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Molecular Landscape of Lung Cancer: Unraveling Oncogenic Drivers, Immune Checkpoints, and Therapeutic Targets.

NextEdge Admin

30 Dec 2023

5 min 9 sec

Identifying these oncogenic driver mutations is crucial for personalized treatment strategies, such as targeted therapies. Targeted therapies aim to specifically inhibit the activity of mutated or rearranged proteins, leading to more effective and less toxic treatment options for patients with these specific mutations.

EGFR (Epidermal Growth Factor Receptor) Mutations:

EGFR mutations are commonly found in non-small cell lung cancer (NSCLC), particularly in adenocarcinoma.
Mutations in the EGFR gene lead to continuous activation of the EGFR signaling pathway, promoting cell growth and survival.

ALK (Anaplastic Lymphoma Kinase) Rearrangements:

ALK gene rearrangements are primarily observed in a subset of NSCLC, especially in adenocarcinoma.
The fusion of ALK with other genes leads to constitutive activation of the ALK tyrosine kinase, driving cancer growth.

ROS1 (ROS Proto-Oncogene 1) Rearrangements:

ROS1 rearrangements are another subset of NSCLC, occurring in adenocarcinomas.
Similar to ALK rearrangements, ROS1 fusions result in the activation of the ROS1 kinase, promoting tumor growth.

KRAS (Kirsten Rat Sarcoma Viral Oncogene Homolog) Mutations:

KRAS mutations are often found in lung adenocarcinoma and are associated with a poor prognosis.
Activating mutations in the KRAS gene lead to persistent signaling, contributing to uncontrolled cell proliferation.

BRAF (V-Raf Murine Sarcoma Viral Oncogene Homolog B) Mutations:

BRAF mutations, including the V600E mutation, are observed in a subset of lung cancers.
These mutations result in the activation of the BRAF kinase, promoting cell growth and survival.

HER2 (Human Epidermal Growth Factor Receptor 2) Mutations:

HER2 mutations are found in a small percentage of lung adenocarcinomas.
HER2 alterations lead to dysregulated signaling and contribute to cancer development.

RET (Rearranged During Transfection) Rearrangements:

RET fusions occur in a subset of NSCLC, primarily in adenocarcinomas.
The fusion of RET with other genes results in the constitutive activation of the RET tyrosine kinase.

NTRK (Neurotrophic Receptor Tyrosine Kinase) Fusions:

NTRK fusions, though relatively rare, can be found in various cancer types, including a subset of lung cancers.
These fusions result in constitutively active TRK fusion proteins, promoting uncontrolled cell growth.

c-MET Dysregulation:

c-MET dysregulation, including gene amplification and overexpression, is observed in lung cancer.
Aberrant c-MET signaling contributes to tumorigenesis and metastasis, making it a potential target for therapy.

PD-L1 (Programmed Death-Ligand 1) Expression:

PD-L1 is expressed on the surface of various cells, including cancer cells, and is involved in immune
regulation.
PD-L1 expression in lung cancer cells can inhibit the immune response, allowing cancer cells to evade detection.
Testing for PD-L1 expression is often performed, and high levels may indicate a potential response to immune checkpoint inhibitors, such as pembrolizumab or nivolumab.

Identifying these oncogenic driver mutations and assessing PD-L1 expression is crucial for personalized treatment strategies, such as targeted therapies and immunotherapies. Targeted therapies aim to specifically inhibit the activity of mutated or rearranged proteins, while immunotherapies aim to enhance the body’s immune response against cancer cells. Ongoing research may uncover additional oncogenic drivers, further refining our understanding of the molecular landscape of lung cancer.

Related Tags

oncogenic

mutations

non-small cell lung cancer

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Molecular Landscape of Lung Cancer: Unraveling Oncogenic Drivers, Immune Checkpoints, and Therapeutic Targets.

NextEdge Admin

30 Dec 2023

5 min 9 sec

EGFR (Epidermal Growth Factor Receptor) Mutations:

EGFR mutations are commonly found in non-small cell lung cancer (NSCLC), particularly in adenocarcinoma.
Mutations in the EGFR gene lead to continuous activation of the EGFR signaling pathway, promoting cell growth and survival.

ALK (Anaplastic Lymphoma Kinase) Rearrangements:

ALK gene rearrangements are primarily observed in a subset of NSCLC, especially in adenocarcinoma.
The fusion of ALK with other genes leads to constitutive activation of the ALK tyrosine kinase, driving cancer growth.

ROS1 (ROS Proto-Oncogene 1) Rearrangements:

ROS1 rearrangements are another subset of NSCLC, occurring in adenocarcinomas.
Similar to ALK rearrangements, ROS1 fusions result in the activation of the ROS1 kinase, promoting tumor growth.

KRAS (Kirsten Rat Sarcoma Viral Oncogene Homolog) Mutations:

KRAS mutations are often found in lung adenocarcinoma and are associated with a poor prognosis.
Activating mutations in the KRAS gene lead to persistent signaling, contributing to uncontrolled cell proliferation.

BRAF (V-Raf Murine Sarcoma Viral Oncogene Homolog B) Mutations:

BRAF mutations, including the V600E mutation, are observed in a subset of lung cancers.
These mutations result in the activation of the BRAF kinase, promoting cell growth and survival.

HER2 (Human Epidermal Growth Factor Receptor 2) Mutations:

HER2 mutations are found in a small percentage of lung adenocarcinomas.
HER2 alterations lead to dysregulated signaling and contribute to cancer development.

RET (Rearranged During Transfection) Rearrangements:

RET fusions occur in a subset of NSCLC, primarily in adenocarcinomas.
The fusion of RET with other genes results in the constitutive activation of the RET tyrosine kinase.

NTRK (Neurotrophic Receptor Tyrosine Kinase) Fusions:

NTRK fusions, though relatively rare, can be found in various cancer types, including a subset of lung cancers.
These fusions result in constitutively active TRK fusion proteins, promoting uncontrolled cell growth.

c-MET Dysregulation:

c-MET dysregulation, including gene amplification and overexpression, is observed in lung cancer.
Aberrant c-MET signaling contributes to tumorigenesis and metastasis, making it a potential target for therapy.

PD-L1 (Programmed Death-Ligand 1) Expression:

PD-L1 is expressed on the surface of various cells, including cancer cells, and is involved in immune
regulation.
PD-L1 expression in lung cancer cells can inhibit the immune response, allowing cancer cells to evade detection.
Testing for PD-L1 expression is often performed, and high levels may indicate a potential response to immune checkpoint inhibitors, such as pembrolizumab or nivolumab.