2024-09-17 14:55:00
New scientific work reveals that genetic heritage confers more or less protection against lung cancer induced by cigarette smoke. The cause: the existence of variations that modulate the effectiveness of the immune system.
Tobacco is the main risk factor for lung cancer: It is estimated that between 80 and 90% of lung cancers are directly linked to it.. However, not all smokers will necessarily be affected by this disease.
While some are spared by simple chance, others are spared for genetic reasons. Indeed, certain characteristics of their genetic heritage reduce their risk of developing the disease. A group of genes linked to the immune system is involved. Explanations.
How does the immune system work against cancer?
Table of Contents
- 1 How does the immune system work against cancer?
- 2 Genetic heritage influences immune response
- 3 How can these results be explained?
- 4 An explanation for the success of immunotherapy
- 5 Proteins can significantly impact the immune response to cancer cells and, consequently, the risk of developing lung cancer.
- 6 – What genetic variations influence the immune response to lung cancer?
Table of Contents
- 1 How does the immune system work against cancer?
- 2 Genetic heritage influences immune response
- 3 How can these results be explained?
- 4 An explanation for the success of immunotherapy
- 5 Proteins can significantly impact the immune response to cancer cells and, consequently, the risk of developing lung cancer.
The immune system is best known for its role in defending against infections. However, its anti-cancer role is just as important. In the lung as in other organs, cells that become cancerous do not systematically end up causing cancer that would threaten the body : recognized by the immune system, they are often eliminated before becoming problematic.
How does the immune system distinguish these cells from healthy cells in the body, which it does not attack? It is important to know that the accumulation of mutations that transform a healthy cell into a cancerous cell ends up modifying it. Its surface, in particular, carries molecules that distinguish it, in the eyes of agents of the immune system, from healthy cells. These molecules recognized as foreign are called antigens.
When antigens are detected on the surface of a cell, specialized immune cells take charge of destroying it. In doing so, they recover the antigens to present them to other immune cells, T lymphocytes, which further strengthen the antitumor response.
Antigens are not presented naked to T lymphocytes: they are bound to what are called major histocompatibility complex proteins. It is through these that the influence of genetic heritage on anti-cancer immunity is manifested, as recently demonstrated by a study published in the prestigious journal Science.
Genetic heritage influences immune response
In the course of this work, the researchers explored two biobanks, one in the United Kingdom and the other in Finland. These databases contain information on the habits, medical history and genetic heritage of hundreds of thousands of volunteers.
Their aim was to compare the profiles of participants who had lung cancer with those who had not developed it. In particular, they focused their attention on the sequences of genes coding for proteins of the major histocompatibility complex, which are therefore associated with the presentation of antigens to T lymphocytes.
Before diving into the heart of the matter, it may be useful to recall some notions of genetics. The information necessary for the production of the proteins that constitute us is carried by genes. Each gene is defined by a “sequence” that is specific to it (this term designates the chain of chemical “bricks” that constitute the gene).
Reading the sequence of a gene allows our cells to make the protein that corresponds to it, a bit like a plan is used to assemble a model.
It is considered that for a given gene, there is a “standard” sequence, which corresponds to that present in the majority of individuals. However, in some people, variations in the sequences are sometimes observed.
Proteins made from these slightly different genes may show variations from those made from the standard sequence. This partly explains the diversity we see in living things.
Furthermore, we all have our genes in duplicate, one received from our father and the other from our mother. Most individuals have the same sequence (most often standard) twice: they are said to be homozygous. The others are heterozygous, with a variation present on one of the two copies.
By studying the British and Finnish biobanks, the researchers observed that participants in the second group, who had not had lung cancer, were more often heterozygous for certain sequences in the gene group. HLA-II than those in the first group, who had had lung cancer.
They then demonstrated that this excess of heterozygous people was limited to participants who were smokers, active or former: it was not observed in people who had never smoked. This observation indicates that the protective effect of genetic variations was therefore specific to smokers.
How can these results be explained?
The presence of two different copies of genes HLA-II leads to a greater diversity of major histocompatibility complex proteins on the surface of antigen-presenting cells. This diversity is accompanied by an increased ability to present cancer antigens to T lymphocytes, and thus a better immune response.
To explain why the protective effect is only observed in smokers, it is assumed that only immunity against the types of cancer caused by tobacco is stimulated.
The first elements aimed at quantifying the effect of these variations suggest that an individual heterozygous in a specific location (we speak of locusplural loci) of a given gene of the complex HLA-II has a lung cancer risk reduced by about 30% compared to a homozygous person. It is conceivable that heterozygosity at multiple loci would be associated with a greater risk reduction.
It is important to remember, however, that regardless of genetics, the absence of exposure to tobacco remains the best way to protect against lung cancer!
