Lung cancer is a widespread problem in the history of cancer disease which has been chosen for this study to concentrate on the understanding of the mechanism of the malignant cell in the human body and how it affects the human body. This type of cancer is very complicated by different factors including the molecular, cellular, and the changes in the pathophysiology. This is going to be a major issue in today's medical field. This study also concentrates on the factors that can focus the different factors of the illness which can vary from man to man depending on their medical history. For those reasons, the treatment and diagnosis are crucial for overcoming the cancer. This study will use the model of the Hanahan-Weinberg which enlisted the ten hallmarks for the cancer disease. From the ten hallmarks of the mechanism of the cancer, the study will discuss four of the hallmarks to describe it more precisely. The first hallmark that has been chosen for this is the resistance to cell death can signify the apoptotic route which allows the malignant cells to escape the programmed cell death. Besides this, another hallmark that is selected for this is the facilitating capacity of replicative immortality which can achieved by the malignant cells by enabling the uncontrolled proliferation of the cells. These help the alteration of the cells for unchecking the growth of the cancer cells in the lung. The third hallmark describes the escaping of the immune destruction. The fourth hallmark which is chosen for this study is the activating of the metastatic growth and the invasion of the cells. This study aims to provide an explanation of the molecular and cellular pathophysiology of the lung cancer which enables to analysis of the importance of the four hallmarks.
Discussion
Resisting Cell Death
The cancer of the lung can be characterized by the resistance to the death of the cell in the host environment. That can be caused by mutations in the important genome which are connected to the apoptotic routes. The genome material which acts as the tumor suppressor or TP53 can coordinate the route in the way the cells respond and encounter destruction of the deoxyribonucleotide or DNA, which can cause the avoiding of the death of cells in the programmed manner (Hanahan, 2022). These incidents can be termed as the ‘guardians of the genome material. The evading can help the cells to survive and can accelerate the progression of lung cancer. This can inhibit the pathway of apoptotic signaling in the malignant cells of the lungs and alter the BCL-2 family of the protein sequence. These protein sequences can be overexpressed by anti-apoptotic ingredients such as the protein sequences of BCL-xl and the BCL-2.
The concept of the immortality of the replicative nature of lung cancer can be interconnected to the ribonucleoprotein enzyme which is referred to as the telomerase. This function of preserving the structural stability of this enzyme can be maintained in this manner (Hanahan, and Monje, 2023). The telomerase enzyme can be reactivated in some instances of lung cancer for the mutation in the genome of the telomerase. For the mutations, the length of the enzyme is sustained and it can delay the senescence of the cellular level which can permit constant cell division. This enables to check the governing of the cell cycle and process of the disruption in the p16INK4a. This can help to understand the mutation process of the CDKN2A which is known as the cyclin-dependent kinase inhibitor of type 2A. This modification of the proliferation of the cells leads to the unchecked of the system. The cancer of the lung cells has the nature of the replicative immortality caused by the reaction of the telomerase enzyme and the regulation of the cell cycle.
Avoiding the Destruction of Immunity
The complicated nature of avoiding the destruction of the immune system can involve the interaction of the genome and the proteins which can be controlled in the way how the cells of the lung cancer and the immune system of the host can interact. The genome sequence of CD274 can encode the ligand of the pd-L1 which can be interacted in the interaction of the immune system. The interaction nature of the ligand between these can block the activation of the t cell of the host body. This pd L1 can be found in the membrane of the cell but when triggered by the malignant cell interacts with the process of immunity. This designed death ligand or the PDL1 is the essential ingredient of the immunological method. The cells of lung cancer which express with this ligand can also react with the t cells (Al-Bedeary et al. 2020).
The T cells can express the programmed death of the cell of the type of protein which is PD 1. This protein can suppress immunity and involves the encouragement of the development of tumor cells. The mutations of the genome which make impact on the KRAS and EGFR. These mutations are the type of deletion in the genome sequence which re in small. These mutations of the carcinoma of the lungs are observed in the exons 19 and 21. So this mutation can influence the environment of the tumor cells and the immunity and on their interactions (Howlader et al. 2020). With these modifications, the landscape of immunology enables the cancer cells of the lungs can be avoided by the destructive nature of the immunity.
Triggering of the Invasion and Metastasis
The modification of the genes which improves the mobility, invasion of the tissues, and the adhesion of the cells are the characteristics of lung cancer which stimulates the metastasis and the invasion. The alterations of the genome sequence including the E-cadherin affected and quickened the process of EMT that is also known as the epithelial-mesenchymal transition. This process can be processed by three stages which include in the first by losing the polarity of the epithelial cells, next is the adhesion of the cells, and adopting the features to become the mesenchymal cell. The mutation of the genome sequence can assist in the development of lung cancer. The development of this type of malignancy can cause the epithelial cells to become more invasive in nature (Senga, and Grose, 2021). The mobility of the cells is increased and the insensitivity can also be triggered by the modifications of the suppressor genome TP 53. By this alteration of the tumor protein the genes including the RAS and MET which can cause carcinoma of the cells. These genes can trigger the inhibitory cells of the malignant cell. The modifications of the increasing capacity of the cancer cells change to metastasis. This allows the cells to spread in the nearby cells and into the far-off location of the host body.
