国际癌症专家莱恩爵士（Professor Sir David Lane）于90年代初成功发现肿瘤抑制基因p53，被视为癌症研究权威，他昨天（29日）首度来港发表演说，透露正努力进行针对p53基因的抗癌药临床研究，预计未来数年会有好消息。
莱恩表示，目前全球有2200万人患癌，每年有1000万宗新症，以往只有私人药厂研制癌症药物，因要赚回研究经费，令药物费用变得昂贵。
他指出，目前英国的癌症药物研究，有50%来自私人捐款支持，这做法可望降低癌症药物价格，令病人受惠。他同意本港单靠政府资助进行药物研究并不足够。
莱恩在90年代初成功发现肿瘤抑制基因p53，这种基因可影响超过一半的人类癌症，他昨日透露，正针对p53基因进行抗癌药研究，目前已在动物身上成功进行临床测试，预计未来数年会在人类身上进行临床研究。
世界卫生组织估计，24%癌症与病毒或细菌感染有关，例如幽门螺旋菌与胃癌有关、乙型肝炎与肝癌有关等，莱恩希望日后会有人研制出不同疫苗，用于防治癌症。
科学家简介：
Professor Sir David Lane FRS FRSE FRCPath
Gibb Fellow of the CRC
Director of the CRC Cell Transformation Group,
Department of Surgery and Molecular Oncology,
Ninewells Hospital and Medical School, Dundee DD1 9SY U. K.
Professor Lane recently moved from the School of Life Sciences to found a new Department of Surgery and Oncology in the University's Medical School with Sir Alfred Cucheiri, one of the pioneers in minimal access ("keyhole") surgery.
Tel: +44 (0)1382 496362
FAX: +44 (0)1382 496363
Email: d.p.lane@dundee.ac.uk
The molecular basis of human cancer
The development of a malignant tumour is a multi-step process involving the mutation of several specific genes involved in the control of cell growth and programmed cell death. Most common solid tumours start from small benign growths. Very rarely an individual cell within such a lesion may undergo additional genetic changes that will confer on it a selective growth or survival advantage. From the progeny of this altered cell further even more damaged cells may arise which have additional selective advantages. Eventually clones may arise that no longer respond at all to normal regulatory signals and grow in an uncontrolled manner spreading to other sites in the body and giving rise to malignant cancer. The goal of our research is to understand the cause and nature of these accumulating genetic changes so that new diagnostic and therapeutic methods can be developed.
The p53 tumour suppressor gene
Our research has become focused on one particular gene, p53, because it is so often mutated in the common tumours and our fast emerging knowledge of its structure and function are beginning to make clear why its normal function is so important in preventing cells from turning malignant. The p53 protein is normally present in minute levels and is probably inactive, but when cells are exposed to DNA damage or start to divide aberrantly p53 levels rise and the protein is switched on (1). For this reason we have called p53 "The guardian of the genome" (2). The function of p53 is critical to the way that many cancer treatments kill cells since radiotherapy and chemotherapy act in part by triggering cell suicide in response to DNA damage. This successful response to therapy is greatly reduced in tumours where p53 is mutant so these tumours are often particularly difficult to treat.
New treatments for cancer
We hope to use our knowledge of p53 to develop new treatments for cancer. Many tumours make mutant forms of p53 that no longer work properly. In the test tube at least we are beginning to find ways to make these damaged p53s work again (3,4,5). We use modern methods of protein chemistry to try and discover novel molecules that will replace p53 or restore its function (6,7). The discovery of such agents would potentially offer a powerful and selective new way of treating the disease.
The message is growth: how growth factor signals are passed on to the MAP kinase cascade which turns on cells to multiply
