Lynch
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Dr. Eugenio Vargas Carbajal CMP 11161 - RNE
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Dr. Eugenio Vargas Carbajal CMP 11161 - RNE
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SINDROME AUTOSOMICO DOMINANTE PRODUCIDO POR MUTACIONES EN LOSGENES REPARADORES DE GENES (son 5 ó 6 genes) Y SE CARACTERIZA POR UN
AUMENTO DEL RIESGO DE DESARROLLAR
CANCER DE COLON.SU ORIGEN ES GENETICO, SE
TRANSMITE EN VARIAS GENERACIONES y SE PUEDE LOCALIZAR TAMBIEN EN
OTROS ÓRGANOS.
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FORMA DE PRESENTACION
:
ORGANOS AFECTADOS
Dr. Eugenio Vargas Carbajal CMP 11161 - RNE
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Importante es realizar en este tipo de pacientes su HISTORIA FAMILIAR.Hay que revisar los ANTECEDENTES FAMILIARES al menos de tres generaciones.Generación Nº 1 : la persona que uno evalúa.Generación Nº 2: los padres.Generación Nº 3: los abuelos.
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EJEMPLO:
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EXISTE MUTACION
SOBRE LA LINEA GERMINAL
DE GENES PARA LA REPLICA DEL ADN
LLAMADOS GENES
REPARADORES DEL ADN
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TUMOR DE COLON CON INESTABILIDAD DE MICROSATELITES, ES PROBABLE QUE TENGA SINDROME DE LYNCH. DEBE PROCEDERSE A EVALUAR EL TUMOR Y VER LAS PROTEINAS ASOCIADAS (AUSENCIA DE PROTEINA MSH2)
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SE CONSIDERA QUE UN TUMOR PRESENTA ALTA IMS* SI MUESTRA INESTABILIDAD EN DOS O MAS CRITERIOS. ES DE BAJA IMS* SI SE MUESTRA EN UN SOLO MARCADOR.
IMS*: INESTABILIDAD DE MICROSATELITESDr. Eugenio Vargas Carbajal CMP 11161 - RNE
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APARECE EN ADULTOS JOVENES
70 – 80 %EDAD 45 AÑOS
(PROMEDIO)
AUMENTA LA INCIDENCIA EN: CA. SINCRONICOS 18 % CA. METASINCRONICOS 24 %
CARACTERISTICAS:
TRASTORNO AUTOSOMICO DOMINANTE CON PENETRANCIA INCOMPLETA. PRESENTA POLIPOS ADENOMATOSICOS QUE PARECEN SUFRIR UNA TRANSFORMACION CANCERIGENA ACELERADA. REPRESENTA EL 5 % DE TODOS LOS CC. PROBABILIDAD DEL 80 % DE DESARROLLAR CC.
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INCREMENTO DEL CA. COLORRECTAL EN PAC. CON SINDROME DE LYNCH
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SE ACELERA LA CARCINOGENESIS EN UN LAPSO DE TIEMPO de 3 – 4 años EN
COMPARACION CON OTROS TUMORES QUE LLEVAN UN LAPSO DE TIEMPO DE 10 AÑOS
MINIMO.
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(SINDROME DE LYNCH)
EL RIESGO DE PADECER
CANCER ESTA LIGADO
UNICAMENTE AL CANCER
COLORRECTAL
SE DESARROLLA CANCER
COLORRECTAL ASOCIADOS A
OTROS CA. EXTRA
COLONICASDr. Eugenio Vargas Carbajal CMP 11161 - RNE
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LOS CANCERES DE COLON EN EL SINDROME DE LYNCH SE LOCALIZAN CON MAYOR
FRECUENCIA EN EL COLON DERECHO.
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Pinol V, Castells A, Andreu M, Castellvi-Bel S, Alenda C, Llor X, et al. Accu-racy of revised Bethesda guidelines, microsat-ellite instability, and immunohistochemistry for the identification of patients with hereditary nonpolyposis colorectal cancer. Jama 2005; 293: 1986-94.
Niessen RC, Berends MJ, Wu Y, Si-jmons RH, Hollema H, Ligtenberg MJ, et al. Identification of mismatch repair gene muta-tions in young colorectal cancer patients and patients with multiple HNPCC-associated tu-mours. Gut 2006; 55: 1781-8.
Domingo E, Niessen RC, Oliveira C, Alhopuro P, Moutinho C, Espin E, et al. BRAF-V600E is not involved in the colorectal tumorigenesis of HNPCC in patients with functional MLH1 and MSH2 genes. Oncogene 2005; 24: 3995-8.
Ogino S, Brahmandam M, Cantor M, Namgyal C, Kawasaki T, Kirkner G, et al. Dis-tinct molecular features of colorectal carcinoma with signet ring cell component and colorectal carcinoma with mucinous component. Mod Pathol 2006; 19: 59-68.
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Dr. Eugenio Vargas Carbajal CMP 11161 - RNE
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CONSULTORIO:Av. SAENZ PEÑA Nº 354 CALLAOPERU ( 5 PM – 8 PM)TELEFONO: [email protected]