• Title/Summary/Keyword: Cancer progression

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Factors that Predict Clinical Benefit of EGFR TKI Therapy in Patients with EGFR Wild-Type Lung Adenocarcinoma

  • Kim, Seo Yun;Myung, Jae Kyung;Kim, Hye-Ryoun;Na, Im Il;Koh, Jae Soo;Baek, Hee Jong;Kim, Cheol Hyeon
    • Tuberculosis and Respiratory Diseases
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    • v.82 no.1
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    • pp.62-70
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    • 2019
  • Background: Epidermal growth factor receptor (EGFR) mutations in non-small cell lung cancers have emerged as key predictive biomarkers in EGFR tyrosine kinase inhibitor (TKI) treatment. However, a few patients with wild-type EGFR also respond to EGFR TKIs. This study investigated the factors predicting successful EGFR TKI treatment in lung adenocarcinoma patients with wild-type EGFR. Methods: We examined 66 patients diagnosed with lung adenocarcinoma carrying wide-type EGFR who were treated with EGFR TKIs. The EGFR gene copy number was assessed by silver in situ hybridization (SISH). We evaluated the clinical factors and EGFR gene copy numbers that are associated with a favorable clinical response to EGFR TKIs. Results: The objective response rate was 12.1%, while the disease control rate was 40.9%. EGFR SISH analysis was feasible in 23 cases. Twelve patients tested EGFR SISH-positive, and 11 were EGFR SISH-negative, with no significant difference in tumor response and survival between EGFR SISH-positive and -negative patients. The overall median progression-free survival (PFS) and overall survival (OS) of 66 patients were 2.1 months and 9.7 months, respectively. Female sex and Eastern Cooperative Oncology Group (ECOG) performance status (PS) of 0-1 were independent predictors of PFS. ECOG PS 0-1 and a low tumor burden of extrathoracic metastasis were independent predictors of good OS. Conclusion: Factors such as good PS, female sex, and low tumor burden may predict favorable outcomes following EGFR TKI therapy in patients with EGFR wild-type lung adenocarcinoma. However, EGFR gene copy number was not predictive of survival.

The clinical outcomes of second-line chemotherapy in patients with advanced pancreatic cancer: a retrospective study

  • Jung, Hyun yeb;Lee, Eun Mi
    • Journal of Yeungnam Medical Science
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    • v.39 no.2
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    • pp.124-132
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    • 2022
  • Background: Despite recent advances in first-line chemotherapy for advanced pancreatic cancer, standard treatment after the failure of initial chemotherapy has not been established. Hence, we aimed to retrospectively analyze the clinical characteristics and outcomes of second-line chemotherapy in patients with advanced pancreatic cancer. Methods: We reviewed the clinical data of patients with advanced pancreatic cancer who underwent palliative chemotherapy at Kosin University Gospel Hospital between January 2013 and October 2020. Results: Among 366 patients with advanced pancreatic cancer who had received palliative chemotherapy, 104 (28.4%) underwent at least one cycle of second-line chemotherapy. The median age of the patients at the time of initiating second-line treatment was 62 years (interquartile range, 57-62 years), and 58.7% (61 patients) of them were male. The common second-line chemotherapy regimens were 5-fluorouracil (FU) plus leucovorin, irinotecan, and oxaliplatin (33 patients, 31.7%); gemcitabine/nab-paclitaxel (29, 27.9%), gemcitabine±erlotinib (13, 12.5%); and oxaliplatin and 5-FU/leucovorin (12, 11.5%). The median overall survival (OS) and progression-free survival were 6.4 months (95% confidence interval [CI], 4.5-8.6 months) and 4.5 months (95% CI, 2.7-6.3 months), respectively. In a multivariate analysis, poor performance status (PS) (hazard ratio [HR], 2.247; p=0.021), metastatic disease (HR, 2.745; p=0.011), and elevated carcinoembryonic antigen (CEA) levels (HR, 1.939; p=0.030) at the beginning of second-line chemotherapy were associated with poor OS. Conclusion: The survival outcome of second-line chemotherapy for advanced pancreatic cancer remains poor. However, PS, disease extent (locally advanced or metastatic), and CEA level may help determine patients who could benefit from second-line treatment.

