historia natural de un tumor ernesto gil deza instituto oncológico henry moore
TRANSCRIPT
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Historia natural de un tumor
Ernesto Gil DezaInstituto Oncológico Henry Moore
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El origen de un tumor…mutación
Por eso puede afirmarse que: “el cáncer es el precio que la vida está dispuesta a pagar para poder evolucionar”
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Se estima que se necesitan al menos 6 eventos para producir
transformación
Probabilidad:de mutación de una de 1013
células:
10-42 X 1013= 1/1029
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GENOMA HUMANO
Genoma nuclear3000 Mb
~30.000 genes
Genoma mitocondrial16.6 kb
37 genes
Genes y secuencias
relacionadas 30 %
DNA extragénico70%
Secuenciascodificantes
Secuenciasno codificantes
pseudogenesIntrones, secuencias no traducidas, etc.
Único o Bajonúmero de copias
Moderado o elevado número de copias
Repeticiones en tandem
Repeticionesdispersas
10% 90%
80%20%
2 rRNA
22 tRNA
13 secuencias codificantes
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Biología molecular
Genómica
Transcriptómica
Proteómica
Complejidad
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Oncogenesis
Hannahan and Weinberg Cell 2000
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Preinvasive
Invasive
Genetic instability
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Historia
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Composición química de la célula
Albrecht Kossel
Premio Nobel de Medicina de 1910: "in recognition of the contributions to our knowledge of cell chemistry made through his work on proteins, including the nucleic substances"
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Cromosomas y herencia
Thomas Hunt Morgan
Premio Nobel de Medicina de 1933
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Mutagenicidad
Hermann Joseph Muller
Premio Nobel de Medicina de 1946“for the discovery of the production of mutations by means of X-ray irradiation"
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Regulación y recombinación genética
George Wells Beadle
Edward Lawrie Tatum
Joshua Lederberg
Premio Nobel de Medicina de 1958
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Síntesis de ADN y ARN
Severo Ochoa Arthur Kornberg
Premio Nobel de Medicina de 1959
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Estructura de ADN y transmisión de la información
Francis Harry Compton Crick
James Dewey Watson
Maurice Hugh Frederick Wilkins
Premio Nobel de Medicina de 1962
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Control enzimático en la replicación viral
François Jacob André Lwoff Jacques Monod
Premio Nobel de Medicina de 1965
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Tumores inducidos por virus
Peyton Rous
Premio Nobel de Medicina de 1966
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Genes y síntesis de proteínas
Robert W. Holley Har Gobind Khorana Marshall W. Nirenberg
Premio Nobel de Medicina de 1968
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Integración de virus tumorales al material genético
David Baltimore Renato Dulbecco Howard Martin Temin
Premio Nobel de Medicina de 1975
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Enzimas de restricción y ADN
Werner Arber Daniel Nathans Hamilton O. Smith
Premio Nobel de Medicina de 1978
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Factores de crecimiento
Stanley Cohen Rita Levi-Montalcini
Premio Nobel de Medicina de 1986
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Oncogenes
J. Michael Bishop Harold E. Varmus
Premio Nobel de Medicina de 1989
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Regulación de ciclo celular
Leland H. Hartwell
R. Timothy (Tim) Hunt
Sir Paul M. Nurse
Premio Nobel de Medicina de 2001
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Apoptosis
Sydney Brenner H. Robert Horvitz
John E. Sulston
Premio Nobel de Medicina de 2002
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Aplicaciones clínicas
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Biología molecularAplicaciones clínicas
EtiologíaFisiopatogeniaDiagnósticoPronósticoTratamiento
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Etiología
MutaciónEdadExposiciónHereditarios son más jóvenes
Por eso es infrecuente hallarlo en animales salvajes.
Era infrecuente hasta el siglo XX
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•Clonogenicidad•Invasión•Traslación•Angiogénesis•Resistencia
Fisiopatogenia
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De Vita - 2001
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¿ Porqué crece un tumor ?
De Vita - 2001
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¿Cómo se explica?
