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Signal transduction in cancer: a cross-talk

Señales de transducción en cáncer: una comunicación cruzada


Resumen gráfico Signal transduction in cancer: a cross-talk
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García Robledo JE, Cardona AF. Signal transduction in cancer: a cross-talk. Rev. colomb. hematol. oncol. [Internet]. 2026 Feb. 17 [cited 2026 Feb. 18];13(1-Supl):38-52. https://doi.org/10.51643/22562915.836

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How to Cite
1.
García Robledo JE, Cardona AF. Signal transduction in cancer: a cross-talk. Rev. colomb. hematol. oncol. [Internet]. 2026 Feb. 17 [cited 2026 Feb. 18];13(1-Supl):38-52. https://doi.org/10.51643/22562915.836

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Juan Esteban Garcia-Robledo,

Médico e investigador con amplia experiencia en investigación traslacional y clínica para le desarrollo de terapias celulares adoptivas para el tratamiento del cáncer. Actualmente se desempeña como subdirector académico y de investigación en IDC Instituto de Cáncer Hemato Oncólogos en Cali.


Andrés F. Cardona ,

Director de investigación, ciencia y educación del Centro de Investigación y Tratamiento del Cáncer Luis Carlos Sarmiento Angulo (CTIC) ubicado en Bogotá, Colombia. Además, es miembro asociado de la Clínica del Country y del Instituto de Oncología de la Fundación Santa Fe de Bogotá (ICCAL). También es profesor asociado en las Facultades de Medicina de la Universidad El Bosque y la Universidad de los Andes. Obtuvo su título de médico en la Universidad del Rosario (Bogotá, Colombia) y luego se especializó en epidemiología en la misma institución. Después de eso, el Dr. Cardona realizó estudios de posgrado en medicina interna (Universidad Javeriana, Bogotá, Colombia), oncología clínica (Universidad El Bosque, Bogotá, Colombia), epidemiología relacionada con el cáncer orientada al desarrollo de ensayos clínicos (Universidades de Barcelona a Sevilla, España) y epidemiología clínica (Universidad de Sevilla, España). También obtuvo un doctorado en genómica tumoral (Universidad Autónoma de Barcelona, ​​España), con énfasis en investigación traslacional.


Introduction: Aberrant signal transduction is a defining feature of cancer, governing proliferation, survival, stemness, immune evasion, and therapeutic resistance. The MAPK, PI3K/AKT/mTOR, and Wnt/β-catenin pathways are frequently altered in solid tumors and function as key regulatory hubs within an interconnected signaling network.

Methods: We conducted a comprehensive literature review focused on the structure, activation mechanisms, oncogenic alterations, and interactions among MAPK, PI3K/AKT/mTOR, and Wnt/β-catenin pathways. We analyzed preclinical and clinical data on therapeutic strategies targeting these pathways and examined specific implementation challenges in Latin America.

Results: MAPK signaling is frequently dysregulated through RAS and BRAF mutations, promoting uncontrolled proliferation. PI3K/AKT/mTOR alterations, including PIK3CA mutations and PTEN loss, drive growth and metabolic reprogramming. Wnt/β-catenin activation supports stemness and immune evasion, often via APC or CTNNB1 mutations. Crosstalk between these pathways amplifies oncogenic signaling and contributes to therapeutic resistance. Dual inhibition strategies show preclinical promise but are limited by toxicity and compensatory feedback. Functional biomarkers and combinatorial regimens are under investigation to overcome resistance. In Latin America, access to molecular diagnostics and targeted therapies remains limited, though efforts to expand precision oncology are underway.

Conclusions: Cancer signaling is shaped by a complex, adaptive network rather than isolated pathways. Therapeutic success will depend on integrated strategies that target signaling interactions. Regional implementation requires context-specific solutions, including minimal biomarker panels, expanded diagnostics, and collaborative infrastructure.


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