• Journal of Chest Surgery
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• v.34 no.12
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• pp.924-929
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• 2001

Backgroun : The long-term survival after operation of patients with lung cancer invading the chest wall is known to be related to regional nodal involvement, completeness of resection and depth of chest wall involvement. In this study results of complete resection are reviewed to determine survival charateristics. Material and Method: Of 680 consecutive patients who were operated on for primary non-small cell carcinoma between 1988 and 1998, we retrospectively reviewed 55 patients(8.0%) who had complete resection for lung cancer invading the chest wall or parietal pleura. Result: Resection of the chest wall was on bloc in 29 patients(47.3％), and extrapleural in 26(52.7％). In the patients undergoing extrapleural resection, the depth of chest wall invasion was confined to the parietal pleura in all patients(100%). In the patients underging en bloc resection, the pathologic depth of invasion was into the parietal pleura alone in 9(31.0%) and into the chest wall in 20(69.0%). The follow-up rate of these patients was 100%. Hospital mortality was 5.4%(n=3). The actuarial 5-year survival rate was 26% for all hospital survivors(n=52). The actuarial 5-year survival rate of patients with T3N0M0 disease(29%) was better than that of T3N2M0 disease(18%), however, there was no significant(p=0.30) difference. The depth of chest wall invasion had no statistically significant effect on survival in our series, neither for patients with involved lymphatic metastasis nor for those without(p=0.99). Conclusion: These observations indicate that the good five year survival in patients with T3 NSCLC invading the chest wall resulted from complete resection. Survival of patients with lung cancer invading the chest wall after complete resection is dependent on the extent of nodal involvement and much less so on the depth of chest wall invasion.

• Radiation Oncology Journal
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• v.29 no.3
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• pp.174-180
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• 2011

Purpose: To evaluate the radiotherapy treatment outcome of patients in stage IE and IIE nasal natural killer/T-cell lymphoma. Materials and Methods: From August 1999 to August 2009, 46 patients with stage IE and IIE nasal natural killer/T-cell lymphoma were treated by definitive radiotherapy and chemotherapy. 33 patients were treated with chemotherapy followed by radiotherapy (CT + RT) and they received 50.4 Gy in 28 fractions. 13 patients were treated with concurrent chemoradiotherapy (CCRT) and they received 40 Gy in 20 fractions. Results: The median follow-up period was 4.6-137.6 months (median, 50.2 months) for all patients. The 4-year overall survival was 68.6% and 4-year disease free survival (DFS) was 61.9%. The 4-year locoregional recurrence free survival was 65.0%, and 4-year distant metastasis free survival (DMFS) was 66.2%. For patients treated with CT + RT, 15 patients (45.5%) achieved complete response after chemotherapy, and 13 patients (39.4%) achieved partial response. 13 patients (81.8%) achieved complete response after radiotherapy, and 6 patients (18.2%) achieved partial response. For patients treated with CCRT, 11 patients (84.6%) achieved complete response, and one patient (7.7%) achieved partial response. In univariate analysis, presence of cervical lymph node metastasis was only significant prognostic factor for DFS and DMFS. Conclusion: This study did not show satisfactory overall survival rate and disease free survival rate of definitive radiotherapy and chemotherapy for stage IE and IIE nasal natural killer/T-cell lymphoma. For patients with cervical lymph node metastasis, further investigation of new chemotherapy regimens is necessary to reduce the distant metastasis.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.3
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• pp.1803-1806
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• 2013

Purpose: Carbohydrate antigen (CA) 242 is inversely related to prognosis in many cancers. However, few data regarding CA 242 in esophageal cancer (EC) are available. The aim of this study was to determine the prognostic value of CA 242 and propose an optimum cut-off point in predicting survival difference in patients with esophageal squamous cell carcinoma (ESCC). Methods: A retrospective analysis was conducted of 192 cases. A receiver operating characteristic (ROC) curve for survival prediction was plotted to verify the optimum cuf-off point. Univariate and multivariate analyses were performed to evaluate prognostic parameters for survival. Results: The positive rate for CA 242 was 7.3% (14/192). The ROC curve for survival prediction gave an optimum cut-off of 2.15 (U/ml). Patients with CA 242 ${\leq}$ 2.15 U/ml had significantly better 5-year survival than patients with CA 242 >2.15 U/ml (45.4% versus 22.6%; P=0.003). Multivariate analysis showed that differentiation (P=0.033), CA 242 (P=0.017), T grade (P=0.004) and N staging (P<0.001) were independent prognostic factors. Conclusions: Preoperative CA 242 is a predictive factor for long-term survival in ESCC, especially in nodal-negative patients. We conclude that 2.15 U/ml may be the optimum cuf-off point for CA 242 in predicting survival in ESCC.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.42 no.6
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• pp.358-364
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• 2016