•Protooncogenes:
PROLIFERACION CELULAR
•Genes Supresores de Tumores:
PREVIENEN LA PROGRESIÓN DEL CICLO CELULAR
INDUCEN APOPTOSIS
REPARACIÓN DE MUTACIONES
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•Factores de crecimientos
•Receptores de membrana
•Transductores de señales
•Proteinas de unión al ADN
•Progresión del ciclo celular: Ciclinas
PROTOONCOGENES
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Perfil genético
Watson and Crick in Cavendish Laboratory, Cambridge
University 1953
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Determinar malignidad Objetivo del estudio
- Determinar sin RNA extraido del estrato córneo puede distinguir melanoma de nevus atípico en lesiones sospechosas.
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Epidermal Genetic Information Retrieval (EGIR) • 4 x 20 mm tapes harvest 4-7 ng total
RNA from normal skin• Lesions of 3 mm can be assayed• RNA stable at ambient temperature for
72 hr
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Hierarchical Clustering of Melanoma and Atypical Nevi Using the 19-Gene Classifier
Atypical nevusMelanoma Atypical nevusMelanoma
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These four histoslides will be superimposed upon one another to create a 3-D model of either the melanoma or the nevi using "3-D Doctor" computer software. This is called segmentation.
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Computer-assisted tracing, or mapping, of the melanocytic nests within either the melanoma or the nevi.
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After the 2-D histoslides are downloaded onto "3-D Doctor" and segmentation has occurred, a 3-D model is created of the melanoma or the nevi. The lighter color represents the nests of melanocytes.
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"3-D Doctor" allows us to separate out the nests of melanocytes (blue color) from the rest of the neoplasm (yellow color).
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•Clonogenicidad•Invasión
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El proceso metastásico
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Invasión
De Vita - 2001
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•Clonogenicidad•Invasión•Traslación
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Adhesión y migración I
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Adhesión y migración II
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•Clonogenicidad•Invasión•Traslación•Angiogénesis
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Angiogénesis
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•Clonogenicidad•Invasión•Traslación•Angiogénesis•Resistencia
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Evolución de un tratamiento
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Van de Vijver y col. NEJM 2002
ResistenciaGenes y sobrevida
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Molecular Breast Cancer Subtype Dendrogram
Carey - ASCO 2005
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Genes y sarcomas
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¿Para qué sirve este conocimiento?CurarPaliarSentar pronósticoSeleccionar pacientesSeleccionar tratamientosModificar el seguimiento
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La innovación tecnológicaEntusiasmo
Tiempo
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Clases moleculares y ER/HER2
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Modelo pronóstico integrado
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21 genes y selección de ttos
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A step-wise (hierarchical) approach to prediction
Clinical & Pathological variables(size, type, grade, PVI, nodes)
HR & HER2 status, Ki67
Molecular profiling
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St Gallen 2009
Should a validated gene profiling assay (when readily available) be considered as an adjunct to high quality classic phenotyping in case of uncertain indication to adjuvant chemotherapy?
• Yes: 80% • No: 18% • Abstension: 2%
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Oncotype Dx
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MINDACT (n=6,000 women) MINDACT (n=6,000 women) Bringing molecular prognostic signatures Bringing molecular prognostic signatures to daily clinical practiceto daily clinical practice
““Low tumor” Low tumor” burden B.C. burden B.C. populationpopulation
•High risk 70-gene signatureHigh risk 70-gene signature + + High risk adjuvant on line High risk adjuvant on line
•Discordant risk groupDiscordant risk group (mostly low risk 70-gene (mostly low risk 70-gene signature but high risk signature but high risk adjuvant on line)adjuvant on line)
•Low risk 70-gene signatureLow risk 70-gene signature + + Low risk adjuvant on line Low risk adjuvant on line
CHEMOTHERAPYCHEMOTHERAPY RANDOMIZE FOR the RANDOMIZE FOR the decision-making tooldecision-making tool
ENDOCRINE ENDOCRINE THERAPYTHERAPY
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Muchas gracias