxel was between 40 mg/m(2) and 80 mg/m(2) per week in a 1-h infusion, and a treatment cycle was 4 weeks until there was no evidence of progressive disease. When a dose of 80 mg/m(2) was administered, the treatment cycle was weekly infusion three times with a 1-week interval per 4-week cycle. The mean treatment period was 5.5 months and the maximal length of administration was 8 months. The overall response rate was 44.4%, including 2 cases of complete response and 6 cases of partial response. Tumor response was observed in 3 of 7 cases of lung metastases (42.8%), 6 of 12 cases of soft tissue metastases (50.0%), and 1 of 3 cases of liver metastases (33.3%), whereas 8 cases with bone metastases did not respond. The mean time to response was 1.8 months and the mean response duration was 4.3 months. The dose between 31.5 mg/m(2)/wk and 79.7 mg/m(2)/wk was not associated with tumor response. Toxicities associated with weekly 1-h low-dose paclitaxel infusion were tolerable, and most were less than grade 2, including alopecia (100%), neutropenia (88.8%), flushing (66.6%), face edema (61.1%), numbness (55.5%), and myalgia (38.8%). There was 1 case of grade 3 neutropenia. Weekly 1-h low-dose paclitaxel might be a therapeutically effective, safe infusion and feasible as a salvage chemotherapy for relapsed breast cancer patients following failure of prior chemotherapy.

Adult↗
PubMedDate not supplied

Novel system for generating cytotoxic effector lymphocytes using carcinoembryonic antigen (CEA) peptide and cultured dendritic cells.

We have established a practical system for generating antitumor effector lymphocytes using the tumor antigen peptide CEA and cultured dendritic cells (DCs), and have also characterized effector cells. DCs were induced from the adherent cell population of autologous peripheral blood mononuclear cells (PBMCs) obtained from HLA-A0201 normal or tumor-bearing donors using IL-4 and GM-CSF. The cultured DCs were shown to express class I, class II, CD80 and CD86 molecules. The PBMCs were stimulated for 7 days with the DCs pulsed with the HLA-A0201-restricted CEA peptide CEA9 671 and then expanded in an anti-CD3 antibody (1 microgram/ml)-coated flask in the presence of a 80 U/ml IL-2 (IL-2/CD3 system). The effector cells, which were designated as CEA peptide-pulsed dendritic cell-activated killer (CEA-PDAK) cells, were preferentially CD3+CD8+, and capable of killing T2 cells pulsed with CEA peptide but not T2 cells alone. The CA-PDAK cells also lysed the gastric cancer cell line KATO III (HLA-A0201, CEA (+)), but not the WiDr (HLA-A2402, CEA(+)) cells. The cytotoxicity was abrogated when the CEA-PDAK cells were treated with anti-TCR alpha beta antibody or when the target cells were treated with the anti-class I antibody prior to the cytotoxicity assay. The CEA-PDAK cells exerted their cytotoxic activity even in the presence of a high amount of CEA protein at the effector phase, which mimicked the clinical setting. The CEA-PDAK cells showed approximately a hundred-fold expansion in total cell numbers yielded without any loss of the specific lysis, when stimulated with the IL-2/CD3 system compared to those stimulated with IL-2 alone. The TCR V beta gene analysis for the CEA-PDAK cells, conducted by means of RT-PCR-Southern blotting, demonstrated oligoclonal expression of TCR beta 7 and 12, and the latter was shown to be responsible for the killing activity. SSCP analysis indicated the clonotype of the TCR V beta 12 gene, indicating a selective expansion of lymphocytes bearing a limited TCR variable region by the stimulation with CEA peptide-pulsed DCs. Taken together, the effector lymphocytes reactive with the CEA antigen can be generated from PBMCs with the antigenic CEA peptide and cultured DCs. The IL-2/CD3 system is effective and practical in activating the effector cells for the clinical use of CEA-PDAK cells. Adoptive immunotherapy using this system may be promising for treating CEA-expressing tumors.

Carcinoembryonic Antigen↗
PubMedDate not supplied

Expression and distribution of human telomerase catalytic component, hTERT, in human breast tissues.

