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随着肺癌发病机制研究的深入,靶向治疗在NSCLC治疗中的地位日渐重要.其中,以厄洛替尼和吉非替尼为代表的表皮生长因子受体酪氨酸激酶抑制剂(epidermal growth factor receptor tyrosine kinase inhibitor,EGFR TKI)的靶向药物取得了一定的疗效. 相似文献
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表皮生长因子受体(epidermal growth factor receptor,EGFR)酪氨酸激酶抑制剂--厄洛替尼,可有效治疗含有EGFR突变的非小细胞肺癌(non-small cell lung cancer,NSCLC),然而,分子靶向药物疗效维持时间较短,几乎所有起初治疗有效的患者最终均会复发,提示对此类药物产生耐药. 相似文献
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人表皮生长因子受体2(HER2)在20%~30%的乳腺癌患者中过表达.针对HER2的分子靶向治疗可从分子水平抑制乳腺癌细胞生长.目前乳腺癌的分子靶向治疗药物主要有作用于HER2的单克隆抗体和酪氨酸激酶抑制剂两类.曲妥珠单抗已临床用于治疗HER2阳性的转移性乳腺癌,对HER2阳性的早期乳腺癌也有一定疗效.拉帕替尼对难治性乳腺癌和乳腺癌脑转移的治疗有很大潜力.该类药物在乳腺癌治疗领域中存在着巨大潜力. 相似文献
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随着分子靶向治疗药物的发展,以吉非替尼(gefitinib,iressa)和厄洛替尼(erlotinib,tarceva)为代表的表皮生长因子受体酪氨酸激酶抑制剂(epidermal growth factor receptor-tyrosine kinases inhibitors,EGFR-TKIs)在治疗非小细胞肺癌中发挥了重要作用。然而在临床前和临床研究中发现许多患者对此药物存在原发性耐药或获得性耐药,使该类药物的使用受到一定限制。本文就近年来对EGFR-TKIs耐药机制的研究进展进行综述。 相似文献
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胃肠道间质瘤靶向治疗新进展 总被引:1,自引:0,他引:1
胃肠道间质瘤(GIST)是最常见的间叶组织源性肿瘤,分子生物学研究已揭示了其发病机制与KIT和PDGFRA基因突变有关。目前,GIST步入了手术及靶向治疗联合的时代,选择性酪氨酸激酶抑制剂伊马替尼等药物已应用于GIST的靶向治疗,干扰肿瘤发展的特定分子环节以延缓肿瘤的进展,并且取得较为理想的疗效,GIST已逐渐成为肿瘤分子靶向治疗的典型。 相似文献
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抗EGFR靶向治疗胃癌 总被引:1,自引:0,他引:1
EGFR家族在胃癌形成中具有重要的作用.针对EGFR的分子靶向药物主要包括胞外单克隆抗体和胞内酪氨酸激酶抑制剂,许多新药如曲妥珠单抗、西妥昔单抗、帕尼单抗、拉帕替尼,已进入胃癌治疗的Ⅲ期临床研究阶段,而ToGA研究结果更给晚期胃癌患者带来希望. 相似文献
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Signal transduction inhibitor 总被引:1,自引:0,他引:1
Numerous molecular targets for cancer chemotherapy have been identified based on the progress made in molecular biology, and new categories of anticancer drugs have been developed. They are variously called target-based drugs, non-cytotoxic drugs and cytostatic drugs. These include inhibitors of signal transduction, cyclin-dependent kinase, angiogenesis, and matrix metalloproteinases. Other new therapies include gene therapy and immunotherapy. There are multiple steps in the signal transduction cascade. Growth factor binds to its cognate receptor tyrosine kinase and the phosphotyrosines on the receptor serve as attachment sites for substrates or adapter molecules. Grb2 functions by directly coupling activated receptor tyrosine kinases to the Ras-activating nucleotide exchange factor SOS. Activation of Ras or Ras family members leads to activation of the mitogen-activated protein kinase (MAPK) cascade pathway. This has been implicated as a necessary component of intracellular signaling to elicit a range of cellular responses including mitogenesis, differentiation, and cell survival. We introduce signal transduction inhibitors including, Ras inhibitors, protein kinase C inhibitors, and MAPK cascade inhibitors. Recently, these drugs have been used in clinical trials and some of them have an antitumor effect. In the near future these drugs may play an important role in cancer chemotherapy. However, these drugs are thought to induce a non-cytotoxic effect different from cytotoxic drugs. Therefore correct and efficient clinical evaluation of these drugs is needed. We look forward to developments from future research on signal transduction inhibitors. 相似文献
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Cortes J Kantarjian H 《Journal of the National Comprehensive Cancer Network : JNCCN》2008,6(Z2):S22-S30
The development of imatinib has changed the management of chronic myeloid leukemia (CML), producing high response rates in most patients. However, most individuals treated with imatinib, 400 mg, have residual molecular disease, and both intrinsic and acquired resistance can occur. The newer tyrosine kinase inhibitors, dasatinib and nilotinib, are effective in patients with imatinib-resistant CML, In patients with relapse or resistance, current guidelines recommend escalating the dose of imatinib or switching to new tyrosine kinase inhibitors. Dasatinib has been investigated in patients who were resistant or intolerant to imatinib. Switching to dasatinib, 70 mg, twice daily has been shown to be more effective than high-dose imatinib. Another study found that dasatinib, 100 mg, once daily was just as effective as the twice-daily regimen but was better tolerated. Nilotinib is also effective in most patients with resistance or intolerance to imatinib and is associated with minimal toxicity. Other inhibitors, such as bosutinib and INNO-406, are being developed with favorable early results. New drugs are still needed, particularly for individuals who are resistant to tyrosine kinase inhibitors or those with the T3151 mutation. Emerging CML therapies, some of which have different mechanisms of action from those of tyrosine kinase inhibitors, have shown promising results and could offer an alternative to these patients as monotherapy or in combination. 相似文献
