{"id":18111,"date":"2020-02-04T20:40:41","date_gmt":"2020-02-04T20:40:41","guid":{"rendered":"https:\/\/dev.inrs.ca\/our-researchers-are-making-a-difference-in-the-fight-against-cancer\/"},"modified":"2021-03-11T10:27:25","modified_gmt":"2021-03-11T15:27:25","slug":"nos-chercheurs-se-demarquent-dans-la-lutte-contre-le-cancer","status":"publish","type":"post","link":"https:\/\/dev.inrs.ca\/en\/news\/our-researchers-are-making-a-difference-in-the-fight-against-cancer\/","title":{"rendered":"Our researchers are making a difference in the fight against cancer"},"content":{"rendered":"\n

Cancer is the leading cause of death in Qu\u00e9bec. In 2019, an estimated 55,600 Quebecers were diagnosed with cancer and 22,100 people died from the disease. On World Cancer Day, February 4, learn more about the work of professors at the Institut national de la recherche scientifique (INRS) to prevent and treat cancer.<\/strong><\/strong><\/p>\n\n\n\n

\"Nos<\/figure>\n\n\n\n

Cellular Communication and Endocrine Disruptors<\/strong><\/strong><\/h2>\n\n\n\n
\"Isabelle
Professor Isabelle Plante<\/figcaption><\/figure><\/div>\n\n\n\n

Mammary gland development is closely linked to the communication between the cells that make up the glands. Dysregulation of this communication has been associated with breast cancer. Proper cellular communication is crucial for the normal development of the mammary gland. Once formed, the cells maintain this communication to ensure proper gland function. \u201cDuring each menstrual cycle throughout a woman\u2019s life, the mammary glands are getting prepared for a possible pregnancy,\u201d says INRS Professor Isabelle Plante<\/a>. \u201cIt\u2019s a constant reorganization that requires tightly orchestration interactions between the cells.\u201d<\/p>\n\n\n\n

However, studies show that cellular communication breaks down in the case of breast cancer. \u201cThe loss of cellular interactions may impact how breast cancer progresses. In my lab, we study mechanisms regulating cell interactions at every stage of mammary gland development to understand how their dysregulation impact breast cancer progression,\u201d she adds.<\/p>\n\n\n\n

Plante is particularly interested in gap junctions\u2014small channels between cells that allow for the direct communication and rapid exchange of signals. This means of communication seems to play an active role in tumour cell growth, depending on the stage. \u201cA cancer cell will sever ties with other cells; this inhibition of interactions will enable other cells to eliminate it, and allow cancer cells to invade other tissues,\u201d explains Plante. \u201cHowever, during metastasis, the cancer cell appears to re-establish contact to facilitate tumour growth in the surrounding tissue.\u201d The role of these interactions also appears to vary depending on the type of breast cancer. For some types, these interactions mean the person will have a better prognosis. In other types, the cancer cells reconnect with each other in ways that make them grow faster.<\/p>\n\n\n\n

In addition to the loss of interactions, Isabelle Plante studies how environmental pollutants may have an impact on breast cancer. Her research in toxicology focuses on endocrine disruptors, substances that mimic hormones. \u201cThis is really important because the mammary glands are highly regulated by hormones. Even a small imbalance can have an impact,\u201d Plante says.<\/p>\n\n\n\n

Endocrine disruptors can cause breast cancer in two ways. Mammary glands grow the most during puberty and during pregnancy when a number of hormones are activated. Exposure during those critical periods can dysregulate the normal hormonal balance and increase the risk for breast cancer. In addition, exposure to endocrine disruptors in utero or during early life, when the hormones governing mammary gland development are not active yet, can trigger early development, which is known to increase the incidence of breast cancer.<\/p>\n\n\n\n

Hormones also play a role in cell proliferation, which is what leads the mammary glands to develop. However, precancerous cells that receive signals from endocrine disruptors can also respond to these signal by increasing their proliferation and cause tumours to form. The effect is amplified in hormone-dependent breast cancer. Professor Plante\u2019s team is starting a new project to study the effect of a family of molecules called brominated flame retardants, chemicals added to various products such as plastics to make them less easily flammable. Several members of this family of molecules are known endocrine disruptors.<\/p>\n\n\n\n

