ACETYL SALICYLIC ACID AND PLATELETS IN COLON CANCER. (Q3177778): Difference between revisions

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(‎Changed label, description and/or aliases in en: translated_label)
(‎Removed claim: summary (P836): Low-dose acetyl salicylic acid (AAS) prevents the development and progression of colorectal cancer (CCR), a process associated with over-expression of COX-2. The AAS seems to be the ideal candidate in CCR chemo-prevention. Regulatory agencies need to know the mechanisms for action before approving their indication. Our hypothesis is that its effect is mainly due to the antiplatelet effect. Primary objective: Check if the AAS causes acetylation...)
Property / summary
Low-dose acetyl salicylic acid (AAS) prevents the development and progression of colorectal cancer (CCR), a process associated with over-expression of COX-2. The AAS seems to be the ideal candidate in CCR chemo-prevention. Regulatory agencies need to know the mechanisms for action before approving their indication. Our hypothesis is that its effect is mainly due to the antiplatelet effect. Primary objective: Check if the AAS causes acetylation (new and validated by us that measures the direct effect on the top) complete COX-1 in platelets and not COX acetylation in colonic tissue. Summary secondary objectives: Evaluate: the degree of acetylation and functionality of platelets and colonic tissue at the time of Tmax with ASA; the effect of ASA on the biosynthesis of eicosanoids, levels of sphingosine-1-phosphate, and protein expression of markers of cell growth and progression, in colonic tissue (normal,adenomas/cancer); C) expression of COX-2 in tumor tissue in patients with familial adenomatose polyposis (FPA). Methods: Phase III randomised clinical trial. The primary and secondary target (a-b) will be evaluated in 40 patients undergoing RCC screening before and after taking 100 mg/day ASA with enteric cover (usual form in cardiovascular patients) for 7 days. Secondary objective (c) will be studied in 12 patients with FAP before and after taking 100 mg/day of enteric-coated ASA for 3 months. Expected results: It is expected to show that COX acetylation and its direct functional effect occurs in platelets rather than colonic tissue. The effect of AAS on COX-2 is indirect. (English)
 
Property / summary: Low-dose acetyl salicylic acid (AAS) prevents the development and progression of colorectal cancer (CCR), a process associated with over-expression of COX-2. The AAS seems to be the ideal candidate in CCR chemo-prevention. Regulatory agencies need to know the mechanisms for action before approving their indication. Our hypothesis is that its effect is mainly due to the antiplatelet effect. Primary objective: Check if the AAS causes acetylation (new and validated by us that measures the direct effect on the top) complete COX-1 in platelets and not COX acetylation in colonic tissue. Summary secondary objectives: Evaluate: the degree of acetylation and functionality of platelets and colonic tissue at the time of Tmax with ASA; the effect of ASA on the biosynthesis of eicosanoids, levels of sphingosine-1-phosphate, and protein expression of markers of cell growth and progression, in colonic tissue (normal,adenomas/cancer); C) expression of COX-2 in tumor tissue in patients with familial adenomatose polyposis (FPA). Methods: Phase III randomised clinical trial. The primary and secondary target (a-b) will be evaluated in 40 patients undergoing RCC screening before and after taking 100 mg/day ASA with enteric cover (usual form in cardiovascular patients) for 7 days. Secondary objective (c) will be studied in 12 patients with FAP before and after taking 100 mg/day of enteric-coated ASA for 3 months. Expected results: It is expected to show that COX acetylation and its direct functional effect occurs in platelets rather than colonic tissue. The effect of AAS on COX-2 is indirect. (English) / rank
Normal rank
 
