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ORIGINAL ARTICLE |
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Year : 2016 | Volume
: 12
| Issue : 8 | Page : 295-297 |
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Gefitinib single drug in treatment of advanced esophageal cancer
Yingjun Xu, Zhihui Xie, Yan Shi, Mengwei Zhang, Jia Pan, Yanming Li, Hong Lu
Department of Oncology, Huaihe Hospital of Henan University, Kaifeng, Henan, P.R. China
Date of Web Publication | 22-Feb-2017 |
Correspondence Address: Hong Lu Department of Oncology, Huaihe Hospital of Henan University, Kaifeng 475000, Henan P.R. China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0973-1482.200760
Objective: The objective of this study is to evaluate the clinical efficacy and toxicity of gefitinib single drug in treatment of advanced esophageal cancer. Materials and Methods: Forty-one case of advanced esophageal cancer were included from February 2012 to June 2016 in the Department of Oncology, Huaihe Hospital of Henan University. All of the included 41 cases were pathology or cytology confirmed of esophageal cancer with advanced stage with previously chemotherapy regimen of cisplatin or fluorouracil. The patients received gefitinib 250 mg/day orally until disease progression or development of unbearable drug-related toxicity. The objective response rate, overall survival, disease-free survival, and drug-related toxicity were recorded. Results: All of the 41 cases had evaluable lesions with complete response rate of 0.0% (0/41), partial response rate of 4.9% (2/41), stable disease rate of 34.1% (14/41), and progression disease rate of 61.0% (25/41). The objective response rate and disease control rate were 4.9% (2/41) and 39.0% (25/41), respectively. At the follow-up, end-point of October 2016, we observed 33 death of the included 41 patients with median disease progression time of 2.2 months and median survival time of 6.1 months; most of the drug-related toxicity was Grade 1–3 nonhematological toxicity with the incidence of Grade 1–2 rash of 51.2% (21/41), Grade 3–4 rash of 17.1% (7/41), Grade 1–2 diarrhea of 26.8% (11/41), Grade 3–4 diarrhea of 7.3% (3/41), Grade 1–2 nausea and vomiting of 14.6% (6/41). Conclusion: Gefitinib can improve the survival rate and quality of life in patients with advanced stage esophageal cancer who failed for first-line chemotherapy. Keywords: Clinical efficacy, esophageal cancer, gefitinib, prognosis, toxicity
How to cite this article: Xu Y, Xie Z, Shi Y, Zhang M, Pan J, Li Y, Lu H. Gefitinib single drug in treatment of advanced esophageal cancer. J Can Res Ther 2016;12, Suppl S4:295-7 |
Yingjun Xu and Zhihui Xie contributed equally to this work.
> Introduction | |  |
Gefitinib is an epidermal growth factor receptor (EGFR) inhibitor, which interrupts signaling through the EGFR in target cells.[1] Therefore, it is only effective in cancers with mutated and overactive EGFR.[2] Many studies have proved that gefitinib can significant improve the survival of nonsmall cell lung cancer patients with mutated EGFR. However, whether gefitinib is effective for esophageal cancer is unknown and seldom reported.[3],[4],[5] In our present study, we analyzed 41 cases of advanced esophageal cancer with previously chemotherapy regimen of cisplatin or fluorouracil to evaluate the clinical efficacy and drug-related toxicity of gefitinib.
> Materials and Methods | |  |
Patients information
Forty-one case of advanced esophageal cancer were included from February 2012 to June 2016 in the Department of Oncology, Huaihe Hospital of Henan University. All of the included 41 cases were pathology or cytology confirmed of esophageal cancer with advanced stage with previously chemotherapy regimen of cisplatin or fluorouracil. All of the patients had evaluable lesions. For the included 41 cases, there were 22 poor differentiated squamous cell carcinoma, 9 moderate differentiated squamous cell carcinoma, and 10 cases of well-differentiated squamous cell carcinoma. The mean age of the 41 patients was 59.6 ± 12.6 (36–78) year old with 33 male and 8 female.
Treatment
The patients received gefitinib 250 mg/day orally until disease progression or development of unbearable drug-related toxicity.
Clinical evaluation
The treatment response was evaluated according to Response Evaluation Criteria In Solid Tumors criteria.[6] Complete response: disappearance of all target lesions; partial response (PR): at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD; stable disease (SD): neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease (PD), taking as reference the smallest sum LD since the treatment started; PD: at least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions.
Statistical analysis
The measured data were expressed by x̄ ± s. The enumeration data were expressed by ratio. SPSS 16.0 software (http://www-01.ibm.com/software/analytics/spss/) was used for all statistical analyses in this study.
> Results | |  |
Objective response rate
All of the 41 cases had evaluable lesions with compete response rate of 0.0% (0/41), PR rate of 4.9% (2/41), SD rate of 34.1% (14/41), and progression disease rate of 61.0% (25/41). The objective response rate and disease control rate were 4.9% (2/41) and 39.0% (25/41), respectively.
Survival
At the follow-up end-point of October 2016, we observed 33 death of the included 41 patients with median disease progression time of 2.2 months and median survival time of 6.1 months.