Cancer and the Environment<\/strong><\/strong><\/h2>\n\n\n\n
\"Marie-\u00c9lise
Professor Marie-\u00c9lise Parent<\/figcaption><\/figure><\/div>\n\n\n\n

What factors increase the risk of developing cancer? This is the question cancer epidemiologist and Professor Marie-\u00c9lise Parent<\/a> is trying to answer. Parent and her team study the role played by the environment as a whole. \u201cWe look at air pollution, light pollution, and the amount of green spaces around where people live. We also look at work environments, because workers are usually exposed to chemicals at higher levels than the general population,\u201d says Parent, specialist in cancer epidemiology at INRS.<\/p>\n\n\n\n

Professor Parent has studied brain, lung, and breast cancer, but is currently focusing on prostate cancer. Prostate cancer is a special case: incidence rates vary widely around the world and it is believed that the environment is the main factor. \u201cThe incidence rate of prostate cancer in some countries is 25 times higher than in others,\u201d Parent explains. \u201cWhen men move to a high incidence area, they acquire this high risk of developing cancer, even if they come from a low incidence area. If it was simply a matter of genetics, the incidence wouldn\u2019t change.\u201d<\/p>\n\n\n\n

After skin cancer, prostate cancer is the most common cancer among men in Canada. Generally speaking, the five-year survival rate is 93%. However, nearly one-third of prostate cancers are aggressive. \u201cThe challenge is to try to understand what factors cause aggressive cancer,\u201d Parent adds. \u201cWe suspect that they\u2019re not the same as more common cancers.\u201d <\/p>\n\n\n\n

To isolate specific risk factors, Parent\u2019s team conducted a major study on prostate cancer in Montr\u00e9al between 2005 and 2012. \u201cIt\u2019s the largest study in the world that looks specifically at environmental factors,\u201d says Parent. \u201cWe recruited 2,000 newly diagnosed men and 2,000 healthy men. We conducted several hours of interviews to go over their history.\u201d<\/p>\n\n\n\n

The sizeable database requires advanced statistical analysis. \u201cOur students are working to analyze the data and everyone has a piece of the puzzle,\u201d says Parent. \u201cFor example, individuals living in areas with high levels of vehicle pollution have an increased risk of prostate cancer. Conversely, men who live surrounded by green spaces are less at risk. Exposure to certain chemical agents, such as benzene, has also been found to be associated with increased risk. Our goal is prevention, so we\u2019re hoping to come up with specific recommendations.\u201d<\/p>\n\n\n\n

Using the Immune System to Fight Tumours<\/strong><\/strong><\/h2>\n\n\n\n
\"Alain
Alain Lamarre, professeur en immunologie, virologie et cancer \u00e0 l\u2019Institut national de la recherche scientifique<\/figcaption><\/figure><\/div>\n\n\n\n

Viruses and tumours have a lot in common. Both have fast replication rates and a tendency to mutate repeatedly to evade the immune system. What if we could use viruses to trigger the immune system to respond to a growing tumour? That was the line of questioning of INRS Professor Alain Lamarre<\/a> considered while studying antiviral response. \u201cIf a virus is injected into a tumour, will it sound the alarm and alert the immune system? Will this then trigger an anti-tumour response?\u201d wonders the immunotherapy expert.<\/p>\n\n\n\n

In his laboratory, the researcher is studying two approaches that take advantage of the immune response. The first uses oncolytic viruses capable of attacking the tumour. \u201cYou inject a virus that infects tumour cells and modifies them to alert the immune system. It could even create an immune memory that would prevent the tumour from coming back,\u201d he explains. <\/p>\n\n\n\n

The problem with the oncolytic approach is that the virus could infect normal cells. \u201cBy creating mutant viruses, we could improve their specificity to tumour cells. The virus has to be aggressive enough to attack tumour cells, but not too aggressive to attack healthy cells,\u201d explains the researcher.<\/p>\n\n\n\n

The second immunotherapy approach is more innovative: introducing a plant virus. This type of virus does not infect humans or animals, but is very foreign to the immune system. According to the professor, \u201cthe plant virus induces production of an antiviral molecule that stimulates the immune response and helps the system recognize the tumour. It triggers a strong anti-tumour response.\u201d<\/p>\n\n\n\n

