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Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
Published on: February 6, 2015
Molecular mechanisms in cancer: what should clinicians know?
Jaffer Ajani1, Victoria Allgood
1Department of Gastrointestinal Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030-4009, USA. jajani@mdanderson.org
Abstract:
Normal cells are influenced by a variety of environmental and host influences that can produce pro-carcinogenic mutations. Either a single or a series of mutations might result in cellular transformation. Like normal cells, most cancer cells use multiple redundant intracellular signaling pathways to ensure the maintenance and viability of functions critical to their survival. Thus, cellular pathways that are integral to cell function, survival, proliferation, and receptor expression are potential targets for therapeutic intervention. One example of this is the epidermal growth factor receptor signaling pathway. Other potential targets are molecules that mediate processes through which tumors produce angiogenic and invasion factors that stimulate host blood vessel growth into tumors and allow tumor growth and metastasis, such as the vascular endothelial growth factor. Targeting of downstream events that result in cellular apoptosis is another potential strategy. Continued investigations may result in the development of proteomic profiling databases through which a patient might be matched with molecular signatures in a library and upon which individualized cancer therapies might be selected. In this way, clinicians might recommend combinations of molecularly targeted agents and other therapies on the basis of an individual patient's proteomic profile.
Insights
Cancer cells rely on signaling pathways for survival, making them targets for new therapies. Personalized cancer treatment may use proteomic profiles to match patients with targeted molecular agents.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Normal cells can acquire pro-carcinogenic mutations from environmental and host factors, leading to cellular transformation.
- Cancer cells, like normal cells, utilize redundant intracellular signaling pathways for survival, proliferation, and receptor expression.
Purpose of the Study:
- To identify and discuss potential therapeutic targets within cellular signaling pathways crucial for cancer cell survival and proliferation.
- To explore the role of angiogenic and invasion factors in tumor growth and metastasis.
- To highlight the potential of proteomic profiling for developing individualized cancer therapies.
Main Methods:
- Review of established knowledge on cellular signaling pathways in normal and cancerous cells.
- Identification of key molecules and pathways involved in cancer cell survival, proliferation, angiogenesis, and metastasis.
- Discussion of therapeutic strategies targeting these pathways and downstream events like apoptosis.
- Exploration of proteomic profiling for personalized medicine.
Main Results:
- Cellular signaling pathways, such as the epidermal growth factor receptor (EGFR) pathway, are critical for cancer cell function and survival.
- Vascular endothelial growth factor (VEGF) and related molecules are key mediators of tumor angiogenesis and metastasis.
- Targeting downstream apoptotic pathways presents another therapeutic strategy.
- Proteomic profiling offers a method to match patients with specific molecular signatures for tailored therapies.
Conclusions:
- Targeting specific molecular pathways, including EGFR and VEGF signaling, offers promising therapeutic avenues for cancer treatment.
- Personalized medicine approaches utilizing proteomic profiling can guide the selection of targeted agents and combination therapies for individual patients.
- Further research into proteomic databases and molecular signatures will advance the development of individualized cancer therapies.
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