Clinical trial · Interventional
Nutritional Intervention and DNA Damage of Patients With HBOC
Effects of a Nutritional Intervention in DNA Damage of Patients With Hereditary Breast and Ovarian Cancer Syndrome
- Source
- ClinicalTrials.gov
- Retrieved
- Sep 8, 2026
- Layer
- normalized (units and labels harmonized; values unchanged)
- Run
- ING-CLINICALTRIALS-20260908-000001
Summary
Brief summary (as posted)
Breast and Ovarian Cancer Syndrome (HBOC) is characterized by mutations in tumor suppressor genes such as BRCA1 and BRCA2, which increase the carrier's risk of developing breast and ovarian cancer, especially before 40. In this pathology the DNA damage is increased because there is a state of chronic inflammation, plus the antineoplastic treatments and changes in body composition result in oxidative stress. The inductions of epigenetic changes by a nutritional intervention with an specific distribution of macronutrients, micronutrients and polyphenols, not only ensures an optimal nutritional status, but also shows a decrease in oxidative stress, and therefore in DNA damage. The aim of this study is to assess if the DNA damage in patients with HBOC decreases after the nutritional intervention.
Conditions
Conditions (3)
Free-text conditions as registered, with the CancerIndex entity they were reconciled to and the match type.
| Condition (as posted) | Mapped entity | Match | Confidence |
|---|---|---|---|
| DNA Damage | — | UNRESOLVED | — |
| HBOC Syndrome | — | UNRESOLVED | — |
| Nutrition Therapy | — | UNRESOLVED | — |
Interventions
Interventions (1)
| Intervention | Type | Mapped drug | Match |
|---|---|---|---|
| Antioxidant therapy | Combination Product | — | UNRESOLVED |
Design
Arms and outcomes
Arms (1)
- type
- OTHER
- label
- Antioxidant therapy
- description
- The patient will get a nutritional personalized treatment with the following characteristics: hypocaloric diet, rich in micronutrients related with DNA reparation and polyphenols, with the next distribution: 45% carbohydrates, 30% lipids, 25% protein, \<10% saturated fats, \>10% unsaturated fats, based on the recommendations of the American Institute for Cancer Research (AICR).
- interventionNames
- Combination Product: Antioxidant therapy
Primary outcomes (1)
- measure
- DNA damage change
- timeFrame
- 12 weeks
- description
- A blood sample will be taken to assess DNA damage (ELISA) by 8-hydroxy-2-deoxyguanosine (8-OHdG), a modified nitrogen base indicating oxidative damage to DNA, before and after nutritional intervention.
Secondary outcomes (5)
- measure
Eligibility
Eligibility (as posted)
- Sex
- Female
- Minimum age
- 18 Years
Show eligibility criteria text
Inclusion Criteria: * Female patients diagnosed with HBOC according to the Mexican Consensus of Breast Cancer * Patients over 18 years who voluntarily agree to participate in the study and sign the informed consent. Exclusion Criteria: * Patients with end-stage chronic kidney failure, heart failure, liver failure, rheumatoid arthritis, non-inherited AC or HIV. * Patients who carry out a structured exercise plan (rehabilitation) at the time of inclusion in the study. * Patients who carry out a structured eating plan (adherence to diet) or who are consuming a food supplement at the time of inclusion in the study. * Patients with significant primary clinical disorders: hematological (hemoglobin \<13 in men and \<12 in women), renal (creatinine\> 3), neurological (other than epilepsy).
References
Publications (5)
- BACKGROUNDKowalska E, Narod SA, Huzarski T, Zajaczek S, Huzarska J, Gorski B, Lubinski J. Increased rates of chromosome breakage in BRCA1 carriers are normalized by oral selenium supplementation. Cancer Epidemiol Biomarkers Prev. 2005 May;14(5):1302-6. doi: 10.1158/1055-9965.EPI-03-0448. PMID 15894690
- BACKGROUNDKasai H. Analysis of a form of oxidative DNA damage, 8-hydroxy-2'-deoxyguanosine, as a marker of cellular oxidative stress during carcinogenesis. Mutat Res. 1997 Dec;387(3):147-63. doi: 10.1016/s1383-5742(97)00035-5. PMID 9439711
- BACKGROUNDGopalakrishnan S, Van Emburgh BO, Robertson KD. DNA methylation in development and human disease. Mutat Res. 2008 Dec 1;647(1-2):30-8. doi: 10.1016/j.mrfmmm.2008.08.006. Epub 2008 Aug 20. PMID 18778722
- BACKGROUNDFerguson LR, Chen H, Collins AR, Connell M, Damia G, Dasgupta S, Malhotra M, Meeker AK, Amedei A, Amin A, Ashraf SS, Aquilano K, Azmi AS, Bhakta D, Bilsland A, Boosani CS, Chen S, Ciriolo MR, Fujii H, Guha G, Halicka D, Helferich WG, Keith WN, Mohammed SI, Niccolai E, Yang X, Honoki K, Parslow VR, Prakash S, Rezazadeh S, Shackelford RE, Sidransky D, Tran PT, Yang ES, Maxwell CA. Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition. Semin Cancer Biol. 2015 Dec;35 Suppl(Suppl):S5-S24. doi: 10.1016/j.semcancer.2015.03.005. Epub 2015 Apr 11. PMID 25869442
- BACKGROUNDHigdon JV, Delage B, Williams DE, Dashwood RH. Cruciferous vegetables and human cancer risk: epidemiologic evidence and mechanistic basis. Pharmacol Res. 2007 Mar;55(3):224-36. doi: 10.1016/j.phrs.2007.01.009. Epub 2007 Jan 25. PMID 17317210