Advances in Lung Cancer
ISSN / EISSN : 21692718 / 21692726
Current Publisher: Scientific Research Publishing, Inc. (10.4236)
Total articles ≅ 41
Latest articles in this journal
Advances in Lung Cancer, Volume 8, pp 1-14; doi:10.4236/alc.2019.81001
Abstract:Objective: The objective of the study was to determine the survival of patients with small-cell lung cancer treated at tertiary hospitals in the East of Thailand. Materials and methods: The researchers conducted this retrospective study by reviewing medical records of patients with small-cell lung cancer treated at Chonburi Cancer Hospital and Prapokklao Hospital from January 2007 to December 2016 and monitored via follow-up until December 2018. Results: This study enrolled 54 patients with a median follow-up time of 8.5 months. The median age of patients was 63 years old. Most patients were male (83.3%) and had a history of smoking (90.7%), and 31.4% had clinical superior vena cava obstruction at initial treatment. The Eastern Cooperative Oncology Group performance status 0-1 was noted for 61.1% of the study population. Median survival time of patients with limited-stage and extensive-stage small cell lung cancer who received systemic chemotherapy and/or radiotherapy was 17.01 months (95% CI, 12.01 - 22.01) and 8.14 months (95% CI, 7.19 - 9.10), respectively, and that of patients receiving supportive care was 2.3 months (95% CI, 0.75 - 4.03). However, the median survival time of patients with extensive-stage small-cell lung cancer receiving only palliative chemotherapy was 5.9 months (95% CI, 0.32 - 17.51). Conclusions: The median survival time of patients with limited-stage small-cell lung cancer treated in the East of Thailand was comparable to those of landmark studies; however, the survival of patients with extensive-stage small-cell lung cancer was shorter than those of Phase III trials. A multidisciplinary team was necessary to improve the quality of patient care.
Advances in Lung Cancer, Volume 7, pp 9-20; doi:10.4236/alc.2018.72002
Abstract:Background: Survivin is an inhibitor of apoptosis that may be a novel diagnostic and prognostic marker of cancer. Our study is to investigate the diagnostic and prognostic value of survivin for pleural effusions. Methods: Sixty-five pleural effusion patients were enrolled prospectively. Pleural effusion samples were examined for survivin level by ELISA. Pleural effusions were divided into three groups: Group I, malignant pleural effusion (MPE) (n = 36); Group II, tuberculous pleurisy (TPE) (n = 18); and Group III, transudative pleural effusion (n = 11). The accuracy of diagnosis and the correlation between survivin level and survival in malignant pleural effusions (MPE) were analyzed. Results: Survivin level was 320.50 ± 228.24 pg/ml in MPE, 328.35 ± 146.79 pg/ml in TPE and 318.87 ± 208.39 pg/ml in transudative pleural effusion respectively. ROC curves for MPE versus TPE were analyzed, area under the ROC curve was 0.419, and for the cutoff value of 254.85 pg/ml sensitivity was 44.4% and specificity 55.6%. Survivin had no discriminative power in differentiating exudative effusions of MPE from non-MPE (p = 0.648). There was no correlation between survivin level and age, sex. However, statistically significant difference was found between primary lung carcinoma (238.66 ± 48.19 pg/ml) and extra-pulmonary metastatic carcinomas (435.09 ± 320.62 pg/ml) according to survivin level (p = 0.033). Survivin levels can distinguish patients who had poor prognosis (median survival 96 days) and those who had good prognosis (median survival 206 days) in MPE. Conclusion: survivin levels detected with ELISA had no discriminative power in differentiating exudative effusions included MPE and TPE. However, over-expression of survivin correlates with poor prognosis in cancer patients. Our results suggest that survivin may be a potential prognostic marker in MPE.
Advances in Lung Cancer, Volume 7, pp 1-8; doi:10.4236/alc.2018.71001
Advances in Lung Cancer, Volume 7, pp 21-31; doi:10.4236/alc.2018.73003
Advances in Lung Cancer, Volume 6, pp 1-11; doi:10.4236/alc.2017.61001
Abstract:The G-CSF is used as a therapeutic drug of the febrile neutropenia in lung cancer chemotherapy, however, there were few reports that showed the effects of combination effects of G-CSF and anticancer drugs against lung cancer. In the present study, we investigated the effects of G-CSF and the combination effects of G-CSF and cisplatin on lung cancer growth. We investigated the effect of G-CSF against the LL-2 and KLN-205 cells by MTT assay and tried to detect the G-CSF receptor by RT-PCR. Next, to analyze the G-CSF effects in vivo, we transplanted the LL-2 into C57BL/6 mice, intraperitoneally administered G-CSF (30 micro/kg/day) with or without cisplatin (5 mg/kg), measured the tumor size and analyzed pathologically by HE and immunostaining. In vitro analyses, G-CSF showed no effects in LL-2 and KLN-205 cells, and RT- PCR revealed no G-CSF receptor mRNA. In vivo analyses, G-CSF alone did not significantly suppress tumor growth. However, concurrent G-CSF administration with cisplatin significantly enhanced the tumor suppressing effect of cisplatin in early stage of tumor growth. The analysis data of vWF immunostaining indicated that the neovascularization in the peripheral region of the tumors was more enhanced in G-CSF treatment mice. ELISA assay revealed that G-CSF did not influence the serum concentration of TNF-alpha and IL- 12 in tumor-bearing mice. This study suggests that concurrent (combination) administration of cisplatin with G-CSF is a safe and effective method for enhancing anticancer effects and reducing chemotherapeutic agent-induced myelosuppression.
Advances in Lung Cancer, Volume 6, pp 13-35; doi:10.4236/alc.2017.62002
Advances in Lung Cancer, Volume 4, pp 37-51; doi:10.4236/alc.2015.43006
Abstract:Cancer is one of the leading causes of death in America, and there is an urgent need for new therapeutic approaches. The progesterone receptor membrane component 1 (PGRMC1) is a cytoch-rome b5 related protein that binds heme and is associated with signaling, apoptotic suppression and autophagy. PGRMC1 is essential for tumor formation, invasion and metastasis, and is upregulated in breast, colon, lung and thyroid tumors. In the present study, we have analyzed PGRMC1 levels in over 600 tumor sections, including a larger cohort of lung tumors than in previous studies, and report the first clinical analysis of PGRMC1 levels in human oral cavity and ovarian tumors compared to corresponding nonmalignant tissues. PGRMC1 was highly expressed in lung and ovarian cancers and correlated with patient survival. PGRMC1 has been previously associated with drug resistance, a characteristic of cancer stem cells. The stem cell theory proposes that a subset of cancerous stem cells contribute to drug resistance and tumor maintenance, and PGRMC1 was detected in lung-tumor derived stem cells. Drug treatment with a PGRMC1 inhibitor, AG-205, triggered stem cell death whereas treatment with erlotinib and the ERK inhibitor, PD98059, did not, suggesting a specific role for PGRMC1 in cancer stem cell viability. Together, our data demonstrate PGRMC1 as a potential tumor biomarker across a variety of tumors, as well as a therapeutic target for cancer stem cells.
Advances in Lung Cancer, Volume 5, pp 1-12; doi:10.4236/alc.2016.51001
Advances in Lung Cancer, Volume 5, pp 21-29; doi:10.4236/alc.2016.53003
Advances in Lung Cancer, Volume 5, pp 30-38; doi:10.4236/alc.2016.53004