Pub Date : 2014-01-01Epub Date: 2014-02-17DOI: 10.1159/000355895
Yujie Zhao, Alex A Adjei
Cancer is a genetic disease caused by a series of somatic and/or germline mutations. The roles of oncogenes and tumor suppressors in cancer molecular origin have been well established. Targeting oncogene products has become an attractive therapeutic strategy with great clinical success, whereas tumor suppressors are considered 'undruggable' because current technology is not able to restore tumor suppressor function in metastatic disease. Although systematic approaches to discover genetic alterations have become available to individual patients, differentiating driver from passenger mutations and identifying and validating drug targets remain challenging. Protein tyrosine kinases play crucial roles in virtually all cellular processes and possess structural features that render them 'druggable'. Monoclonal antibodies and small-molecule inhibitors represent two major classes of targeted therapeutic agents, each possessing its own strength and weakness. Although initial successes have been achieved, targeted therapy faces many challenges that need to be addressed and hurdles to overcome.
{"title":"Targeting oncogenic drivers.","authors":"Yujie Zhao, Alex A Adjei","doi":"10.1159/000355895","DOIUrl":"https://doi.org/10.1159/000355895","url":null,"abstract":"<p><p>Cancer is a genetic disease caused by a series of somatic and/or germline mutations. The roles of oncogenes and tumor suppressors in cancer molecular origin have been well established. Targeting oncogene products has become an attractive therapeutic strategy with great clinical success, whereas tumor suppressors are considered 'undruggable' because current technology is not able to restore tumor suppressor function in metastatic disease. Although systematic approaches to discover genetic alterations have become available to individual patients, differentiating driver from passenger mutations and identifying and validating drug targets remain challenging. Protein tyrosine kinases play crucial roles in virtually all cellular processes and possess structural features that render them 'druggable'. Monoclonal antibodies and small-molecule inhibitors represent two major classes of targeted therapeutic agents, each possessing its own strength and weakness. Although initial successes have been achieved, targeted therapy faces many challenges that need to be addressed and hurdles to overcome.</p>","PeriodicalId":49661,"journal":{"name":"Progress in Tumor Research","volume":"41 ","pages":"1-14"},"PeriodicalIF":0.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000355895","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32258500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cancers of the head and neck.","authors":"Hans Krueger, David McLean, Dan Williams","doi":"10.1159/000151875","DOIUrl":"https://doi.org/10.1159/000151875","url":null,"abstract":"","PeriodicalId":49661,"journal":{"name":"Progress in Tumor Research","volume":"40 ","pages":"62-84"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000151875","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27684454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This comment is found in a German report covering what were probably the first documented cases of second primary cancer (SPC) [1]. In the intervening 120 years, the research focus on this important area of oncology and epidemiology has been established and gradually intensified. Recently, investigation of prevention options has begun to dominate the agenda. It is well known that cancer survivors are at risk for recurrence of the primary cancer. The chance of getting a so-called SPC is also increased. Simply put, a SPC is a new primary cancer developing in a person with a history of cancer. Interest in SPCs has paralleled the extraordinary improvement in curing primary cancers, which in turn has increased both the longevity and the absolute number of survivors. The concomitant reduction in mortality rates attached to (in particular) cardiovascular disease has augmented the general increase in longevity. Accordingly, the cumulative incidence of SPC has grown, essentially driven by patients surviving long enough for other cancers to develop. It is accurate to say that the SPC story has expanded as a by-product of increasing health awareness, early diagnosis of primary cancers and therapeutic success. The outcome of these forces is that SPCs are now more common; indeed, as a class they are estimated to be the sixth most common form of malignancy in the world [2]. Consequently, research on such cancers has intensified. The last comprehensive textbook on the area covered data up to about 1997 [3]. It appears that the volume of publishing since that point has already matched the academic output in all the previous decades combined. There are 3 imperatives that have prompted the continuing wave of research and analysis. First, there is a need to completely understand the epidemiology of SPC. This
