How to predict the occurrence of cancer?
Cancer-causing genes
Justin Stebbing, Professor of Cancer Medicine and Oncology at King's College London, talks about family cases of cancer, preventive intervention and modern methods of treatment.
I will tell you about the genes that cause cancer, because cancer is a genetic disease. But it is important to understand what we mean by the word "genetic": innate genes that directly lead to the occurrence of cancer are quite rare. If I start doing weightlifting, I will become big and strong: obviously, because I lift a barbell every day. But seriously, I can build muscle mass, but I won't pass it on to my children. I'll give them the color of their eyes, the color of their hair (at least what's left of them). When I say that cancer is a genetic disease, I mean new genes that were not part of me –like muscles that grow as a result of weightlifting. I will not pass them on to the children.
We know that cancer is a genetic disease, because it does not contain normal genes in its cells, but mutant, merged ones; or the wrong number of copies of genes, the wrong components of genes. But the genes responsible for familial cases of cancer, fortunately, are relatively rare. We have all heard about the BRCA1 and BRCA2 genes, which are responsible for about 5% of breast cancer cases and a slightly larger number of ovarian cancer cases. Now we are scanning for BRCA genes of all women with ovarian cancer and the vast majority of girls and women who have had cases of breast cancer in their family. We know that if our cells, that is, all cells of the body, contain the mutant BRCA1 or BRCA2 gene, then the chances of developing breast cancer or ovarian cancer during life are very high – higher with the BRCA1 gene than with the BRCA2 gene. In these cases, we often recommend a bilateral mastectomy and removal of the ovaries. If people with these genes develop cancer, we can attack it with "synthetic lethality" drugs that affect these genes – we call them "PARP inhibitors", there are several of them.
As part of the 100,000 Genomes project in England and other genome analysis projects, we are also looking for other genes that affect familial cases of cancer. We know that mutant BRCA genes play an important role in other tumors – for example, in pancreatic cancer, and not just breast or ovarian cancer. Perhaps they are also important in other diseases, such as prostate cancer. We find other genes, say CHEK1 or NBN. Their presence does not guarantee a huge risk of developing these types of cancer, but we are studying them and beginning to understand how such genetic information can be used in the daily treatment of cancer patients.
Cancer and its causes are a huge puzzle for us, but sometimes we know that people in ordinary cells have a gene that turns these ordinary cells into cancer cells. We are able to prevent this, for example, with the help of surgical intervention or special drugs. For example, Angelina Jolie has the BRCA gene, and she had a bilateral mastectomy and oophorectomy. This reduces her chances of developing breast cancer or ovarian cancer from 80-95% to almost 0% for both types of cancer. We will not be able to get 0%, because even after a mastectomy there will always be a few breast cells left, but even this approach reduces the risk of developing the disease from almost 100% to almost 0% – this is an amazing difference. Sometimes we can use preventive therapy for breast cancer, and there are also other ways for other types of tumors. We can send people to scan programs with imaging and radiological examination. We are doing all this much better now than at any time in the past.
If people develop cancer, we can treat it – again with surgery, radiotherapy and medications. We can monitor these patients to detect cancer at an early stage. This can be done not only during scanning, but also in blood tests and medical examinations. We need to understand how we can introduce these procedures into people's daily lives in order to remove this stigma from cancer, so that people can live happily ever after with this information, and not die of cancer and not think that cancer is the end of the world.
In the field of gene and cancer research, everything is changing. We use a variety of treatment methods based on information about genes that change in cancer. The use of immunotherapy is based on understanding the work of the PD1 and PD-L1 genes or another gene, CTLA4. There are specific drugs, clinical trials are being conducted, and medications based on understanding EGFR gene mutations or mergers in the OUT gene are used on a daily basis. There is a gene called BCR, which, as a result of merging with the ABL gene, leads to chronic myeloid leukemia, and on its basis we created the drug imatinib, so that people with chronic myeloid leukemia can now count on a normal life expectancy. We treat breast cancer based on data on the genes of estrogen receptors, progesterone receptors and HER2. If a patient has breast cancer with overexpression of the HER2 gene on chromosome 17, we prescribe herceptin, or trastuzumab, or kadsila, or other genes if the disease progresses. By studying the work of these genes, we can understand what activates cancer cells, and if we understand what activates them, we can also understand how to deactivate them.
We take an individual approach to the treatment of each tumor. We personalize the treatment regimen by using specific drugs to treat a specific type of cancer in a specific patient at a specific time. And because we use personalized treatment, we maximize the chances that our drugs and approaches will work, and minimize their side effects and toxicity. With this approach, as well as through the study of "cancer" genes and inherited genes that affect the development of cancer, we hope to increase the percentage of recovery. But even if we can't do this and cancer turns into a chronic disease, as with chronic myeloid leukemia, people continue to live with it, and do not die from it.
My laboratory at Imperial College London specializes in the regulation of gene expression. There are 3 billion letters in our DNA that are present in the cells of our brain, mouth, lungs and breast. What determines whether breast cells will turn out, or breast cancer cells, or breast cancer stem cells that can remain dormant for many years and that we can cultivate, or breast stem cells? There is a mechanism by which these 3 billion letters turn on and off, and we call it the regulation of gene expression. By better understanding these processes, we will be able to improve the lives of patients who live with cancer, as well as increase the level of early diagnosis and, consequently, increase the recovery rate by understanding cancer genes, which we can now detect with a simple blood test, without invasive diagnosis. We call this extracellular DNA analysis, and we are also studying this issue at Imperial College London. In this area, everything is developing at supersonic speed, and we will be able to understand what modifies the "cancer" genes, how they change over time and how we can better interact with them during treatment.
Portal "Eternal youth" http://vechnayamolodost.ru