Molecular Carcinogenesis: Structures and Therapeutic Targeting of Cancer-Related Molecules
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- Educational and scientific content explaining the genetic and epigenetic mechanisms behind cancer development.
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What Is Molecular Carcinogenesis?
Molecular carcinogenesis refers to the process where genetic and epigenetic changes accumulate in cells, transforming them from normal to malignant. Key factors include:
- Mutations in oncogenes (e.g., KRAS, MYC)
- Inactivation of tumor suppressor genes (e.g., TP53, RB1)
- Epigenetic alterations such as DNA methylation and histone modification
- External agents like carcinogens, viruses, and radiation
These molecular events disrupt cell cycle control, promote uncontrolled growth, and enable cancer cells to avoid programmed cell death (apoptosis).
Key Molecules Involved in Cancer Development
Oncogenes and Proto-Oncogenes
Proto-oncogenes normally regulate cell growth. When mutated, they become oncogenes that drive tumor progression.
Examples:
- KRAS (colorectal, lung cancers)
- MYC (various tumors)
- BRAF (melanoma)
Tumor Suppressor Genes
These genes prevent abnormal cell growth. Loss or mutation removes natural growth brakes.
Examples:
- TP53, the “guardian of the genome”
- RB1, regulator of the G1/S cell cycle checkpoint
- BRCA1/2, involved in DNA repair
Epigenetic Regulators
Abnormal epigenetic changes can silence tumor suppressor genes without altering DNA sequence.
Key targets include: DNMT1, HDACs, EZH2.
Questions?
It is the study of how genetic and epigenetic changes cause cancer at the cellular level.
Mutated oncogenes promote uncontrolled cell division and survival, fueling tumor growth.
They normally prevent cancer; their loss allows unchecked cell proliferation.
By analyzing target protein 3D structures, researchers design molecules that bind specifically to inhibit them.
KRAS is frequently mutated in colorectal and lung cancers.
MYC regulates cell cycle and metabolism and is overexpressed in many tumor types.
BRAF mutations (especially V600E) are common in melanoma and affect the MAPK signaling pathway.
Tumor suppressor genes are protective genes that stop abnormal cell growth, repair DNA damage, or trigger apoptosis. When inactivated or deleted, they lose their ability to control tumors.
TP53: Known as the “guardian of the genome,” it controls DNA repair and apoptosis.
RB1: Regulates the G1/S checkpoint in the cell cycle.
BRCA1/2: Critical for DNA double-strand break repair; mutations increase risk of breast and ovarian cancers.
Key epigenetic regulators include:
- DNMT1: Involved in maintaining DNA methylation
- HDACs: Control histone acetylation
- EZH2: A histone methyltransferase associated with gene repression
Drugs targeting these proteins (e.g., HDAC inhibitors) are being developed or tested for cancer treatment.
| Title | Summary | PDF Link | |
|---|---|---|---|
| 1 | Tumor-Associated Macrophages Induce Vascular Endothelial Cell Capillary Formation | Explores how TAMs interact with lymphatic endothelial cells to form capillary-like structures using time-lapse and 3D visualization. | View PDF |
| 2 | Tumor-Associated Macrophage: Its Role in Cancer Invasion and Metastasis | Describes how TAMs facilitate invasion, metastasis, and vasculogenic mimicry through cytokine and growth factor signaling. | View PDF |
| 3 | Matriptase: Its Role in Cancer Development and Malignancy | Reviews the role of matriptase in ECM degradation, metastasis, and oncogenic signaling. | View PDF |
| 4 | Roles of p53 in Carcinogenesis, Diagnosis and Treatment | Discusses p53’s structure, mutation impact, apoptosis regulation, and therapeutic implications. | View PDF |
| 5 | Sesamin Inhibits Endothelial Growth and Angiogenesis | Shows sesamin’s role in inhibiting pathological angiogenesis via VEGFA pathways without harming normal vessel formation. | View PDF |
| 6 | Tumor-Associated Macrophage in Tumor Angiogenesis | Explores TAMs' role in secreting VEGFA, MMP9, and other factors driving angiogenesis and therapy resistance. | View PDF |
| 7 | p53: Structure, Function and Therapeutic Applications | Offers detailed analysis of p53’s molecular biology and its therapeutic relevance in cancer treatment. | View PDF |
| 8 | TNF-α, IL-8, IL-6 in Capillary Tube Formation | Highlights the angiogenic and antiangiogenic effects of pro-inflammatory cytokines, especially TNF-α. | View PDF |
| 9 | VEGF-A Expression in Colorectal Cancer | Reviews the role of VEGF-A in colorectal tumor vascularization and its clinical implications. | View PDF |
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