BJR supplement最新文献_第3页

BJR supplement Pub Date : 1992-01-01

G D Wilson

引用次数: 0

Cell kinetics of human solid tumours. 人实体瘤细胞动力学。

BJR supplement Pub Date : 1992-01-01

J H Laing, D A Rew, G D Wilson

引用次数: 0

Accelerated fractionation using the concomitant boost: a contribution of radiobiology to radiotherapy. 使用伴随增强的加速分馏:放射生物学对放射治疗的贡献。

BJR supplement Pub Date : 1992-01-01

L J Peters

引用次数: 0

Intrinsic radiosensitivity as a predictor of patient response to radiotherapy. 内在放射敏感性作为患者放射治疗反应的预测因子。

BJR supplement Pub Date : 1992-01-01

C M West, J H Hendry

引用次数: 0

Cell kinetics: from tritiated thymidine to flow cytometry. 细胞动力学:从氚化胸苷到流式细胞术。

BJR supplement Pub Date : 1992-01-01

N H Terry, R A White, M L Meistrich

引用次数: 0

Modelling altered fractionation schedules. 模拟改变了分馏时间表。

BJR supplement Pub Date : 1992-01-01

J F Fowler

引用次数: 0

Oncogenes and tumour suppressor genes in human cancers: clinical implications. 人类癌症中的癌基因和肿瘤抑制基因:临床意义。

BJR supplement Pub Date : 1992-01-01

J Bourhis

引用次数: 0

Molecular analysis of radiation damage and repair in normal and mutant cells. 正常和突变细胞辐射损伤与修复的分子分析。

BJR supplement Pub Date : 1992-01-01

J E Arrand, B Kysela

引用次数: 0

Fluorescence in situ hybridization: an improved method of quantitating chromosome damage and repair. 荧光原位杂交:一种改进的染色体损伤与修复定量方法。

BJR supplement Pub Date : 1992-01-01

J M Brown, J W Evans

引用次数: 0

Inadequate vasculature in solid tumours: consequences for cancer research strategies. 实体肿瘤中血管不足:癌症研究策略的后果。

BJR supplement Pub Date : 1992-01-01

J Denekamp

{"title":"Inadequate vasculature in solid tumours: consequences for cancer research strategies.","authors":"J Denekamp","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In the last decade, since we first postulated that antiproliferating endothelial therapy was a promising new approach to therapy, there have been remarkable developments. Vascular effects have been recognized from completely unrelated and unexpected agents, including hyperthermia, photodynamic therapy, misonidazole, tumour necrosis factor, FAA, interferon and interleukins. These vascular effects may coexist with direct cytotoxicity to the tumour cells or they may explain all of the antitumour activity. In order to benefit from such vascular effects, we need to monitor them, understand their mechanisms of action and ensure that the clinical scheduling is optimized to give the greatest therapeutic advantage. The biologist must re-evaluate the validity of his or her tumour models and the clinician must question whether drugs targeted at tumour cells should be sought or whether it would be more productive to target the nutrient supply through the neovasculature. The molecular biology approaches of oncogene expression in tumour cells and growth factor dependency must be weighed against angiogenesis, the pathophysiology of the tumour mass and its supporting normal stromal elements. Since this is a highly complex field there will be many fascinating years of work elucidating tumour versus normal vascular differences. In the meantime, we need to ensure that we do not reject useful therapeutic agents by inappropriate scheduling based on a misunderstanding of their mode of action, or by the use of inappropriate models for testing potential anticancer agents.</p>","PeriodicalId":77044,"journal":{"name":"BJR supplement","volume":"24 ","pages":"111-7"},"PeriodicalIF":0.0,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12465453","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}

引用次数: 0