Association between the Interleukin-17A -197G>A (rs2275913) Polymorphism and Risk of Digestive Cancer

  • Duan, Yin;Shi, Ji-Nan;Pan, Chi;Chen, Hai-Long;Zhang, Su-Zhan
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.21
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    • pp.9295-9300
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    • 2014
  • Interleukin-17A (IL-17A) is a multifunctional cytokine which plays a crucial role in the initiation and progression of cancer. To date, several studies have investigated associations between IL-17A -197G>A (rs2275913) polymorphism and digestive cancer risk, but the results remain conflicting. We here aimed to confirm the role of this single nucleotide polymorphism (SNP) in susceptibility to digestive cancer through a systemic review and meta-analysis. Ten eligible case-control studies were identified by searching electronic databases, involving 3,087 cases and 3,815 controls. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were used to estimate the strength of the association. The results of overall analyses indicated that the variant A allele was associated with an increased risk of digestive cancer (AA vs GG: OR=1.51, 95%CI=1.18-1.93; AA vs GG+GA: OR=1.45, 95%CI=1.12-1.87; A vs G: OR=1.21, 95%CI=1.05-1.39). In subgroup analysis stratified by specific cancer type, elevated risk among studies of gastric cancer was found (AA vs GG: OR=1.68, 95%CI=1.24-2.28; AA vs GG+GA: OR=1.62, 95%CI=1.16-2.26; A vs G: OR=1.23, 95%CI=1.04-1.46). According to ethnicity, there was evidence in the Asian populations for an association between this polymorphism and cancer risk (GA vs GG: OR=1.19, 95%CI=1.05-1.36; AA vs GG: OR=1.56, 95%CI=1.15-2.12; AA+GA vs GG: OR=1.28, 95%CI=1.13-1.44; AA vs GG+GA: OR=1.42, 95%CI=1.01-2.00; A vs G: OR=1.24, 95%CI=1.08-1.44), while in the Caucasian populations an association was found in the recessive model (AA vs GG+GA: OR=1.62, 95%CI=1.17-2.24). In conclusion, the results of this meta-analysis suggest that the IL-17A -197G>A polymorphism contributes to an increased risk of human digestive cancer, both in the Asian and Caucasian populations and especially for gastric cancer.

Model for Cancer Cachexia using C26 Adenocarcinoma-Induced Wasting Syndrome for Newer Therapeutic Approach (새로운 치료 방법 접근을 위한 C26 선암세포 기반의 Cancer Cachexia 동물모델 수립)

  • Eun A Kang;Jong Min Park;Young Min Han;Sung Pyo Hong;Joo Young Cho;In Kyung Yoo;Ji Young Oh;Ki Baik Hahm
    • Journal of Digestive Cancer Research
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    • v.5 no.2
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    • pp.97-104
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    • 2017
  • Background: Cachexia is a multi-factorial syndrome presenting with chronic illness, decreases in body weight, and loss of adipose tissue and skeletal muscle, mostly in patients with advanced cancer and chronic wasting disease. Even after years of intensive researches, there remains no convincing therapy to prevent cancer cachexia. Methods: In this in vivo study, we have established C26 adenocarcinoma-induced cancer cachexia model in mice to explore the underlying core changes in cytokine, signal transduction, and muscle wasting. The ultimate aim of establishing animal model is to find optimal therapeutics to mitigate cancer cachexia. Results: We have administered C26 adenocarcinoma cells onto BALB/c mice and observed 4 weeks to assess the progression of cancer cachexia. Significant loss of weight accompanied with loss of appetite was noted. As C26 adenocarcinoma xenograft progressed, mortality was started from 3 weeks, accompanied with significant sarcopenia and decreased mice movement. Surges in TNF-α and IL-6 were noted with the commencement of cancer cachexia. Conclusion: Using C26 adenocarcinoma cancer cachexia model, we can screen the optimal therapeutics to mitigate cancer cachexia, in which agents to modulate IL-6, TNF-α, and NF-κB were essential.