Property / summary: Low-dose acetyl salicylic acid (AAS) prevents the development and progression of colorectal cancer (CCR), a process associated with over-expression of COX-2. The AAS seems to be the ideal candidate in CCR chemo-prevention. Regulatory agencies need to know the mechanisms for action before approving their indication. Our hypothesis is that its effect is mainly due to the antiplatelet effect. Primary objective: Check if the AAS causes acetylation (new and validated by us that measures the direct effect on the top) complete COX-1 in platelets and not COX acetylation in colonic tissue. Summary secondary objectives: Evaluate: the degree of acetylation and functionality of platelets and colonic tissue at the time of Tmax with ASA; the effect of ASA on the biosynthesis of eicosanoids, levels of sphingosine-1-phosphate, and protein expression of markers of cell growth and progression, in colonic tissue (normal,adenomas/cancer); C) expression of COX-2 in tumor tissue in patients with familial adenomatose polyposis (FPA). Methods: Phase III randomised clinical trial. The primary and secondary target (a-b) will be evaluated in 40 patients undergoing RCC screening before and after taking 100 mg/day ASA with enteric cover (usual form in cardiovascular patients) for 7 days. Secondary objective (c) will be studied in 12 patients with FAP before and after taking 100 mg/day of enteric-coated ASA for 3 months. Expected results: It is expected to show that COX acetylation and its direct functional effect occurs in platelets rather than colonic tissue. The effect of AAS on COX-2 is indirect. (English) / qualifier
point in time: 12 October 2021
Timestamp+2021-10-12T00:00:00Z
Timezone+00:00
CalendarGregorian
Precision1 day
Before0
After0
 

Revision as of 19:22, 12 October 2021

Project Q3177778 in Spain
Language Label Description Also known as
English
ACETYL SALICYLIC ACID AND PLATELETS IN COLON CANCER.
Project Q3177778 in Spain

    Statements

    country
    Spain
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    EU contribution
    50,750.0 Euro
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    budget
    101,500.0 Euro
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    co-financing rate
    50.0 percent
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    start time
    1 January 2015
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    end time
    31 March 2019
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    beneficiary name (string)
    INSTITUTO ARAGONES DE CIENCIAS DE LA SALUD
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    coordinate location

    41°39'7.67"N, 0°52'51.38"W
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    postal code
    50297
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    summary
    El ácido acetil salicílico a dosis bajas (AAS) previene el desarrollo y la progresión del cáncer colorrectal (CCR), proceso asociado a sobre-expresión de COX-2. El AAS parece el candidato ideal en quimio-prevención de CCR. Las agencias reguladoras requieren conocer los mecanismos de acción antes de aprobar su indicación. Nuestra hipótesis es que su efecto se debe fundamentalmente al efecto antiplaquetario. Objetivo primario: Verificar si el AAS causa acetilación (técnica nueva y validada por nosotros que mide el efecto directo en la encima) completa de la COX-1 en plaquetas y no acetilación de COX en tejido colonico. Objetivos secundarios resumidos: Evaluar: a) el grado de acetilación y funcionalidad de plaquetas y en tejido colónico en el momento de Tmax con AAS; b) el efecto de AAS en la biosíntesis de eicosanoides, niveles de esfingosina-1-fosfato, y expresión proteica de marcadores de crecimiento celular y progresión, en tejido colónico (normal,adenomas/cáncer); c) la expresión de COX-2 en el tejido tumoral de pacientes con poliposis adenomatosa familiar (PAF). Métodos: Ensayo Clínico aleatorizado en fase III. El objetivo primario y secundarios (a-b) se evaluaran en 40 pacientes sometidos a cribado de CCR antes y después de la toma de 100 mg/día AAS con cubierta entérica (forma habitual en pacientes cardiovasculares) durante 7 días. El objetivo secundario c) se estudiará en 12 pacientes con PAF antes y tras la toma de 100 mg/día de AAS con cubierta entérica durante 3 meses. Resultados esperados: Se espera demostrar que la acetilación de la COX y su efecto funcional directo ocurre en plaquetas y no el tejido colónico. El efecto de AAS sobre la COX-2 es indirecto. (Spanish)
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    location (string)
    Zaragoza
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    Identifiers

    Spanish Kohesio ID
    PI14_01218
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