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Leow Pay Chin Ross A. Soo Richie Soong Sai-Hong I. Ou 《Journal of thoracic oncology》2012,7(11):1625-1630
Chromosomal rearrangements involving the ROS1 receptor tyrosine kinase have been described in a variety of human malignancies including non–small-cell lung cancer (NSCLC), cholangiocarcinoma and glioblastoma multiforme. Recently, clinicopathologic characteristics of c-ros oncogene 1, receptor tyrosine kinase (ROS1)-rearranged NSCLC patients have been described. Furthermore, anaplastic lymphoma kinase inhibitor, novel class of drugs targeting this tyrosine kinase receptor is currently under clinical trial in this molecular subset of NSCLC patients. This review will focus on the current knowledge of ROS1 rearrangements in NSCLC, methods to detect ROS1 rearrangement, and targeting ROS1-rearranged NSCLC patients with anaplastic lymphoma kinase inhibitors. 相似文献
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难治性白血病诊治进展 总被引:2,自引:0,他引:2
难治性白血病因其本身特性难达完全缓解和长期无病生存,始终是恶性血液病领域研究的热点和难点,国内外关于难治性白血病的诊断标准在不断调整,引起白血病难治高危的因素也在不断的被发现;新的分子标志,基因突变或某些基因高表达,如FLT3 跨膜区内部串联重复等,这些分子标志将决定急性白血病患者的预后。治疗难治性或复发性急性髓细胞性白血病仍然具有挑战性。多种新药正在开发和临床试验。临床许多新的治疗方法正在探讨。如应用耐药逆转剂、加强分子靶向治疗、改进造血干细胞移植和开发新药、组成新的化疗方案等;单克隆抗体和多肽疫苗与白血病相关抗原为治愈急性白血病带来了希望。 相似文献
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Gulden Menderes Jonathan Black Carlton L. Schwab 《Expert review of anticancer therapy》2016,16(1):83-98
The prognosis of patients with metastatic cervical cancer is poor with a median survival of 8–13 months. Despite the potency of chemotherapeutic drugs, this treatment is rarely curative and should be considered palliative only. In the last few years, a better understanding of Human papillomavirus tumor-host immune system interactions and the development of new therapeutics targeting immune check points have renewed interest in the use of immunotherapy in cervical cancer patients. Moreover, next generation sequencing has emerged as an attractive option for the identification of actionable driver mutations and other markers. In this review, we provide background information on the molecular biology of cervical cancer and summarize immunotherapy studies, targeted therapies, including those with angiogenesis inhibitors and tyrosine kinase inhibitors recently completed or currently on-going in cervical cancer patients. 相似文献
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Pajares B Torres E Trigo JM Sáez MI Ribelles N Jiménez B Alba E 《Clinical & translational oncology》2012,14(2):94-101
The adverse effects associated to traditional chemotherapy are well known and broadly studied. In the recent years several
tyrosine kinase inhibitors have been approved for cancer treatment and numerous are under investigation. These drugs target
specific mutated/overexpressed tyrosin kinase receptors and frecuently their pharmacokinetic/pharmacodinamic behavior is not
fully elucidated. These new drugs may interact with non-antineoplastic drugs leading to undesirable adverse effects. In this
article, we will discuss different types of drug interactions and briefly review the pharmacokinetics and mechanisms of action
of tyrosine kinase inhibitors in clinical use, with a particular emphasis on the risk of the occurrence of such interactions
based on currently available scientific evidence. 相似文献
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Reinmuth N Meister M Muley T Steins M Kreuter M Herth FJ Hoffmann H Dienemann H Thomas M 《International journal of cancer. Journal international du cancer》2006,119(4):727-734
Receptor tyrosine kinases (RTKs) are essential components of the cellular signaling apparatus and are often mutated or otherwise deregulated in nonsmall cell lung cancer (NSCLC). These receptors are not solely expressed by cancer cells but also by multiple other cell types, including stromal cells that, in turn, may modulate cancer cell functions by various direct and indirect interactions. Recently, clinical studies have successfully evaluated the inhibition of RTKs by specific RTK-targeting agents, including tyrosine kinase inhibitors (TKIs). Although the response was impressive in some studies, only a limited proportion of patients benefit from these new drugs. Therefore, an intensive search for markers has started to determine which patients and tumor types are most likely to respond favorably to this new kind of treatment. Considerable attention has been focused onto molecular changes in cancer cells such as receptor expression, gene amplification, changes in intracellular signaling and receptor mutations. In this article, we explore the current data regarding molecular alterations as surrogate markers of response to specific RTK-targeting agents in NSCLC. Defined alterations may serve as key markers helping to preselect NSCLC patients for an individualized therapeutic approach in the future. 相似文献