Changing The Lung Cancer Perspective: A Tale Of Hope And Survival
Confined to a wheelchair, and unable to breathe at the age of 50 without extra oxygen, Maria was running out of time— and hope. Her oncologist recommended hospice, but Maria wanted a second opinion from another specialist, not ready to surrender to lung cancer.
After learning that she had never smoked, the consulting oncology care team recommended treatment involving a new drug that showed a lot of promise for patients of lung cancer who never smoked. Within days, Maria was out of her wheelchair and was breathing without the support of supplemental oxygen. Her future was unclear but she had her life back for the moment— and with it, a renewed sense of hope and joy.
“I will never forget her story,” said William Pao, M.D., Ph.D., who witnessed Maria’s second chance as a fellow at the Memorial Sloan-Kettering Cancer Center before becoming Head of Pharma Research and Early Development. “We hadn’t yet known at the time why never-smokers with lung cancer responded well to the drug but based on clinical evidence, we saw in patients with similar profiles, we were able to put Maria on a treatment course that targeted her specific type of tumour. Soon afterward, we worked with others to identify the genetic basis of the tumour response to check those which are most likely to benefit from it routinely.
With the tremendous progress made in screening for lung cancer over the past decade, Maria’s tale is an early example of how successful collaboration can be in the battle against lung cancer between diagnostics and pharmaceuticals.
Survival And More
Lung cancer is the most prevalent type of cancer worldwide. It is also the most aggressive, taking the lives of 1.8 million people each year — more than the combination of breast, colorectal and prostate cancers[1]. More than two-thirds of patients with lung cancer are diagnosed at a late stage after the disease has spread to other parts of the body[2].
Yet we’ve entered an era of new hope today. “We have a much greater understanding of what is happening in lung cancer cells, how the immune system controls lung cancers, and how this new knowledge can be applied,” said Dr. Pao. “It is an incredibly exciting time for research, both in terms of diagnostics and development of new medicines. New information empowers us to help patients with lung cancer like never before.’
Different Treatment For Different Patients And Different Cancer
At the heart of these revolutionary developments, is an emphasis on understanding the genetic mechanisms behind cancer . “We used to believe that there were only two major types of lung cancer, but we now know that there are multiple different subsets,” said Dr. Pao. “When you take it further— when you look at the genetic make-up— we now know that everybody has a different tumour individually.”
Genetic testing and advanced diagnostics will detect mutations in patients like Maria and determine the best therapy, ultimately giving doctors and other healthcare professionals the ability to deliver personalised healthcare. In the case of Maria, she had an EGFR mutation, which was the explanation for the outcome of her successful treatment. Knowing the genetic footprint of any patient allows for greater accuracy in risk assessment, disease diagnosis, accurate prognosis, and therapy assignment. Researchers today can stratify and develop new, life-saving drugs and can track patients during their treatment process.
Targeting Gene Mutations
The gene rearrangement of anaplastic lymphoma kinase (ALK) triggers the formation of an ALK fusion protein, which controls the abnormal growth and survival of cancer cells[3, 4]. This is typically found in people who are non-smokers or light smokers.[5] ALK gene rearrangement patients can benefit from a medication directly targeting the ALK fusion protein, shutting down its signalling and leading to tumour cell death.
Epidermal Growth Factor Receptor (EGFR) is a signalling protein that sits across the cell membrane.[7] It stimulates cell growth and division when the Epidermal Growth Factor (EGF) binds to the EGFR. Mutations lead to prolonged activation of cell growth in EGFR-mutant lung cancer, leading to the formation of cancerous tumours [5,6]. Patients with this type of lung cancer may benefit from a medication that targets the mutant EGFR protein, shutting down its signalling and leading to tumour cell death.
From Science To Medicine
Collaborative work in the fields of diagnostics and pharmaceutics stimulates creativity that can eventually change the lives of patients. Targeted therapies, which are used alone or in conjunction with other treatments, help to stop the growth and metastases of lung cancer cells. Immunotherapy continues to show tremendous potential by harnessing the immune system’s ability to detect and kill cancer cells; cancer immunotherapy has been shown to prolong the lives of metastatic disease patients by five years and beyond — much longer than standard therapies, Dr Pao said. Routine biopsies will show which drug can overcome resistance for patients whose tumours initially shrink on treatment but then become resistant. Lung cancer remains a complex disease but current pipeline work, clinical trials, and investigational therapies will continue to discover responses that will save and improve lives.
Even though no single intervention is likely to cure cancer — and much work remains to be done — new possibilities change perspectives and prognosis. Experts like Dr Pao and many others are trying to turn lung cancer into a chronic disease rather than a fatal disease. Driven by the promise of the future and the rewards that come with offering patients such as Maria, the opportunity to experience more of the unforgettable moments of life, today’s collaboration between diagnostics and pharmaceutical science instills optimism where once there was none.
References:
- https://www.lung.org/lung-health-and-diseases/lung-disease-lookup/lung-cancer/learn-about-lung-cancer/what-is-lung-cancer/how-serious-is-lung-cancer.html
- Ellis, PM, Vandermeer, R. J Thorac Dis, 2011 Wetp; 3(3):183-188.: http://jtd.amegroups.com/article/view/159/html_79
- Choi YL, et al. Cancer Res 2008; 68:4971–4976: https://pubmed.ncbi.nlm.nih.gov/18593892/
- Roskoski Jr, R. Pharmacol Res 2013;68:68-94: https://pubmed.ncbi.nlm.nih.gov/23201355/
- Gridelli C, et al. Cancer Treat Rev 2014;40:300-306: https://pubmed.ncbi.nlm.nih.gov/23931927/
- Britten CD. Mol Cancer Ther 2004;3:1335-1342.: https://mct.aacrjournals.org/content/molcanther/3/10/1335.full.pdf
- Prenzel, N et al. Endocrine-Related Cancer 2001;8:11-31.: https://pubmed.ncbi.nlm.nih.gov/11350724/