Everyone needs their lungs. From birth, it is the first sign of life. From the first breath to the last human lungs  never stop working. Perhaps because they are constantly working, the lungs, their decline, and cessation of function are one of the most noticeable signs of aging. Respiratory disease and lung cancer are among some of the leading causes of death in the developed world. As they accumulate damage their decline eventually contributes to poorer health – even with the healthiest of lifestyles. Everyone deserves the right to breathe, but everyone’s lungs eventually fail.

Maintenance is crucial because respiratory decline creates multiple negative feedback loops that  can accelerate overall bodily decline (Veldhuizen, Mccaig, Pape, & Gill, 2019). Everyone needs to breathe, and gradually getting less of it is a part of getting older. Once some parts of the body all suffer from the same problem, lack of vital oxygen, deterioration for other parts becomes inevitable.

Treatments for the chronic lung diseases have traditionally been painful and expensive. Lung cancer is especially dangerous. For example, less than a quarter of those diagnosed with NSCLC (by far the most common type of lung cancer) survive the next five years. NSCLC is by far the most common type. SCLC, comprising most remaining lung cancers, has an even lower survival rate (Siegel, Miller, & Jemal, 2020). Lung cancer overall is the most common type of cancer, and because of its lethality, it has become a death sentence for a large segment of the population.

While patient options have been limited in the past, the rise of gene therapies promise treatments which will increase survival rates, eventually to a near certainty. Once the necessary genes are identified and well understood enough that they may be upregulated or downregulated accordingly to alter  the  trajectory of the condition.

Gene therapy has the potential to change all this, but not just for lung cancer.

Gene therapy can be used for almost all forms of cancer.  The point is that if gene therapy works for lung cancer, then a huge portion of cancer victims can be cured, which would really change medicine as we know it.   According to the National Cancer Institute, over 90% of cancer occurs in people over the age of 45, so Integrated Health System’s work towards addressing the hallmarks of aging also prevents most cancer related deaths (White et al., 2014). Cancer is dreaded for good reason, it is not only deadly, it is one of the more painful diseases a person suffer, but with the future comes a promise that one day we will stop this dreadful disease.

Both PGC-1α and Klotho can have roles in treating and/or preventing lung cancer and there is promise for gene therapies to, for example, treat conditions like cystic fibrosis, pulmonary fibrosis, and in preventing transplant rejections (Cruz-Bermúdez et al., 2017) (Shin, Shin, Kim, & Lee, 2014) (Villate-Beitia at al., 2017) (Walweel et al., 2020). The specific roles each individual gene plays in such conditions is not perfectly understood yet, but progress has been made in identifying which ones carry the most weight.

As promising as gene therapies may be, research into solutions for lung cancer has been cross-disciplinary. Some of the most exciting advancements include the use of bioinformatics in the identification of what researchers consider to be seven key genes in NSCLC  (Wang et al., 2020). In the future, medicine may be able to stop or prevent lung cancer by changing the way these genes are expressed in the bloodstream.

This advancement would not have been possible without the databases of genetic and biological data the researchers made full use of. They leveraged and applied bioinformatics in order to glean important details about the body’s complex mechanisms (Deng, Huang, Wang, & Chen, 2020). As information about how the lungs work become more available, and more accessible, researchers can use the new information to isolate certain genes and create new therapies. This is a relatively new field, the more information is gathered about the body, the more research teams can glean from the data.

Also, on the precipice is the emerging field of nanomedicine, while application for these kinds of advancements may be further away, possibilities for integrating nanomedicine with gene therapies are already being explored with promising results (Feldmann, Heyza, Zimmermann, Patrick, & Merkel, 2020) (Han et al., 2015). In the future, regulation of the lungs, and many other systems, may be curated by smart cells, nanites placed throughout the body and talk to each other in order to ensure everything remains in perfect order.

The day may come when, fueled by bioinformatics, nanites deliver care to the lungs, sometimes in the form of upregulation of proteins or gene therapies which IHS uses now. IHS is at the forefront of these kinds of innovations and will do its best to keep people  breathing.

