Issue Contents

Publication date: April 2016
Source:Cancer/Radiothérapie, Volume 20, Issue 2





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Editorial Board

Publication date: April 2016
Source:Cancer/Radiothérapie, Volume 20, Issue 2





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Radiation-enhancing effect of sodium glycididazole in patients suffering from non-small cell lung cancer with multiple brain metastases: A randomized, placebo-controlled study

Publication date: Available online 1 April 2016
Source:Cancer/Radiothérapie
Author(s): Y.C. Zeng, R. Wu, R. Xing, F. Chi, S.L. Wang, X.D. Chen, Y. Xuan, L.N. Wu, Q.Y. Duan, M.Y. Tang, N. Niu, Y.N. Sun, G.L. Fan, H.M. Wang
PurposeMedian survival of patients with brain metastases from non-small cell lung cancer is poor. This study was to investigate the radiation-enhancing effect of sodium glycididazole combined with whole-brain radiotherapy of multiple brain metastases from non-small cell lung cancer.Patients and methodsSixty-four patients with multiple brain metastases from non-small cell lung cancer were included: the study group (n=32) received whole-brain radiotherapy combined with sodium glycididazole at a dose of 700mg/m² intravenous infusion 30minutes before radiotherapy, three times a week; the control group (n=32) only received whole-brain radiotherapy. The primary end point was central nervous system (CNS) progression-free survival and overall survival. The treatment-related toxicity was also recorded.ResultsThe CNS disease control rate was better (90.6% vs 65.6%, P=0.016) in the study group than in the control group at 3 month of follow-up. The median CNS progression-free survival time was longer in the study group than in the control group (7.0 months vs 4.0 months, P=0.038). There was no significant difference of the median overall survival time between the study group and the control group (11.0 months vs 9.0 months, P=0.418). On the other hand, the treatment-related toxicity showed no statistically significant difference between these two groups (P>0.05).ConclusionsThe study indicated that sodium glycididazole was an effective, promising radiation-enhancing agent that improved CNS disease control rate, extended the median CNS progression-free survival time and was well tolerated in patients suffering from non-small cell lung cancer with multiple brain metastases.



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Reducing understaging of bladder cancer with the aid of photodynamic cystoscopy

Publication date: Available online 1 April 2016
Source:Journal of the Egyptian National Cancer Institute
Author(s): K. Sfetsas, D. Mitropoulos
BackgroundThe authors evaluated the role of photodynamic cystoscopy in the detection of additional urothelial lesions, mainly carcinoma in situ, that would not be detected solely with white light cystoscopy, leading to disease understaging.MethodsFrom 2009 to 2011, 70 patients underwent white light cystoscopy, followed by photodynamic cystoscopy (blue light system, Karl Storz, Tuttlingen, Germany). Preoperatively they were instilled intravesically with 50ml of Hexvix (Hexaminolevulinate hexylester). We recorded all lesions found with white light cystoscopy and the additional lesions revealed by blue light cystoscopy. Afterward all lesions were removed and sent for pathologic evaluation.ResultsSeventeen patients (24.3%) had primary tumors while 53 patients (75.7%) had recurrent disease. In 53 out of 70 patients (75.7%) white light cystoscopy revealed urothelial lesions. In the rest 17 patients who had no findings with white light cystoscopy, blue light cystoscopy revealed 7 cases of Cis (41.2%) and 8 cases of dysplasia (47%). In the group of patients with visible lesions in white light cystoscopy photodynamic cystoscopy revealed additional carcinoma in situ in 22 patients. Altogether additional carcinoma in situ cases found with the aid of photodynamic cystoscopy were 29 out of 70 cases (41.4%).ConclusionsPhotodynamic cystoscopy is the most efficient diagnostic procedure for flat urothelial lesions and especially for carcinoma in situ. It is significantly more sensitive than conventional white light cystoscopy in Cis diagnosis, thus reducing understaging of the disease and consequently improving recurrence and progression rates.



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[What's next in glioblastoma treatment: Tumor-targeted or immune-targeted therapies?]

[What's next in glioblastoma treatment: Tumor-targeted or immune-targeted therapies?]

