• Title/Summary/Keyword: Iressa$^{(R)}$

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A Case of Non-small Cell Lung Cancer Patient Whose Dermatologic Adverse Reactions Associated with the Epidermal Growth Factor Receptor-inhibitors were Relieved with the Treatment of a Herbal medicine, Samultang-gagambang (비소세포폐암 환자의 표피성장인자 수용체 억제제 치료와 관련된 피부의 이상반응이 사물탕 가감방 투여로 호전된 1례)

  • Park, Hyeong-Jun;Chae, Jean;Lee, Jin-Soo;Jung, Hyun-Sik;Lee, Sang-Hun;Choi, Won-Cheol;Kim, Kyung-Suk
    • Journal of Korean Traditional Oncology
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    • v.16 no.1
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    • pp.55-61
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    • 2011
  • Objectives : Epidermal growth factor receptor-inhibitors have demonstrated improved overall survival in patients with non-small cell lung cancer, but their use is associated with dermatologic adverse reactions that often require symptomatic treatment. Methods : A 44-year-old woman, who started the chemotherapy of Iressa$^{(R)}$ on August 2010, developed cutaneous symptoms such as papulopustular rash, dry skin, and pruritus on her face and scalp after taking Iressa$^{(R)}$ for four weeks. The patient visited our clinic with such symptoms on March 2011 and underwent herebal remedy targeted to alleviate the skin reactions. The severity of dermatologic symptoms was evaluated with the numeric rating scale and the Common Terminology Criteria for Adverse Events version 4.0. Results : Noticeable changes on the skin lesion were observed after the two months of treatment, without any dose modification of the Iressa$^{(R)}$. The cutaneous symptoms as papulopustular rash, dry skin and pruritus were improved and there was no adverse event induced by the treatment with herbal medicine. Conclusions : This case report suggests that the treatment with a herbal medicine, Samultang-gagambang be considered as a useful treatment to relieve EGFR-inhibitor induced dermatologic adverse reactions.

Novel Quinazoline Derivatives Targeting on EGFR Kinase Mediated Signal Pathway in A431 Human Epidermoid Carcinoma Cells (A431 피부암세포의 EGFR kinase 신호체계에 선택적으로 작용하는 새로운 퀴나졸린계 억제제)

  • Jeong, Chul-Woo;Son, Byeng-Wha;Ha, Jae-Du;Kim, Gun-Do
    • Journal of Life Science
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    • v.21 no.3
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    • pp.349-357
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    • 2011
  • Inhibitors of EGFR (epidermal growth factor receptor) kinase activity may prove useful to therapeutically intervene in cancer and to treat other proliferative diseases. In this study, we investigated the inhibitive effects of two compounds named 63013 and 63033 possess a [1,4]-dioxino quinazoline structure that links the alkoxy side chains together and their structural characteristics are considered to allow better solubility than the dialkoxyquinazoline derivatives. The EGFR kinase activities of A431 human epidermoid carcinoma cells, stimulated by EGF were inhibited by treatment with 63013 and 63033 in a dose-dependent manner respectively. Consistent with the compound-mediated EGFR kinase suppression, the major EGF-related downstream target molecules, such as MEK1/2, MAPK p44/42, AKT and STAT3, were also suppressed by both compounds. Interestingly, both compounds led to cell growth inhibition at a lower concentration than that of Gefitinib (Iressa$^{(R)}$). Collectively, our study showed that both compounds may have good therapeutic potential as an EGFR kinase specific inhibitor to treat EGFR-related diseases.

The Concurrent Use of Rhus verniciflua Stokes as Complementary Therapy with Second or More Line Regimens on Advanced Non-small-cell Lung Cancer: Case Series

  • Lee, Sang-Hun;Kim, Kyung-Suk;Choi, Won-Cheol;Yoon, Seong-Woo
    • The Journal of Korean Medicine
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    • v.30 no.6
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    • pp.112-117
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    • 2009
  • Objective: Rhus verniciflua Stokes (RVS) has anticancer effect confirmed by preclinical studies and historical records. We thus tried to evaluate retrospectively the effect of RVS as a complementary medicine for patients with advanced non-small-cell lung cancer (NSCLC) showing refractory to conventional chemotherapy. Patients and Methods: From June 1, 2006 to June 30, 2007, patients with advanced NSCLC who received both the standardized RVS extract and a standard course of second or more line therapy such as pemetrexed ($Alimta^{(R)}$), erlotinib ($Tarceva^{(R)}$), and gefitinib ($Iressa^{(R)}$) were checked. A total of 13 patients were eligible for the final analysis after fulfilling inclusion/exclusion criteria. Time to progression (TTP) of these patients treated with the standardized RVS extract was checked in the aftercare period. Results: Patients received RVS treatment for a median period of 296 (range 84-698) days. The median TTP was 220.5 (range 36-489) days, and three patients (23.1%) had TTP values of 15 more months. No significant side effects from RVS treatment have been observed. Conclusion: The standardized RVS extract might have synergetic effects by assisting apoptosis in advanced NSCLC with concurrent standard therapy agents, since it prolonged TTP without significant adverse effects. This study suggests that the standardized RVS extract is beneficial to patients with chemotherapy-refractory NSCLC. Further clinical trials and preclinical studies are necessary to determine the efficacy and safety of the standardized RVS extract in NSCLC.

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Enhancement of Sensitivity of Human Lung Cancer Cell Line to TRAIL and Gefitinib by IGF-1R Blockade (폐암세포주에서 IGF-1R 억제를 이용한 TRAIL 및 gefitinib에 대한 감수성 증가를 위한 연구)

  • Lee, Yoon-Jin;Park, Mi-Young;Kang, Young-Ae;Kwon, Sung-Youn;Yoon, Ho-Il;Lee, Jae-Ho;Lee, Choon-Taek
    • Tuberculosis and Respiratory Diseases
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    • v.63 no.1
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    • pp.42-51
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    • 2007
  • Background: TRAIL is a cytokine that selectively induces apoptosis in various cancer cell lines. Gefitinib is new targeted drug applied in lung cancer that selectively inhibits EGFR tyrosine kinase. However, lung cancers have shown an initial or acquired resistance to these drugs. This study examined the effect of IGF-1R and its blockade on enhancing the sensitivity of lung cancer cell lines to TRAIL and gefitinib. Methods: Two lung cancer cell lines were used in this study. NCI H460 is very sensitive to TRAIL and gefitinib. On the other hand, A549 shows moderate resistance to TRAIL and gefitinib. The IGF-1R blockade was performed using adenoviruses expressing the dominant negative IGF-1R and shRNA to IGF-1R and AG1024 (IGF-1R tyrosine kinase inhibitor). Results: The adenovirus expressing dominant negative IGF-1R(950st) induced the increased expression of defective IGF-1R on the lung cancer cell surface, and the adenovirus-shIGF-1R effectively decreased the level of IGF-1R expression on cell surface. The genetic blockade of IGF-1R by the adenovirus-dnIGF-1R and AG1024 increased the sensitivity of A549 cells to TRAIL. The reduction of IGF-1R by transduction with ad-shIGF-1R also increased the sensitivity of the A549 cells to gefitinib. Conclusion: The blockade of IGF-1R through various mechanisms increased the sensitivity of the lung cancer cell line that was resistant to TRAIL and gefitinib. However, further studies using other cell lines showing acquired resistance as well as in vivo animal experiments will be needed.