Immune Markers in Non-Small Cell Lung Cancer: What Else Beyond Pd-L1 and Tumour Mutational Burden is there?
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2019, Vol 12, Issue 5
Abstract
The advancement of immune-oncology and immunotherapy in recent decades is unprecedented. Immune evasion and cancer promoting inflammation have been added as new hallmarks of malignancy. This opened a view of cancer as an immunological disease. Non-small cell lung cancer [NSCLC] is one of the leading cancer types in terms of immunotherapy research and implication. The need for predictive markers to immune checkpoint inhibitors fuels the search for immune markers in NSCLC. However, since the importance of immune evasion is now recognised, defining the immunological phenotype of NSCLC can have broader implications. Immune markers may aid in better defining the prognosis, supplement TNM staging and predict response to all modalities of treatment. PD-L1 and TMB are immune markers firmly established in clinical practice. However, 2 markers can hardly capture the full scope of immune response in cancer. We have searched PubMed, Cochrane and clinicaltrials.gov databases to compile a brief review of immune markers that seem closest to daily clinical practice in NSCLC other than PD-L1 and TMB. Our aim is to review the possible implications of these markers in personalization of treatment of NSCLC patients. The immune markers helpful in defining prognosis, staging and predicting response to various treatment modalities.After being abandoned for the several decades, immune-oncology has since made huge leaps to establish itself as one of the cornerstones of cancer research. The ability to evade the destruction by the immune system has been included as one of the hallmarks of a malignant disease [1]. The complexity of the relationship between the cancer and the immune system should be stressed out. The evolving view of this topic has led to the change of the original immune-surveillance theory into immune-editing [2]. The immune editing theory considers the possibility of selection of less immunogenic clones and the eventual evolution of cancer that allows it to evade or even take advantage of immune systems’ elements. The great progress made in this field has resulted in advance of immune checkpoint inhibitors into daily practice. These clinical trials have even placed it as a preferred 1st line treatment in some chemosensitive cancer types. NSCLC with high PD-L1 expression is one such example. However, a considerable number of patients do not benefit from this treatment and long-lasting responses are seen only in few responders.The means to immune evasion are many and are not limited to expression of immune checkpoints. The formation and execution of anticancer immune response is described by cancer immunity cycle [3]. Cancer may inactivate the immune response at any step of this cycle: formation of neoantigens, antigen uptake, DC maturation and migration, antigen presentation and T cell priming, T cell migration/ tumour infiltration and finally effector functions of T cells at the tumour. Based on this, three cancer immune phenotypes have been described: immune-desert, excluded and inflamed tumours [4]. Each phenotype is associated with immune response inactivation at various points of the cancer immunity cycle. Furthermore, every step of this cycle may be impaired by several distinct mechanisms. The identification of the immune phenotype and the underlying mechanisms of immune evasion may therefore be crucial in personalization of therapy.
Authors and Affiliations
JB Jaroslav Bublevič, SC Saulius Cicėnas, VP Vita Pašukonienė
Keywords
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- EP ID EP598524
- DOI 10.26717/BJSTR.2019.12.002325
- Views 155
- Downloads 0
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