國(guó)際癌癥專家萊恩爵士（Professor Sir David Lane）于90年代初成功發(fā)現(xiàn)腫瘤抑制基因p53，被視為癌癥研究權(quán)威,，他昨天（29日）首度來(lái)港發(fā)表演說(shuō)，透露正努力進(jìn)行針對(duì)p53基因的抗癌藥臨床研究,，預(yù)計(jì)未來(lái)數(shù)年會(huì)有好消息,。
萊恩表示，目前全球有2200萬(wàn)人患癌,，每年有1000萬(wàn)宗新癥,，以往只有私人藥廠研制癌癥藥物，因要賺回研究經(jīng)費(fèi),，令藥物費(fèi)用變得昂貴,。
他指出，目前英國(guó)的癌癥藥物研究,，有50%來(lái)自私人捐款支持,，這做法可望降低癌癥藥物價(jià)格，令病人受惠,。他同意本港單靠政府資助進(jìn)行藥物研究并不足夠,。
萊恩在90年代初成功發(fā)現(xiàn)腫瘤抑制基因p53,，這種基因可影響超過(guò)一半的人類癌癥，他昨日透露,，正針對(duì)p53基因進(jìn)行抗癌藥研究,，目前已在動(dòng)物身上成功進(jìn)行臨床測(cè)試，預(yù)計(jì)未來(lái)數(shù)年會(huì)在人類身上進(jìn)行臨床研究,。
世界衛(wèi)生組織估計(jì),，24%癌癥與病毒或細(xì)菌感染有關(guān)，例如幽門螺旋菌與胃癌有關(guān),、乙型肝炎與肝癌有關(guān)等,，萊恩希望日后會(huì)有人研制出不同疫苗，用于防治癌癥,。
科學(xué)家簡(jiǎn)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: [email protected]
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