BACKGROUND: Activation of telomerase is essential in a variety of malignant tumors. However, the regulation of its activation and the expression of human telomerase reverse transcriptase (hTERT) are not fully understood in breast tissues. MATERIALS AND METHODS: In order to clarify this point, the telomerase activity was examined by telomeric repeat amplification protocol (TRAP) assay and quantified by hybridization protection assay (HPA) and, moreover, the expressions of hTERT mRNA and protein were examined by RT-PCR and immunohistochemistry, respectively. RESULTS: Telomerase activity and the expression of hTERT mRNA were detected in 41(75%) and 37(67%) cases among 55 breast carcinomas, respectively. However, the telomerase ZV activity was detected in only 14(40%) among 35 benign breast tumors. Strong correlation was observed between telomerase activity and hTERT mRNA expression, as described previously. Moreover, the strong expression of hTERT protein in the nucleus of the cell was detected in 30 (57%) cases among 53 breast carcinomas and weak expression of the protein was also detected in 11 (35%) cases among 31 benign breast tumors by immunohistochemistry. There were 12 breast carcinomas which had no telomerase activity. Three of them had hTERT mRNA and protein and in 3 other cases, only hTERT protein was detected. Five cases had the expression of mRNA but not the protein and it was only one case which had no activity and expression of hTERT mRNA and protein. However, in benign tumors, 14 (87.5%) cases among 16 TRAP-negative tumors had no mRNA and protein expression. CONCLUSION: These results indicate that complicated regulation might be involved in the regulation of telomerase activity and also the activation of the gene may be important in the carcinogenesis of human breast carcinomas.

Breast Neoplasms↗
PubMedDate not supplied

Induction mechanism of apoptosis by troglitazone through peroxisome proliferator-activated receptor-gamma in gastric carcinoma cells.

BACKGROUND: It has been reported recently that the antidiabetic thiazolidinediones not only induce fibroblast differentiation but also inhibit the growth of carcinoma cells. MATERIALS AND METHODS: In the present study, in order to elucidate the further mechanism of growth inhibition by troglitazone, the expression of cell cycle regulators and apoptotic regulators were examined by cDNA microarrays and Western blot analysis by gastric carcinoma cells. RESULTS: Six gastric carcinoma cell lines (TMK-1, MKN-1,7,28,45,74) were treated with 0.1, 1, 10, 100 microM of troglitazone in vitro. The growth of 5 cell lines were inhibited by troglitazone in a time- and dose-dependent manner. Interestingly, the expression of cyclin D mRNA and protein was decreased and that of p27 was increased in TMK-1 cells at 12 hours after troglitazone treatment, suggesting the induction of cell cycle arrest of the cells. On the other hand, DNA ladder formation was observed at 12 hours after treatment. Moreover, the expression of cytochrome C, caspases 3 and 8 and PARP genes was increased after treatment and the gradual reduction of Bcl-XL protein was observed, which indicate that the apoptotic signals were induced after treatment by troglitazone. CONCLUSION: These results suggest that the thiazolidinediones can be a new therapeutic tool for gastric carcinoma via cell cycle regulation and apoptosis.

Antineoplastic Agents↗
PubMedDate not supplied

Screening of gastrointestinal hormone release in patients with lung cancer.

The aim of this study was the screening of gastrointestinal (GI) hormones release as possible sensitive tumor markers. The subjects were eight patients with carcinoma of the lung compared with nine healthy controls. Six kinds of GI hormones were measured by the specific radioimmunoassay. It was evaluated by fasting level (F), increased integrated responses (IIR60, IIR180 pmol/l/min) and total integrated responses (TIR60, TIR180 pmol/l/min) after a meal. The data were analyzed by the Student's t-test. The F of pancreatic polypeptide (PP) was significantly higher in patients than that in healthy controls (24.4 vs. 12.3 pmol/l, p = 0.002). Consequently, the sensitivity was 75% (6 out of 8) and specificity was 100% (9 out of 9). Almost all parameters of IIR60, IIR180, TIR60 and TIR180 in PP and peptide YY were significantly higher in patients than in healthy controls (p value: 0.00020-0.021). The other four kinds of hormones showed similar results to the healthy controls. These results seem to indicate that PP and PYY would be useful tumor markers for lung cancer in clinical management.

Aged↗