Mini Review - Biology & Medicine Case Reports (2022) Volume 6, Issue 4

Molecular pathophysiology in lung cancer, detection, treatment and various clinical applications.

Department of Surgery, Yale University, 330 Cedar Street, New Haven, Connecticut, United States

*Corresponding Author:

Elizabeth Francis
Department of Surgery
Yale University, 330 Cedar Street
New Haven, Connecticut, United States
E-mail: francisE@yale.edu

Received: 01-Jul-2022, Manuscript No. AABMCR-22-70596; Editor assigned: 04-Jul-2022, PreQC No. AABMCR-22-70596 (PQ); Reviewed: 18-Jul-2022, QC No AABMCR-22-70596; Revised: 21-Jul-2022, Manuscript No. AABMCR-22-70596(R); Published: 28-Jul-2022, DOI:10.35841/aabmcr-6.4.117

Citation: Francis E. Molecular pathophysiology in lung cancer, detection, treatment and various clinical applications. J Pub Health Nutri. 2022;6(4):117

Keywords

Pathophysiology, Lung cancer, Genetic abnormalities.

Introduction

Amplifying proto-oncogenes like MET, FGFR1, and DDR2 in adenocarcinomas and squamous cell lung cancers. MicroRNA-mediated oncogenic gene overexpression (miRNAs) [1]. TP53, RB1, CDKN2A, FHIT, RASSF1A, and PTEN are examples of tumour suppressor genes (TSG) that are inactivated. Telomerase activity is increased, which promotes cellular longevity by preserving telomere length through telomere synthesis from scratch and extension of already-existing telomeres (100 percent of SCLCs and 80% to 85% of NSCLCs). hTERT gene amplification occurs in 57% of NSCLCs.

Diagnosis and clinical applications in treating lung cancer

There has been a tremendous amount of effort done to enhance patient care in the clinic, including early discovery, treatment, and prognosis prediction, using the knowledge about these genetic defects that has been gathered.

Identification of biomarkers for both initial and recurring illness Lung cancer is now diagnosed solely based on symptoms, and it is frequently discovered when curative action, such as surgery, is no longer an option. The fiveyear survival rate for individuals with early-stage, operable NSCLC ranges from 50 to 70%, but it reduces to 2 to 5% for those whose tumours have gone far. Numerous possible indicators for the early identification of lung cancer have been studied. However, due to the absence of high sensitivity and specificity or functional relevance of these biomarkers to lung carcinogenesis, there are still no biomarkers for the detection of lung cancer in clinical application [2].

The creation of innovative treatments: Lung cancer patients can presently access EGFR- and ALK-targeted medicines. Bevacizumab is one angiogenesis inhibitor that can be used to treat lung cancer. These tailored treatments provide a potential and practical means of individualised lung cancer care. However, side effects might be a problem and treatment resistance is frequently developed. The therapeutic issue is to identify the most efficient combination therapy for each patient that may deliver the best possible care with the fewest adverse effects [3].

Standard treatment for advanced lung cancer involves platinum-based regimens. However, accumulated haematoand neuro-toxicities restrict their therapeutic efficacy, stressing the necessity for alternate treatment plans. A crucial enzyme for nucleotide excision repair is ERCC1 (NER) [4]. High ERCC1 expression is correlated with a better overall prognosis in NSCLC, whereas low ERCC1 expression is correlated with higher susceptibility to platinum-based treatment [4]. Nearly 50% of NSCLC patients have low ERCC1 levels, making them candidates for alternative treatments that take advantage of this tumour ERCC1 deficit. The ribonucleotide reductase regulatory subunit RRM1 is required for the production of deoxyribonucleotides (dNTPs).

The antimetabolite medication gemcitabine, which is a cornerstone cancer therapy in the treatment of numerous malignancies including lung cancer, primarily targets RRM1. Ribonucleotide reductase is permanently inactivated by gemcitabine, which binds directly to RRM1. High RRM1 levels are linked to tumour resistance to gemcitabine therapy, whereas low RRM1 levels are linked to tumour sensitivity.

A number of novel potentially treatable changes were revealed in NSCLC, such as the amplification of FGFR1 and the mutation of DDR1 in squamous cell lung cancers. These changes might have a significant prognostic and predictive role in determining how well patients respond to FGFR inhibitor or DDR1 inhibitor therapies (e.g., Dasatinib).

Finding prognostic and predictive biomarkers: In both early and late stages of lung cancer, a large panel of molecular markers has been evaluated for prognostic and/or predictive relevance. It has been demonstrated that the presence of an EGFR mutation (10–15% of advanced NSCLC) or an ALK rearrangement (ALK-EML4 fusion) (5-7% of advanced NSCLC) is predictive of a therapeutic benefit with EGFR tyrosine kinase inhibitors (TKIs) or an ALK TKI (crizotinib) in advanced NSCLC.

Conclusion

The survival statistics for people with lung cancer and mesothelioma are still low, despite the rigorous research and development of several novel targeted treatments and immunotherapies. To pinpoint the underlying genetic changes and predispositions influencing clinical outcome, more research is still required. Early diagnosis and treatment of these malignancies may significantly increase patient survival. In reality, more than 60% of lung cancer patients receive their diagnosis in the latter stages of the illness, when it is improbable that the available treatments would be successful. In order to support the best treatment decision for each patient, as well as for early identification of lung cancer that might enhance the prognosis, reliable biomarkers are urgently needed to predict sensitivity to each therapeutic modality in thoracic malignancies.

References

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