Objectives: To evaluate the results of elective neck dissection versus those of observation in the treatment of early stage oral squamous cell carcinoma and to identify factors related to recurrence and survival. Materials and Methods: This was a retrospective study of 52 patients who underwent elective neck dissection and 27 who did not receive neck dissection. Results: In survival analyses, elective neck dissection showed a benefit in overall recurrence (P=0.027), especially in stage I patients (P=0.024). With regard to survival, the benefit was statistically insignificant (P=0.990). In multivariable analysis, overall recurrence was independently related to poor histologic grade (odds ratio [OR]=9.65, P=0.006), and cancer-specific death was independently related to advanced age (OR=6.3, P=0.022), higher clinical T stage (OR=15.2, P=0.01), and poorly differentiated histologic grade (OR=6.6, P=0.025). Conclusion: Though there was lower recurrence in the elective neck dissection group, there were no statistically significant results on survival. The characteristics of the tumor itself, such as clinical T stage and poor histologic grade, may be more important in cancer-specific survival.

• BMB Reports
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• v.49 no.1
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• pp.63-68
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• 2016

The serine/threonine kinase mTOR is essential for the phosphoinositide 3-kinases (PI3K) signaling pathway, and regulates the development and function of immune cells. Aberrant activation of mTOR signaling pathway is associated with many cancers including leukemia. Here, we report the contributions of mTOR signaling to growth of human leukemic cell lines and mouse T-cell acute leukemia (T-ALL) cells. Torin, an ATP-competitive mTOR inhibitor, was found to have both cytotoxic and cytostatic effects on U-937, THP-1, and RPMI-8226 cells, but not on Jurkat or K-562 cells. All cells were relatively resistant to rapamycin even with suppressed activity of mTOR complex 1. Growth of T-ALL cells induced by Notch1 was profoundly affected by torin partially due to increased expression of Bcl2l11 and Bbc3. Of note, activation of Akt or knockdown of FoxO1 mitigated the effect of mTOR inhibition on T-ALL cells. Our data provide insight on the effect of mTOR inhibitors on the survival and proliferation of leukemic cells, thus further improving our understanding on cell-context-dependent impacts of mTOR signaling. [BMB Reports 2016; 49(1): 63-68]

• IMMUNE NETWORK
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• v.14 no.1
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• pp.14-20
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• 2014

CD28/T cell receptor ligation activates the NF-${\kappa}B$ signaling cascade during CD4 T cell activation. NF-${\kappa}B$ activation is required for cytokine gene expression and activated T cell survival and proliferation. Recently, many reports showed that NF-${\kappa}B$ activation is also involved in T helper (Th) cell differentiation including Th17 cell differentiation. In this review, we discuss the current literature on NF-${\kappa}B$ activation pathway and its effect on Th17 cell differentiation.

• Parasites, Hosts and Diseases
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• v.52 no.6
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• pp.595-603
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• 2014

Trichomonas vaginalis secretes a number of proteases which are suspected to be the cause of pathogenesis; however, little is understood how they manipulate host cells. The mammalian target of rapamycin (mTOR) regulates cell growth, cell proliferation, cell motility, cell survival, protein synthesis, and transcription. We detected various types of metalloproteinases including GP63 protein from T. vaginalis trophozoites, and T. vaginalis GP63 metalloproteinase was confirmed by sequencing and western blot. When SiHa cells were stimulated with live T. vaginalis, T. vaginalis excretory-secretory products (ESP) or T. vaginalis lysate, live T. vaginalis and T. vaginalis ESP induced the mTOR cleavage in both time-and parasite load-dependent manner, but T. vaginalis lysate did not. Pretreatment of T. vaginalis with a metalloproteinase inhibitor, 1,10-phenanthroline, completely disappeared the mTOR cleavage in SiHa cells. Collectively, T. vaginalis metallopeptidase induces host cell mTOR cleavage, which may be related to survival of the parasite.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.5
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• pp.2297-2302
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• 2014