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Weight Loss Correlates with Macrophage Inhibitory Cytokine-1 Expression and Might Influence Outcome in Patients with Advanced Esophageal Squamous Cell Carcinoma

  • Lu, Zhi-Hao;Yang, Li;Yu, Jing-Wei;Lu, Ming;Li, Jian;Zhou, Jun;Wang, Xi-Cheng;Gong, Ji-Fang;Gao, Jing;Zhang, Xiao-Tian;Li, Jie;Li, Yan;Shen, Lin
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.15
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    • pp.6047-6052
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    • 2014
  • Background: Weight loss during chemotherapy has not been exclusively investigated. Macrophage inhibitory cytokine-1 (MIC-1) might play a role in its etiology. Here, we investigated the prognostic value of weight loss before chemotherapy and its relationship with MIC-1 concentration and its occurrence during chemotherapy in patients with advanced esophageal squamous cell carcinoma (ESCC). Materials and Methods: We analyzed 157 inoperable locally advanced or metastatic ESCC patients receiving first-line chemotherapy. Serum MIC-1 concentrations were assessed before chemotherapy. Patients were assigned into two groups according to their weight loss before or during chemotherapy:>5% weight loss group and ${\leq}5%$ weight loss group. Results: Patients with weight loss>5% before chemotherapy had shorter progression-free survival period (5.8 months vs. 8.7 months; p=0.027) and overall survival (10.8 months vs. 20.0 months; p=0.010). Patients with weight loss >5% during chemotherapy tended to have shorter progression-free survival (6.0 months vs. 8.1 months; p=0.062) and overall survival (8.6 months vs. 18.0 months; p=0.022), and if weight loss was reversed during chemotherapy, survival rates improved. Furthermore, serum MIC-1 concentration was closely related to weight loss before chemotherapy (p=0.001) Conclusions: Weight loss both before and during chemotherapy predicted poor outcome in advanced ESCC patients, and MIC-1 might be involved in the development of weight loss in such patients.

Efficacy of Taxane-Based Regimens in a First-line Setting for Recurrent and/or Metastatic Chinese Patients with Esophageal Cancer

  • Jiang, Chang;Liao, Fang-Xin;Rong, Yu-Ming;Yang, Qiong;Yin, Chen-Xi;He, Wen-Zhuo;Cai, Xiu-Yu;Guo, Gui-Fang;Qiu, Hui-Juan;Chen, Xu-Xian;Zhang, Bei;Xia, Liang-Ping
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.13
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    • pp.5493-5498
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    • 2014
  • Objective: To compare the efficacy of taxane-based regimens in the first line setting retrospectively in Chinese patients with recurrent and/or metastatic esophageal cancer. Methods: We analyzed 102 recurrent and/or metastatic esophageal cancer patients who received taxanes-based regimens in a first-line setting from January 2009 to December 2013. Sixteen (15.7%) patients were administered Nab-PTX based chemotherapy and 86 patients (84.3%) received paclitaxel (PTX) or docetaxel (DTX) based chemotherapy. Patients in the PTX/DTX group could be further divided into TP (71 patients) and TPF (15 patients) groups. Results: The objective response rate (ORR) of all patients was 20.6%, and the disease control rate (DCR) was 67.6%. The median overall survival (OS) was 10.5 months (95% CI 10.1-16.4) and the median progression-free survival (PFS) was 6.04 months (95% CI 5.09-7.91). The DCR was higher in the TPF group than the TP group (93.3% vs. 59.1%; p = 0.015 ). There were no significant differences in ORR, OS, and PFS among Nab-PTX, TPF and TP groups. Conclusions: The three regimens of Nab-PTX based, TP and TPF proved active in a first line setting of Chinese patients with recurrent and/or metastatic esophageal cancer, and should thus be regarded as alternative treatments.

