Commentary - Journal of Pulmonology and Clinical Research (2023) Volume 6, Issue 5
Cancers of the human lung are classified molecularly and genetically.
Matthew Franklin *
Department of Medical Oncology, University Hospital of Parma, Parma, Italy
- *Corresponding Author:
- Matthew Franklin
Department of Medical Oncology
University Hospital of Parma
Received:30-Aug-2023, Manuscript No. AAJPCR-23-112900; Editor assigned:02- Sep -2023, PreQC No. AAJPCR-23-112900 (PQ); Reviewed:16-Sep-2023, QC No. AAJPCR-23-112900; Revised:21-Sep-2023, Manuscript No. AAJPCR-23-112900 (R); Published:28-Sep-2023, DOI:10.35841/ /aajpcr-6.5.170
Citation: Franklin F. Cancers of the human lung are classified molecularly and genetically. J Pulmonol Clin Res. 2023;6(5):170
Given its high incidence and fatality rates, lung cancer continues to be one of oncology's most difficult problems, posing a threat to global health. In the complex web of this illness, one genetic change—KRAS mutations—stands out clearly as a major force behind the onset and spread of lung cancer. Because of their widespread prevalence and important implications for patient outcomes, these mutations, which affect the Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) gene, have become a focus of study and clinical attention .
A crucial protein in the intracellular signaling pathways that control cell growth, differentiation, and survival is encoded by the KRAS gene. This gene's mutations set off a chain reaction of abnormal cellular functions that promote unchecked cell growth and survival, two characteristics that characterize cancer. Although KRAS mutations are not particular to lung cancer, their prevalence and clinical importance in this situation have led to a lot of research on them .
Lung cancer is one of the most common and deadly types of cancer in the world, and it are a complex and diverse illness. Scientists have using molecular and genetic classifications to untangle the complex web of causes driving this deadly illness' growth and progression in their attempt to understand and treat it. Instead of being one illness, lung cancer is a spectrum of conditions, each with a distinct molecular make-up and clinical behavior. Non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) are the two principal histological subtypes of lung cancer, respectively. However, developments in genetics and molecular biology have uncovered a greater level of intricacy .
The lung cancer therapy landscape has undergone a revolution thanks to molecular and genetic classifications. With the use of personalized medicine, oncologists may now adapt treatments to each patient's particular genetic profile, enhancing therapeutic effectiveness and minimizing side effects. Erlotinib and osimertinib are two examples of EGFR tyrosine kinase inhibitors that may be helpful for people with EGFR mutations. ALK inhibitors like crizotinib can treat people with ALK rearrangements. For some lung cancer patients, particularly those with strong PD-L1 expression, immunotherapy has also shown promise .
Lung cancers are a heterogeneous set of diseases that can be categorized according to their histological and molecular features; they are not one single disease. Small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) were historically the two main subtypes of lung cancer. Modern developments in molecular biology have nonetheless painted a considerably more complex picture .
We now have a better understanding of lung cancer thanks to molecular and genetic classifications, which also expose the heterogeneity of this disease and provide a window into more potent treatment options. The future holds hope for even more precise and tailored medicines, ultimately improving the prognosis and quality of life for those affected by this difficult disease. Lung cancer is a complicated disease that is still being fully understood at the molecular level by research. Lung cancer treatment is changing thanks to the incorporation of genetics and genomics into clinical practice, and we're getting closer to a time when every patient is given a course of action that is customized to their particular genetic profile.
- Dacic S, Ionescu DN, Finkelstein S, et al. Patterns of allelic loss of synchronous adenocarcinomas of the lung. Am J Surg Pathol. 2005;29(7):897-902.
- Peifer M, Fernández-Cuesta L, Sos ML, et al. Integrative genome analyses identify key somatic driver mutations of small-cell lung cancer. Nat Genet. 2012;44(10):1104-10.
- Sos ML, Michel K, Zander T, et al. Predicting drug susceptibility of non-small cell lung cancers based on genetic lesions. J Clin Invest. 2009;119(6):1727-40.
- Huang M, Shen A, Ding J, et al. Molecularly targeted cancer therapy: Some lessons from the past decade. Trends Pharmacol Sci. 2014;35(1):41-50.
- Mataki H, Enokida H, Chiyomaru T, et al. Downregulation of the microRNA-1/133a cluster enhances cancer cell migration and invasion in lung-squamous cell carcinoma via regulation of Coronin1C. J Hum Genet. 2015;60(2):53-61.