Objective: To evaluate early treatment for extranodal natural killer/T cell lymphoma (ENK/TCL) in China and provide reference for clinical treatment of these patients. Methods: Computer-based retrieval was performed in PubMed, CNKI, CBM, VIP and WanFang Data to search for randomized controlled trials (RCTs) of treatment for early ENK/TCL, and a meta-analysis was conducted with RevMan 5.0 software. Results: A total of 11 RCTs, including 871 patients, were selected, of which the first radiotherapy had a higher complete response (CR) than the first chemotherapy [OR=14.16, 95%CI (8.68, 23.10), P<0.00001] and CR was not different between combined treatment group and radiotherapy group [OR=1.86, 95%CI (0.47, 3.58), P=0.61], but long-term survival rate was higher with combined treatment[OR=1.88, 95%CI (1.09, 3.19), P=0.02]. No difference in survival rate was observed between radio-chemotherapy and chemo-radiotherapy groups [OR=1.11, 95%CI (0.73, 1.69), P=0.63]. Conclusions: Radiotherapy is of great significance in the treatment of early ENK/TCL, but combined therapy could further enhance long-term survival rate of patients. This conclusion still requires further confirmation using RCTs with high quality and large sample size.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.14
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• pp.5687-5690
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• 2015

Background: Factors predictive of survival have been identified in Western patients with metastatic clear cell renal cell carcinoma (mCCRCC) treated with sunitinib. Less is known, however, about factors predictive of survival in Japanese patients. This study evaluated factors prognostic of survival in Japanese patients with mCCRCC treated with first-line sunitinib. Materials and Methods: This retrospective study evaluated 46 consecutive Japanese mCCRCC patients treated with sunitinib as first line therapy. Clinical and biochemical markers associated with progression-free survival (PFS) were analyzed, with prognostic factors selected by uniand multivariate Cox regression analyses. Results: Univariate analysis showed that factors significantly associated with poor PFS included Memorial Sloan-Kettering Cancer Center poor risk scores, International Metastatic RCC Database Consortium poor risk and high (>0.5 mg/dl) serum C-reactive protein (CRP) concentrations (p<0.001 each). Multivariate analysis showed that high serum CRP was independently associated with poorer PFS (p=0.040). Six month disease control rate (complete response, partial response and stable disease) in response to sunitinib was significantly higher in patients with normal (${\leq}0.5mg/dl$) than elevated baseline CRP (p<0.001). Conclusions: CRP is a significant independent predictor of PFS for Japanese patients with mCCRCC treated with first-line sunitinib. Pretreatment CRP concentration may be a useful biomarker predicting response to sunitinib treatment.

• Parasites, Hosts and Diseases
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• v.51 no.3
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• pp.279-287
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• 2013

Autophagy is a process of cytoplasmic degradation of endogenous proteins and organelles. Although its primary role is protective, it can also contribute to cell death. Recently, autophagy was found to play a role in the activation of host defense against intracellular pathogens. The aims of our study was to investigate whether host cell autophagy influences Toxoplasma gondii proliferation and whether autophagy inhibitors modulate cell survival. HeLa cells were infected with T. gondii with and without rapamycin treatment to induce autophagy. Lactate dehydrogenase assays showed that cell death was extensive at 36-48 hr after infection in cells treated with T. gondii with or without rapamycin. The autophagic markers, LC3 II and Beclin 1, were strongly expressed at 18-24 hr after exposure as shown by Western blotting and RT-PCR. However, the subsequent T. gondii proliferation suppressed autophagy at 36 hr post-infection. Pre-treatment with the autophagy inhibitor, 3-methyladenine (3-MA), down-regulated LC3 II and Beclin 1. The latter was also down-regulated by calpeptin, a calpain inhibitor. Monodansyl cadaverine (MDC) staining detected numerous autophagic vacuoles (AVs) at 18 hr post-infection. Ultrastructural observations showed T. gondii proliferation in parasitophorous vacuoles (PVs) coinciding with a decline in the numbers of AVs by 18 hr. FACS analysis failed to confirm the presence of cell apoptosis after exposure to T. gondii and rapamycin. We concluded that T. gondii proliferation may inhibit host cell autophagy and has an impact on cell survival.