Advances in Cancer Therapy: Targeted Therapies

伊马替尼 主旨 髓系白血病 酪氨酸激酶 癌症研究 甲磺酸伊马替尼 癌症 酪氨酸激酶抑制剂 达沙替尼 靶向治疗 阿布勒 医学 受体酪氨酸激酶 间质细胞 内科学 受体
作者
Dieter Marmé
出处
期刊:Oncology Research and Treatment [Karger Publishers]
卷期号:39 (12): 758-759 被引量:3
标识
DOI:10.1159/000453340
摘要

As we learned to understand many of the mechanisms which drive cancer development and progression, a paradigmatic change for new treatment options occurred. Instead of focusing mostly on unspecific cytotoxic therapeutics, new substances directed against cancer-driving molecules made their way to the clinic. The idea behind this concept of ‘targeted cancer therapies' is quite simple: if we are able to bring cancer-driving molecules under control, we might be able to stop cancer development and progression. An outstanding example confirming this hypothesis is the successful treatment of chronic myeloid leukemia (CML) with imatinib. This treatment works so perfectly because the underlying genetic alteration of CML is a chromosomal translocation that leads to a constitutive activation of the BCL-Abl tyrosine kinase - imatinib inhibits its activity.Interestingly, after the successful use of imatinib against CML, it was found that the same compound could also be applied to treat gastrointestinal stromal tumors (GIST). Here again, the explanation is rather simple: imatinib not only inhibits the BCL-Abl-tyrosine kinase (one of about 500 protein kinases coded in the human genome), but also the c-KIT tyrosine kinase, which is mutated and activated in GIST. Furthermore in about 5-7% of GIST patients, the platelet-derived growth factor receptor alpha (PDGFRA) is mutated and activated. Its activity is also inhibited by imatinib. This explains to some degree the successful use of imatinib in the treatment of GIST.What does the imatinib story tell us? (i) ‘Targeted therapy' does work effectively (CML); (ii) a targeting compound does not necessarily have to be extremely specific. In the case of GIST, imatinib modulates the activity of 2 tumor-driving mutated protein kinases: BCL-Abl tyrosine kinase and PDGFRA tyrosine kinase. (iii) Activated protein kinases are often involved in tumor development and thus are potential targets for treatment.However, most tumors have a much more complex etiology than CML. Over time, sometimes over decades, they progress by accumulating many mutations, occurring in so-called oncogenes and/or tumor suppressor genes. This process results in progression of the disease and formation of metastases. This process (the types of mutations and their temporal occurrence) differs from tumor type to tumor type. Furthermore, within a given tumor entity, this process also differs from patient to patient. Thus, at present we are faced with quite a number of problems, which have to be solved in order to proceed with the development of ‘targeted therapies': - Identification of the molecular identities of tumor-driving mechanisms and their validation as ‘therapeutic targets'. In this area considerable progress has been made over the last years. - Diagnostic verification of the presence of therapeutic targets in the tumor of each individual patient. This gives us the necessary information as a prerequisite for ‘personalized cancer therapy'. Molecular pathology has successfully developed novel technologies, i.e. molecular and histological methods, such as next-generation sequencing or semi-quantitative immuno-histochemistry. A large effort has to be made to integrate these technologies into clinical studies and thus eventually to facilitate more refined guidelines, combining validated diagnostics with precision therapy in clinical practice. - Development of more compounds suited for targeted therapy. A large number of molecules and antibodies is already available. Many of them have been investigated in clinical studies and some of these have already found their way to the clinic. The knowledge of the individual transforming entities will help to stratify