Professor Lamarre\u2019s team is trying to combine these approaches with other anti-tumour therapies, such as immune checkpoint inhibitors (anti-PD-1). \u201cThe tumour creates an immunosuppressive environment, which acts like a brake in the immune response. Using Anti-PD-1 is like lifting your foot off the brake, and the viral approach is like stepping on the gas. We\u2019re hitting it from both sides at the same time.\u201d<\/p>\n\n\n\n

However, Professor Lamarre cautions that immunotherapy approaches do not work for all types of cancer. \u201cIt\u2019s mostly for cancers with a high mutation rate, such as melanoma,\u201d he says. \u201cSince cancer comes from our own cells and our immune system is trained not to attack them, there may be a response if the build-up of mutations makes the cell appear abnormal to the immune system. If the cancer progresses more slowly with fewer mutations, as with prostate or breast cancers, the approach is less effective.\u201d<\/p>\n\n\n\n

Inhibiting a Protein to Counteract Metastasis<\/strong><\/strong><\/h2>\n\n\n\n
\"Yves
Professor Yves St-Pierre<\/figcaption><\/figure><\/div>\n\n\n\n

For the past 15 years or so, a class of proteins has been attracting attention among cancer researchers: galectins. This interest stems from the protein\u2019s ability to promote tumour growth. Professor Yves St-Pierre<\/a> of INRS focuses on galectin-7, which is responsible for metastasis formation. \u201cWe are the first to demonstrate the role this protein plays in how aggressive certain cancer cells are,\u201d said the cellular biology expert.<\/p>\n\n\n\n

His team is particularly interested in triple-negative breast cancer. \u201cIt\u2019s a very difficult subtype to treat, and the level of galectin-7 found in these cases is abnormally high,\u201d said Professor St-Pierre, who has been studying cancer for 25 years. Cancer cells produce this protein and release some of it outside their membrane. Once released, part of the galectin-7 will bind to immune system cells to neutralize them and create an immunosuppressive environment. The rest will attach to surrounding cancer cells. This allows the protein to promote the division of cancer cells so they are better able to spread throughout the body and form metastases. <\/p>\n\n\n\n

\"Nicolas
Professor Nicolas Doucet<\/figcaption><\/figure><\/div>\n\n\n\n

How can we counter the negative effects of this protein? \u201cYou can\u2019t really stop the cell from expressing galectin-7. So the challenge is finding a drug to neutralize it once it is released,\u201d explained Professor Yves St-Pierre. To solve this problem, he has been working with INRS professors Nicolas Doucet<\/a>, an expert in the structural biology of proteins, and David Chatenet<\/a>, a pharmacotherapy specialist.  <\/p>\n\n\n\n

The three laboratories with complementary expertise wanted to find a way to inhibit galectin-7. The problem is that the entire galectin family has a similar molecular structure. So the researchers needed to target something specific only to galectin-7 without inhibiting other types of galectin. \u201cCertain types of galectins are beneficial to cells, so a massive carpet bombing approach is out of the question because it would have major side effects,\u201d said Professor Doucet.  <\/p>\n\n\n\n

\"David
Professor David Chatenet<\/figcaption><\/figure><\/div>\n\n\n\n

What separates galectin-7 from the rest of the galectin family? \u201cThese proteins cannot function on their own at the molecular level,\u201d said Professor Doucet. \u201cThey must be coupled with another identical galectin molecule to form pairs. The pairing configuration varies by subtype. For instance, certain galectins have a side-by-side molecular organization. But galectin-7 proteins can only pair up back-to-back.\u201d To disrupt this unique galectin-7 configuration, Professor David Chatenet has developed a peptide (small chain of amino acids) specific to the targeted protein. The peptide will only stick to the back of galectin-7 proteins to prevent them from recognizing each other and forming pairs. Blocking galectin-7 from pairing effectively inhibits the protein so it can no longer function effectively. <\/p>\n\n\n\n

The inhibitors developed in the lab of Professor Yves St-Pierre in Laval target triple-negative breast cancer, but they could potentially be used with other types of cancers that present overexpression of galectin-7, such as lymphoma and ovarian cancer, which are responsible for the deaths of over 4,000 Canadians each year. <\/p>\n","protected":false},"excerpt":{"rendered":"

Cancer is the leading cause of death in Qu\u00e9bec. In 2019, an estimated 55,600 Quebecers were diagnosed with cancer and 22,100 people died from the disease. 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