Efficacy and Toxicity of Sunitinib in Metastatic Renal Cell Carcinoma Patients in Egypt

  • Edesa, Wael Abdelgawad;Abdelmalek, Raafat Ragaey
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.5
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    • pp.1971-1976
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    • 2015
  • Background: To evaluate our results in terms of response, survival and toxicity profile of sunitinib among Egyptian patients with metastatic renal cell carcinoma. Materials and Methods: Between January 2010 and December 2013, 44 patients with metastatic renal cell carcinoma who received sunitinib at an oncology center of Cairo university hospitals were enrolled in this retrospective analysis. Results: The median age of the patients was 53 years, 22 (50%) having localized disease at presentation, while the remaining half of the patients presented with metastasis. At a median follow up of 19 months, 9 (21%) patients achieved partial remission, while disease was reported stable in 20 cases (45%) and progressive in 7 (16%), 4 (9%) being lost to follow up, and 4 (9%) had discontinued therapy due to toxicity. The median overall survival was 23 months (95%CI 15.2 - 30.9), while progression free survival was 12 months (95%CI 11.6 - 12.3). The most commonly reported non hematological grade 3 adverse events included mucositis (15.9%), hand-foot syndrome (13.6%), and fatigue (9%), while the predominant grade 3 or 4 laboratory abnormalities were neutropenia (6.8%), followed by anemia in 4.5% of patients. Conclusions: Our efficacy data were comparable to the published literature in terms of progression free survival and overall survival, while toxicity profile is different from Asian and western countries. However, sunitinib adverse events were manageable and tolerable in most of our Egyptian patients.

Psycho-oncology : A Historical Review (정신종양학의 역사와 개관)

  • Lee, Chul
    • Korean Journal of Psychosomatic Medicine
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    • v.2 no.1
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    • pp.3-9
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    • 1994
  • The psychobiological model of cancer has a long history, with Galen's view on melancholic woman being often quoted. From a historical perspective, the 1950s witnessed a surge of interest in psychosomatic medicine and in researches linking psychological, social, and environmental factors to disease onset and progression. The 1960s witnessed the growth of animal experiements, in the hope of better understanding the effects of psychological and behavioral factors on carcinogenesis while controlling confounding variables. The 1970s saw rapid advances in immunology and neurochemistry. Further researches in the 1980s in psychoneuroimmunology explored relationships between immunological responses and psychosocial variables, and their implications for cancer vulnerability and progression. In this review, the interacting aspects of oncology and psychiatry are presented with selected major findings in the fold of psychooncology researches.

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Development and Characterization of a Specific Anti-Caveolin-1 Antibody for Caveolin-1 Functional Study in Human, Goat and Mouse

  • Ke, Meng-Wei;Jiang, Yan-Nian;Li, Yi-Hung;Tseng, Ting-Yu;Kung, Ming-Shung;Huang, Chiun-Sheng;Cheng, Winston Teng-Kuei;Hsu, Jih-Tay;Ju, Yu-Ten
    • Asian-Australasian Journal of Animal Sciences
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    • v.20 no.6
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    • pp.856-865
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    • 2007
  • Caveolin-1 of the caveolin family of proteins regulates mammary gland development and has been shown to play a contradictory role in breast tumor progression. A specific anti-Caveolin-1 antibody will be useful for functional study of Caveolin-1 in different tissues. In this study, we generated a rabbit polyclonal antibody that specifically recognizes the N-terminal amino acids 50-65 of Caveolin-1. This polyclonal antibody specifically reacted with Caveolin-1 extracted from cells of different species, including human epithelial A431 cells, goat primary mammary epithelial cells and mice fibroblast NIH 3T3 cells, by Western blotting. Endogenous Caveolin-1 protein expressing in cells and normal human tissues was detected by this polyclonal antibody using immunocytofluorescent and immunohistochemical staining, respectively. Furthermore, an apparent decrease in Caveolin-1 expression in tumorous breast and colon tissues was detected by this polyclonal antibody. In conclusion, we have identified amino acids 50-65 of Caveolin-1, which contains an epitope that is specific to Caveolin-1 and is conserved in the human, goat and mouse. In future, this anti-Caveolin-1 antibody can be used to examine the progression of breast and colon cancers and to study functions of Caveolin-1 in human, goat and mouse cells.