Drug-related toxicity
Most of the drug-related toxicity was Grade 1–3 nonhematological toxicity with the incidence of Grade 1–2 rash of 51.2% (21/41), Grade 3–4 rash of 17.1% (7/41), Grade 1–2 diarrhea of 26.8% (11/41), Grade 3–4 diarrhea of 7.3% (3/41), Grade 1–2 nausea and vomiting of 14.6% (6/41) [Table 1].
> Discussion | |  |
Esophageal cancer is an aggressive disease with poor prognosis. It is one of the most diagnosed malignant carcinoma in the world.[7] Operation is the only treatment for cure. However, most of the patients are at advanced stage for lack of specific symptoms in early, losing the chance of curative resection. For these advanced patients, chemoradiotherapy is major treatment method for control disease progression.[8],[9] Platinum or fluorouracil-containing chemotherapy was generally used for advanced stage esophageal cancer patients. However, the general objective response rate for chemotherapy is <30%. For patients with failure first-line chemotherapy, there was no standard second-line chemotherapy treatment modality. Gefitinib is an EGFR inhibitor, which interrupts signaling through the EGFR in cancer cells. Therefore, it is only effective in cancers with mutated and overactive EGFR. Many studies have proved that gefitinib can significant improve the survival of nonsmall cell lung cancer patients with mutated EGFR.[4],[5] However, seldom studies have reported the efficacy of gefitinib in the treatment of advanced esophageal cancer.[10] In this study, we analyzed 41 cases of advanced esophageal cancer with previously chemotherapy regimen of cisplatin or fluorouracil to evaluate the clinical efficacy and drug-related toxicity of gefitinib. We found the complete response rate, PR rate, SD rate, and progression disease rate were 0.0%, 4.9%, 34.1%, and 61.0%, respectively, with the objective response rate and disease control rate were 4.9% (2/41) and 39.0% (25/41). For prognosis evaluation, the median disease progression time was 2.2 months and median survival time was 6.1 months. These results were superior to best supportive care. For drug-related toxicity, most of the drug-related toxicity was Grade 1–3 nonhematological toxicity. The results indicated that gefitinib can improve the survival rate and quality of life in patients with advanced stage esophageal cancer who failed for first-line chemotherapy. However, the conclusion needs further confirmed by clinical randomized controlled trials or high-quality meta-analysis.
This work was supported by science and technology project of Henan Province (No. 11210231009).
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
> References | |  |
1. | Ono M, Kuwano M. Molecular mechanisms of epidermal growth factor receptor (EGFR) activation and response to gefitinib and other EGFR-targeting drugs. Clin Cancer Res 2006;12:7242-51. |
2. | Tartarone A, Lazzari C, Lerose R, Conteduca V, Improta G, Zupa A, et al. Mechanisms of resistance to EGFR tyrosine kinase inhibitors gefitinib/erlotinib and to ALK inhibitor crizotinib. Lung Cancer 2013;81:328-36. |
3. | Watanabe S, Inoue A, Nukiwa T, Kobayashi K. Comparison of Gefitinib Versus Chemotherapy in Patients with Non-small Cell Lung Cancer with Exon 19 Deletion. Anticancer Res 2015;35:6957-61. |
4. | Soria JC, Wu YL, Nakagawa K, Kim SW, Yang JJ, Ahn MJ, et al. Gefitinib plus chemotherapy versus placebo plus chemotherapy in EGFR-mutation-positive non-small-cell lung cancer after progression on first-line gefitinib (IMPRESS): A phase 3 randomised trial. Lancet Oncol 2015;16:990-8. |
5. | Yu H, Zhang J, Wu X, Luo Z, Wang H, Sun S, et al. A phase II randomized trial evaluating gefitinib intercalated with pemetrexed/platinum chemotherapy or pemetrexed/platinum chemotherapy alone in unselected patients with advanced non-squamous non-small cell lung cancer. Cancer Biol Ther 2014;15:832-9. |
6. | Yanagawa M, Tatsumi M, Miyata H, Morii E, Tomiyama N, Watabe T, et al. Evaluation of response to neoadjuvant chemotherapy for esophageal cancer: PET response criteria in solid tumors versus response evaluation criteria in solid tumors. J Nucl Med 2012;53:872-80. |
7. | Siegel RL, Miller KD, Jemal A. Cancer statistics, 2016. CA Cancer J Clin 2016;66:7-30. |
8. | D'Journo XB, Thomas PA. Current management of esophageal cancer. J Thorac Dis 2014;6 Suppl 2:S253-64. |
9. | Keditsu KK, Jiwnani S, Karimundackal G, Pramesh CS. Multimodality management of esophageal cancer. Indian J Surg Oncol 2013;4:96-104. |
10. | Sohal DP, Rice TW, Rybicki LA, Rodriguez CP, Videtic GM, Saxton JP, et al. Gefitinib in definitive management of esophageal or gastroesophageal junction cancer: A retrospective analysis of two clinical trials. Dis Esophagus 2015;28:547-51. |
[Table 1]
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