Bull Cancer. 2016 Mar 28;

Authors: Schernberg A, Marabelle A, Massard C, Armand JP, Dumont S, Deutsch E, Dhermain F

Abstract
INTRODUCTION: Glioblastoma (GBM) is associated with a poor prognosis. This review will discuss different directions of treatment, mostly regarding immunotherapies and combinatorial approaches.
DEVELOPMENT: Standard treatment for newly diagnosed GBM is maximal and safe surgical resection followed by concurrent radiochemotherapy (RCT) based on temozolomide, allowing 14.6 months median survival. Nowadays, no combination with molecular-targeted therapy had significantly improved prognosis. Phases I and II data are emerging, highlighting the potential efficacy of associations with other therapies. Studies have suggested the potential of targeting tumor stem cells, at less partially responsible for resistance to RCT. There is now some evidence that immunotherapy is also relevant for brain tumors. Treatment strategies have mainly explored vaccines strategies, such as the dendritic cell, heat shock protein or EGFRvIII vaccines. Of the work initiated in melanoma, immune checkpoints inhibitors have exhibited stimulating results. Others trials have demonstrated potential of autologous stimulated lymphocytes. Moreover, strong data indicates that radiation therapy has the potential to promote immunogenicity and create a sort of in situ personalized vaccine.
CONCLUSION: These data provide strong evidence to support the potential of associating combinatorial targeted and/or immunotherapeutic regimens in patients with GBM that may change patient outcome.

PMID: 27032303 [PubMed - as supplied by publisher]

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Optimal combination of gemcitabine, sorafenib, and S-1 shows increased efficacy in treating cholangiocarcinoma in vitro and in vivo.

Cholangiocarcinoma (CCA) is one of the most difficult cancers to treat and lacks an established standard chemotherapy regimen. This study evaluated the effects of different combinations of gemcitabine, sorafenib, and S-1 on CCA cells to identify the optimal drug combination. A fractional factorial design method was applied in drug combination experiments to determine the optimal combination of these three drugs (gemcitabine=1.4 mmol/l, sorafenib=0.03 mmol/l, S-1=0.185 mmol/l). We constructed a mathematical model with a small number of runs (Y=1.14-0.377A-23.0B-1.81C+0.084A2+109B2+6.06C2+3.83AB+0.175AC-40.4BC) to predict the efficacy of combinations of the drugs. The optimal combination can significantly inhibit the AKT/mTOR pathway, and thus CCA cell proliferation, and can induce cell apoptosis. In vivo, this combination (gemcitabine=1.4 mmol/l, sorafenib=0.03 mmol/l, S-1=0.185 mmol/l) can significantly inhibit tumor growth. The present study showed that the mathematical model was reliable and could predict the efficacy of the different drug combinations. The optimal combination of these drugs may aid the development of a promising standard chemotherapy regimen for CCA. Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved.

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IL-6 blockade in K-ras mutant lung cancer

Activating mutations of K-ras are the most common oncogenic alterations found in lung cancer. Unfortunately, attempts to target K-ras mutant lung tumors have thus far failed, clearly indicating the need for new approaches in patients with this molecular profile. We have previously shown NF-κB activation, release of IL-6, and activation of its responsive transcription factor STAT3 in K-ras mutant lung tumors, which was further amplified by the tumor enhancing effect of chronic obstructive pulmonary disease (COPD)-type airway inflammation. These findings suggest an essential role for this inflammatory pathway in K-ras mutant lung tumorigenesis and its enhancement by COPD. Therefore, here we blocked IL-6 using a monoclonal anti-IL-6 antibody in a K-ras mutant mouse model of lung cancer in the absence or presence of COPD-type airway inflammation. IL-6 blockade significantly inhibited lung cancer promotion, tumor cell intrinsic STAT3 activation, tumor cell proliferation, and angiogenesis markers. Moreover, IL-6 inhibition reduced expression of pro-tumor type 2 molecules (Arginase 1, Fizz 1, Mgl, and IDO), number of M2 type macrophages and G-MDSCs, and pro-tumor T-regulatory/T helper 17 cell responses. This was accompanied by increased expression of anti-tumor type 1 molecule (Nos2), and anti-tumor T helper 1/CD8 T cell responses. Our study demonstrates that IL-6 blockade not only has direct intrinsic inhibitory effect on tumor cells, but also re-educates the lung microenvironment toward an anti-tumor phenotype by altering the relative proportion between pro-tumor and anti-tumor immune cells. This information introduces IL-6 as a potential druggable target for prevention and treatment of K-ras mutant lung tumors.

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