References and Further Reading

Chwistek M. (2017). Recent advances in understanding and managing cancer pain. F1000Research, 6,

  1. https://doi.org/10.12688/f1000research.10817.1

Cruz-Bermúdez, A., Vicente-Blanco, R.J., Laza-Briviesca, R. et al. PGC-1alpha levels correlate with survival

in patients with stage III NSCLC and may define a new biomarker to metabolism-targeted therapy. Sci Rep 7, 16661 (2017). https://doi.org/10.1038/s41598-017-17009-6

Deng, H., Huang, Y., Wang, L., & Chen, M. (2020). High Expression of UBB, RAC1, and ITGB1 Predicts

Worse Prognosis among Nonsmoking Patients with Lung Adenocarcinoma through Bioinformatics Analysis. BioMed Research International, 1–14. https://doi.org/10.1155/2020/2071593

Feldmann, D. P., Heyza, J., Zimmermann, C. M., Patrick, S. M., & Merkel, O. M. (2020). Nanoparticle-

mediated gene silencing for sensitization of lung cancer to cisplatin therapy. Molecules, 25(8), 1994. doi:http://dx.doi.org.library.capella.edu/10.3390/molecules25081994

Han, Y., Li, Y., Zhang, P., Sun, J., Li, X., Sun, X., & Kong, F. (2016). Nanostructured lipid carriers as novel

drug delivery system for lung cancer gene therapy. Pharmaceutical Development & Technology, 21(3), 277–281. https://doi.org/10.3109/10837450.2014.996900

Risk Factors: Age. (n.d.). Retrieved November 02, 2020, from https://www.cancer.gov/about-


Shin, I., Shin, H., Kim, J., & Lee, M. (2015). Role of klotho, an antiaging protein, in pulmonary fibrosis.

Archives of Toxicology.Archiv Für Toxikologie, 89(5), 785-795. doi:http://dx.doi.org.library.capella.edu/10.1007/s00204-014-1282-y

Siegel, R. L., Miller, K. D., & Jemal, A. (2020). Cancer statistics, 2020. CA: A Cancer Journal for

Clinicians, 70(1), 7-30. doi:10.3322/caac.21590

Veldhuizen, R. A. W., McCaig, L. A., Pape, C., & Gill, S. E. (2019). The effects of aging and exercise on lung

mechanics, surfactant and alveolar macrophages. Experimental Lung Research, 45(5/6), 113–122. https://doi.org/10.1080/01902148.2019.1605633

Villate-Beitia, I., Zarate, J., Puras, G., & Pedraz, J. L. (2017). Gene delivery to the lungs: pulmonary gene

therapy for cystic fibrosis. Drug Development & Industrial Pharmacy, 43(7), 1071–1081. https://doi.org/10.1080/03639045.2017.1298122

Walweel, K., Skeggs, K., Boon, A. C., See Hoe, L. E., Bouquet, M., Obonyo, N. G., Pedersen, S. E., Diab, S.

D., Passmore, M. R., Hyslop, K., Wood, E. S., Reid, J., Colombo, S. M., Bartnikowski, N. J., Wells, M. A., Black, D., Pimenta, L. P., Stevenson, A. K., Bisht, K., & Marshall, L. (2020). Endothelin receptor antagonist improves donor lung function in an ex vivo perfusion system. Journal of Biomedical Science, 27(1), 1–9. https://doi.org/10.1186/s12929-020-00690-7

Wang, L., Qu, J., Yu, L., Zhao, D., Rehman, F. U., Kang, Q., & Zhang, X. (2020). Identification and

validation of key genes with prognostic value in non‐small‐cell lung cancer via integrated bioinformatics analysis. Thoracic Cancer, 11(4), 851-866. doi:http://dx.doi.org.library.capella.edu/10.1111/1759-7714.13298

White, M. C., Holman, D. M., Boehm, J. E., Peipins, L. A., Grossman, M., & Henley, S. J. (2014). Age

and Cancer Risk. American Journal of Preventive Medicine, 46(3). doi:10.1016/j.amepre.2013.10.029

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