patients into subgroups suited for specific targeted treatments. This has already been shown to be a successful strategy. However, this approach might require large amounts of tumor tissue (and does not necessarily solve the problem of tumor heterogeneity). Thus alternative sources of tumor samples, such as blood (i.e. liquid biopsies), have to be explored to gain access to the complete signature of an individual tumor. First successful examples encourage us to proceed in this direction.These activities are ongoing. Together with the availability of more and quantitated target-specific diagnostic assays, targeted therapies will become increasingly successful in treating cancer. As in general tumors are driven by more than one oncogenic process, the combination of two or even more targeted compounds could increase their curative potential. So far, many of these novel treatment options are applied in combination with traditional cytotoxic substances. In this issue of Oncology Research and Treatment experts in the field summarize the achievements reached so far in selected tumor entities. They also address the deficits as they show up at present and give an outlook on the urgent needs in order to accomplish successful targetined therapy. Lung cancer is a prominent example where substantial progress has been made. Michels and Wolf [1] in particular address resistance problems and also the blood/brain barrier as a major hurdle to treat brain metastases. The therapy of chronic lymphocytic leukemia (CLL) can be improved in certain cases by combining different agents addressing different targets [2]. Head and neck cancer requires substantially more clinical studies investigating new compounds addressing the targets that have been shown to be involved in this disease [3]. To proceed with targeted therapy of esophagogastric cancer, we need much better diagnostics and more information on markers. This should considerably improve the evaluation of clinical investigations [4]. Metastatic colorectal cancer (mCRC) is treated basically by targeting an oncogenic molecule at the surface of the cancer cell on the one hand and tumor angiogenesis as a target coming from the cellular environment on the other [5]. As targeted therapies require substantial support from molecular pathology, Manfred Dietel [6] describes the current situation in this field and addresses the problems and the future developments.In summary, personalized targeted therapies are at present the most encouraging treatment strategies to advance in the battle against cancer. The first steps in this direction have been successful. However, there is still a long way to go. The Author declares no conflicts of interest.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
研友_O8W2PZ发布了新的文献求助10
刚刚
1秒前
1秒前
深情安青应助Aye采纳,获得10
2秒前
hahahalha完成签到,获得积分10
3秒前
lkymxt完成签到,获得积分10
3秒前
JISOO发布了新的文献求助10
4秒前
谦让新竹完成签到,获得积分10
6秒前
今后应助蝶步韶华采纳,获得10
7秒前
orixero应助威武的雨筠采纳,获得10
7秒前
8秒前
奋斗沛文发布了新的文献求助10
8秒前
8秒前
9秒前
9秒前
10秒前
李健应助buno采纳,获得30
11秒前
ty发布了新的文献求助10
12秒前
lxg发布了新的文献求助10
13秒前
CHOW发布了新的文献求助10
13秒前
田様应助xwwwww采纳,获得10
13秒前
Vicky发布了新的文献求助10
14秒前
AN完成签到,获得积分0
15秒前
豚豚完成签到,获得积分10
15秒前
明亮夜云完成签到,获得积分10
16秒前
姜雪毅完成签到 ,获得积分10
16秒前
shunshun51213发布了新的文献求助10
16秒前
17秒前
永远的Tmac发布了新的文献求助10
18秒前
所所应助我爱学习采纳,获得10
18秒前
18秒前
dd完成签到,获得积分10
18秒前
19秒前
天天快乐应助wbqdssl采纳,获得10
19秒前
xinxiangshicheng完成签到 ,获得积分10
20秒前
yolo完成签到,获得积分10
20秒前
21秒前
无花果应助xl采纳,获得10
23秒前
852应助ty采纳,获得10
23秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
AnnualResearch andConsultation Report of Panorama survey and Investment strategy onChinaIndustry 1000
Continuing Syntax 1000
Signals, Systems, and Signal Processing 610
简明药物化学习题答案 500
Quasi-Interpolation 400
脑电大模型与情感脑机接口研究--郑伟龙 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 物理 内科学 复合材料 催化作用 物理化学 光电子学 电极 细胞生物学 基因 无机化学
热门帖子
关注 科研通微信公众号,转发送积分 6276231
求助须知:如何正确求助?哪些是违规求助? 8095927
关于积分的说明 16924256
捐赠科研通 5345695
什么是DOI,文献DOI怎么找? 2842174
邀请新用户注册赠送积分活动 1819385
关于科研通互助平台的介绍 1676587