{"title":"Overview of the topic.","authors":"Hans Krueger, David McLean, Dan Williams","doi":"10.1159/000151866","DOIUrl":"https://doi.org/10.1159/000151866","url":null,"abstract":"This comment is found in a German report covering what were probably the first documented cases of second primary cancer (SPC) [1]. In the intervening 120 years, the research focus on this important area of oncology and epidemiology has been established and gradually intensified. Recently, investigation of prevention options has begun to dominate the agenda. It is well known that cancer survivors are at risk for recurrence of the primary cancer. The chance of getting a so-called SPC is also increased. Simply put, a SPC is a new primary cancer developing in a person with a history of cancer. Interest in SPCs has paralleled the extraordinary improvement in curing primary cancers, which in turn has increased both the longevity and the absolute number of survivors. The concomitant reduction in mortality rates attached to (in particular) cardiovascular disease has augmented the general increase in longevity. Accordingly, the cumulative incidence of SPC has grown, essentially driven by patients surviving long enough for other cancers to develop. It is accurate to say that the SPC story has expanded as a by-product of increasing health awareness, early diagnosis of primary cancers and therapeutic success. The outcome of these forces is that SPCs are now more common; indeed, as a class they are estimated to be the sixth most common form of malignancy in the world [2]. Consequently, research on such cancers has intensified. The last comprehensive textbook on the area covered data up to about 1997 [3]. It appears that the volume of publishing since that point has already matched the academic output in all the previous decades combined. There are 3 imperatives that have prompted the continuing wave of research and analysis. First, there is a need to completely understand the epidemiology of SPC. This","PeriodicalId":49661,"journal":{"name":"Progress in Tumor Research","volume":"40 ","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000151866","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27684090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The literature regarding SPC following urological cancers is limited. The main sites of interest include the kidney, the upper urinary tract in general and the bladder. Regarding kidney cancer, the 2 most recent studies were based on a similar sample size. In 2006, Beisland et al. [1] investigated 1,425 patients with renal cell carcinoma. Only 3 types of SPC showed a significant excess risk (table 44). The results support the common understanding of bladder cancer as a key sequela to renal cancer. For instance, Rabbani and colleagues found that only bladder cancer was seen to exhibit an excess risk among a small series of renal carcinoma patients [2]. The common risk factor posited to explain this phenomenon involves smokingrelated carcinogens excreted through the kidneys and thence to the bladder and its tissues [3]. The other population-based study, from 2003, specifically focused on papillary kidney cancer (n 1,733). It demonstrated a slightly wider range of SPCs with a significant excess risk – though the most dramatic result was still for bladder cancer (table 45) [4]. Augmenting these results, Thompson and colleagues noted in a 2006 report that patients with papillary renal cell carcinoma have an overall greater risk of a SPC, particularly related to colon and prostate cancer, than patients with clear cell renal carcinoma [5]. The theory concerning tobacco smoking and increased bladder cancer noted earlier may also explain any excess of second primary lung cancers. Consequently, smoking cessation could be an effective preventive measure. In the studies just described, prostate cancer joins the list of sites with excess risk, a result that has been confirmed by other research [3, 6]. No definitive explanation of this association has been offered.
{"title":"Genitourinary cancers.","authors":"Hans Krueger, David McLean, Dan Williams","doi":"10.1159/000151877","DOIUrl":"https://doi.org/10.1159/000151877","url":null,"abstract":"The literature regarding SPC following urological cancers is limited. The main sites of interest include the kidney, the upper urinary tract in general and the bladder. Regarding kidney cancer, the 2 most recent studies were based on a similar sample size. In 2006, Beisland et al. [1] investigated 1,425 patients with renal cell carcinoma. Only 3 types of SPC showed a significant excess risk (table 44). The results support the common understanding of bladder cancer as a key sequela to renal cancer. For instance, Rabbani and colleagues found that only bladder cancer was seen to exhibit an excess risk among a small series of renal carcinoma patients [2]. The common risk factor posited to explain this phenomenon involves smokingrelated carcinogens excreted through the kidneys and thence to the bladder and its tissues [3]. The other population-based study, from 2003, specifically focused on papillary kidney cancer (n 1,733). It demonstrated a slightly wider range of SPCs with a significant excess risk – though the most dramatic result was still for bladder cancer (table 45) [4]. Augmenting these results, Thompson and colleagues noted in a 2006 report that patients with papillary renal cell carcinoma have an overall greater risk of a SPC, particularly related to colon and prostate cancer, than patients with clear cell renal carcinoma [5]. The theory concerning tobacco smoking and increased bladder cancer noted earlier may also explain any excess of second primary lung cancers. Consequently, smoking cessation could be an effective preventive measure. In the studies just described, prostate cancer joins the list of sites with excess risk, a result that has been confirmed by other research [3, 6]. No definitive explanation of this association has been offered.","PeriodicalId":49661,"journal":{"name":"Progress in Tumor Research","volume":"40 ","pages":"92-101"},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000151877","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27684456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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