An explanation for the success of immunotherapy
The links between genetic heritage and lung cancer have been known for several years. For example, we know that variations in genes that ensure DNA integrity can cause the disease in young non-smokers. The genes involved in smoker’s cancer therefore seem to be very different from those involved in cancer occurring in people who have never smoked.
However, this work is the first to convincingly demonstrate the link between genetic heritage, smoking, immune response and lung cancer.
This association between immunity and lung cancer explains the success of immunotherapies. These approaches, which consist of promoting the patient’s immune response by lifting blocking mechanisms triggered by the body, have been integrated for several years The therapeutic arsenal used in thoracic cancerologybecause of their sometimes spectacular effectiveness.
In the coming years, we can expect an explosion of knowledge in this field, which will certainly have implications for medical practice. Pulmonology and thoracic cancer teams are already seeking to develop lung cancer screening programs adapted to individual risk. There is little doubt that the progressive integration of genetic data will allow increasingly precise estimates.
Thanks to Professor Jacques Cadranel for his proofreading and comments.
1726666539
#tobacco #smokers #equal
Proteins can significantly impact the immune response to cancer cells and, consequently, the risk of developing lung cancer.
Unlocking the Secret to Lung Cancer Prevention: How Genetic Heritage Affects Immunity
Lung cancer is one of the leading causes of cancer-related deaths worldwide, and tobacco smoking is the primary risk factor, accounting for 80-90% of all lung cancer cases. However, not all smokers are equally susceptible to developing the disease. Recent scientific research has shed light on the role of genetic heritage in conferring protection against lung cancer induced by cigarette smoke. The key lies in the variations of genes linked to the immune system, which modulate its effectiveness in fighting cancer cells.
The Immune System’s Anti-Cancer Role
The immune system is often associated with defending against infections, but it also plays a crucial role in preventing cancer. In the lungs and other organs, cells that become cancerous do not always lead to cancer that threatens the body. Recognized by the immune system, these cells are often eliminated before becoming problematic. The immune system distinguishes cancer cells from healthy cells by identifying specific molecules on their surface, called antigens.
Antigens and the Immune Response
When antigens are detected, specialized immune cells, such as T lymphocytes, take charge of destroying the cancer cells. In this process, the antigens are bound to major histocompatibility complex proteins, which are influenced by an individual’s genetic heritage. A recent study published in the prestigious journal Science has demonstrated that variations in the genes coding for these
– What genetic variations influence the immune response to lung cancer?
Genetic Heritage and Lung Cancer: How Immune System Variations Affect Cancer Risk
Tobacco is the leading risk factor for lung cancer, accountable for 80-90% of cases. However, not all smokers develop the disease, and researchers have discovered that certain genetic characteristics can confer protection against lung cancer induced by cigarette smoke. The key lies in variations that modulate the effectiveness of the immune system.
How the Immune System Works Against Cancer
The immune system plays a crucial role in defending against infections and cancer. In the lung, cells that become cancerous can be recognized by the immune system and eliminated before they become problematic. The immune system distinguishes cancerous cells from healthy cells through the presence of antigens on their surface, which are molecules recognized as foreign. Specialized immune cells then destroy these cancerous cells and present the antigens to T lymphocytes, further strengthening the antitumor response.
Genetic Heritage Influences Immune Response
A recent study published in the journal Science explored the genetic profiles of hundreds of thousands of volunteers in two biobanks in the UK and Finland. Researchers compared the profiles of participants who had lung cancer with those who had not developed the disease, focusing on genes coding for proteins of the major histocompatibility complex (MHC). This complex plays a crucial role in presenting antigens to T lymphocytes.
The study revealed that variations in the sequences of MHC genes can impact the immune response to cancer cells, consequently affecting the risk of developing lung cancer. These variations can influence the effectiveness of the immune system in recognizing and eliminating cancer cells.
How Can These Results Be Explained?
The research team found that certain genetic variations in the MHC genes can affect the presentation of antigens to T lymphocytes, impacting the immune system’s ability to recognize and respond to cancer cells. This means that individuals with these variations may have a reduced risk of developing lung cancer.
An Explanation for the Success of Immunotherapy
The study’s findings may also provide an explanation for the success of immunotherapy, a type of cancer treatment that boosts the immune system’s ability to fight cancer. By understanding how genetic variations affect the immune response, researchers may be able to develop more targeted and effective immunotherapies.
Proteins Can Significantly Impact the Immune Response to Cancer Cells
The study highlights the importance of proteins in the immune response to cancer cells and the subsequent risk of developing lung cancer. The proteins involved in the MHC complex play a critical role in presenting antigens to T lymphocytes, and variations in these proteins can significantly impact the