So the molecular complexities important to the signs of cellular breakdown in the lungs explain an intricate scan of transmissible transformations and dysregulated pathways. From evasion call passing to еmpowеring replicative еvеrlasting status, staying away from the invasion, and triggering it and metastasis, these molecular changes by and large coordinate the dеtеrminеd movement of cellular breakdown in the lungs (Ravi et al. 2022). Understanding this systems at the sub-atomic level gives a еstablishmеnt to the improvement of designated treatments pointed toward upsetting explicit pathways driving the disorder.
Molecular Mechanism of Lung Cancer
Cellular breakdown in the lungs commеncеmеnt is frequently credited to the collection of hereditary transformations, a cycle much of the time set off by the several factors like smoking or cancer-causing substances (Bull, and Byrne, 2022). The prеsеncе of the mutation, rеmеmbеring those for TP53, KRAS, and EGFR, fills in as early development of the molecular level that makes way for uncontrolled cell dеvеlopmеnt. TP53 transformations compromise the capacity of the cell to control the cell cycle and go through apoptosis for damaging DNA, while changes in KRAS and EGFR lead to dysregulating the messaging pathways that can advance the cell multiplication, establishing a favorable climate for the commеncеmеnt and drive of cellular breakdown in the lungs (Moraes et al. 2021). These characteristics of the molecular mechanism in the progression of the tumor cell which can be initiated by this molecular mechanism. The development of carcinoma cells in the lungs can be followed by the specific nature of the cellular breakdown which led to the progression of the malignant cell.
The mutations of the cancer-causing genes including the KRAS and EGRF can perform a significant part in the processing of the unusual signaling route of the cancer cell. The capability of the cancer cell is altered to survive in the host environment and make proliferation. The malignancies in the genome of the EGRF can be the reason of the stimulation of the receptor along with the signaling process (Saha et al. 2021). That can also encourage the proliferation of the carcinoma cell. In a similar perspective, the mutations in the KRAS genome can be the reason for the irrepressibly activating of the route of action that is involved in the event of cell proliferation. The lung cancer represents the deregulatory nature of the pathway of the p13k/AKT/mTOR and this pathway involves the route in a way that can respond to the nutrients which are available and stimulate the regulation of the hormone.
The molecular mechanism of angiogenesis is the essential to understanding the biological mechanism of the development of carcinoma cells and how they spread in the host body (Mouillet et al. 2021). The major factors of the angiogenesis can include the factors which is HIF -1 alpha or the hypoxia-inducible factor 1. The other factor is the VEGF or the vascular endothelial factor. The expression of these factors can encourage the expression of these genomes that help to develop the blood vessels which are in new. This event ensures the tumor cells are receiving of a sufficient amount of nutrients and the oxygen. The enhancement of the HIF-1 alpha can be induced by the hypoxia situation in the environment of the host’s body. The genes which are modified are expressed in the tumor cell by reacting with the changes of angiogenesis. This mechanism can lead to the latent phase to become the destructive phase which are heavily vascularized.
The pathway of the epithelial-mesenchymal transition which is also referred to as the EMT can be affected by the spreading capability of lung cancer which is accompanied by genetic alterations (Thandra et al. 2021). The genes which are linked to the EMT pathway include the e-cadherin and the twist 1 gene which play a significant role in the prior development of the cell. These are mutated for the modifications in the epithelial cells to becoming the destructive nature of the mesenchymal phenotype. The modifications of the lung cells are becoming of very capable of invading into the associated organs (Nooreldeen et al. 2021). The alteration of the genomic sequence in the lung cell can be facilitated by the spreading of the cancer cell which is also very far from the origin.
Conclusion
In conclusion, it can be concluded that the study of the cellular, molecular, and pathophysiology of lung cancer which is thoroughly described in this helped to gain an understanding of the development of the cancer cell by choosing the four hallmarks. These hallmarks are designed by Hanahan and Weinberg which help to get the benefits of the understanding of the genetic moderations of lung cancer. The four hallmarks which are chosen for this are enabling to describe the molecular mechanism by which way the carcinoma cell can grow and spread to the far way of the origin of the malignancy. This helps to gather the information about the spreading mechanism of the oncogene and the suppressor proteins in the environment of the host body. The cells of lung cancer use various techniques to escape the destruction of immunity which allows them to survive in the host and enables them. The four hallmarks of this framework reveal the mechanism of the mutation process of the specific gene which led to the development of the cancer cell. The information of the molecular mechanism helps to customize the process of treatments which can give ways to overcome the genetic profile of the patient and enabling to provide the faith in the advancement of more effective interventions.
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Reference List
Journals
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