Pub Date : 2013-04-01DOI: 10.13172/2052-9635-1-1-759
A Bollig-Fischer, Sk Michelhaugh, R Ali-Fehmi, S Mittal
INTRODUCTION Metastatic brain tumours remain an intractable clinical problem despite notable advances in the treatment of the primary cancers. It is estimated that 30-40% of breast and lung cancer patients will develop brain metastases. Typically, brain lesions are not diagnosed until patients exhibit neurological symptoms because there are currently no tests that can predict which patients will be afflicted. Brain metastases are resistant to current chemotherapies, and despite surgical resection and radiotherapy, the prognosis for these patients remains very poor with an average survival of only 6-9 months. Cancer is ultimately a genetic disease, involving patient genetics and aberrant tumour genomics; therefore the pursuit of an explanation for why or how brain metastases occur requires investigation of the associated somatic mutations. In this article, we review the current literature surrounding the molecular and genome-based mechanistic evidence to indicate driver oncogenes that hold potential biomarkers for risk, or therapeutic targets for treatment of brain metastases. CONCLUSION Patients afflicted with metastatic brain tumours are in dire need of more effective therapies, and clinicians need predictive laboratory tests to identify patients at risk of developing metastatic brain tumours. The as yet unrealized comprehensive analysis of metastatic brain tumour genomics is necessary to meet these needs. Moreover, without improved understanding of the genomic aberrations that drive metastatic brain tumours, development of biomarkers and molecularly targeted therapies will remain stalled and patient outcomes will continue to be dismal.
{"title":"The molecular genomics of metastatic brain tumours.","authors":"A Bollig-Fischer, Sk Michelhaugh, R Ali-Fehmi, S Mittal","doi":"10.13172/2052-9635-1-1-759","DOIUrl":"https://doi.org/10.13172/2052-9635-1-1-759","url":null,"abstract":"INTRODUCTION\u0000Metastatic brain tumours remain an intractable clinical problem despite notable advances in the treatment of the primary cancers. It is estimated that 30-40% of breast and lung cancer patients will develop brain metastases. Typically, brain lesions are not diagnosed until patients exhibit neurological symptoms because there are currently no tests that can predict which patients will be afflicted. Brain metastases are resistant to current chemotherapies, and despite surgical resection and radiotherapy, the prognosis for these patients remains very poor with an average survival of only 6-9 months. Cancer is ultimately a genetic disease, involving patient genetics and aberrant tumour genomics; therefore the pursuit of an explanation for why or how brain metastases occur requires investigation of the associated somatic mutations. In this article, we review the current literature surrounding the molecular and genome-based mechanistic evidence to indicate driver oncogenes that hold potential biomarkers for risk, or therapeutic targets for treatment of brain metastases.\u0000\u0000\u0000CONCLUSION\u0000Patients afflicted with metastatic brain tumours are in dire need of more effective therapies, and clinicians need predictive laboratory tests to identify patients at risk of developing metastatic brain tumours. The as yet unrealized comprehensive analysis of metastatic brain tumour genomics is necessary to meet these needs. Moreover, without improved understanding of the genomic aberrations that drive metastatic brain tumours, development of biomarkers and molecularly targeted therapies will remain stalled and patient outcomes will continue to be dismal.","PeriodicalId":90276,"journal":{"name":"OA molecular oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4229688/pdf/nihms-586868.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32817159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2013-04-01DOI: 10.13172/2052-9635-1-1-708
Mw Van Dyke, Ld Nelson
While most naturally occurring DNA and RNA adopt the now quite familiar double-helix structure, certain sequences can under the appropriate conditions adopt a three-stranded, triple-helical structure. Both intramolecular and intermolecular triplexes have been described. Evidence for the existence of triplex structures in vivo is limited, although cellular proteins have been identified that avidly and specifically interact with such species. The postulated roles of triplexes and the proteins that interact with them in cancer and their potential utility as diagnostic markers are discussed in this review.
{"title":"Triple helix-interacting proteins and cancer.","authors":"Mw Van Dyke, Ld Nelson","doi":"10.13172/2052-9635-1-1-708","DOIUrl":"https://doi.org/10.13172/2052-9635-1-1-708","url":null,"abstract":"<p><p>While most naturally occurring DNA and RNA adopt the now quite familiar double-helix structure, certain sequences can under the appropriate conditions adopt a three-stranded, triple-helical structure. Both intramolecular and intermolecular triplexes have been described. Evidence for the existence of triplex structures <i>in vivo</i> is limited, although cellular proteins have been identified that avidly and specifically interact with such species. The postulated roles of triplexes and the proteins that interact with them in cancer and their potential utility as diagnostic markers are discussed in this review.</p>","PeriodicalId":90276,"journal":{"name":"OA molecular oncology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2013-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4047974/pdf/nihms528189.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32408809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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