Presentation Information
[kNAyHR2S-06]Revealing the crosstalk between gut and breast microbiota and the role of their metabolites with breast cancer in obese females: A case control study
*walaa saad hanafy mahmoud1, Mahmoud M. Kamel2, Mohammed Abu-Elghait3, Osama Azmy4 (1. Assistant professor, faculty of medicine, Galala university (Egypt), 2. Clinical Pathology, National Cancer Institute, Cairo University, Cairo, Egypt (Egypt), 3. Department of Botany and Microbiology, Faculty of Science, Al-Azhar University, Cairo, Egypt (Egypt), 4. Department of Reproductive Health Research, Cairo, Egypt (Egypt))
Keywords:
breast microbiota,metabolites,breast cancer,obese females
Background: The relationship between the microbiome and breast cancer pathogenesis remains incompletely understood. This study aimed to compare the abundance of selected bacterial genera (Lactobacillus, Bifidobacterium, and Streptococcus) and associated metabolite levels in stool and breast tissue samples between breast cancer patients and healthy controls.
Methods: In a case-control study, stool and breast tissue samples from 137 newly diagnosed, treatment-naive breast cancer patients and 57 healthy controls were analyzed. Bacterial abundance was quantified using real-time PCR with genus-specific primers targeting the 16S rRNA gene. Levels of seven metabolites (estradiol, cadaverine, propionic acid, isobutyric acid, isovaleric acid, caproic acid, and heptanoic acid) were measured using liquid chromatography-mass spectrometry. Statistical analyses included Mann-Whitney U tests, Wilcoxon signed-rank tests, and Spearman correlations.
Results: Breast cancer patients showed significantly lower abundances of Lactobacillus and Bifidobacterium in both stool and breast tissue samples compared to controls (p < 0.05 for all comparisons). Within the patient group, stool samples showed higher concentrations of Lactobacillus and Bifidobacterium than matched breast tissue samples (p < 0.001). Streptococcus abundance did not differ between groups or sample types. Levels of estradiol, cadaverine, propionic acid, isovaleric acid, and caproic acid were significantly elevated in patient stool samples compared to controls (p < 0.01 for all). A weak negative correlation was observed between tissue Bifidobacterium concentration and caproic acid levels (r = -0.254, p = 0.003). No significant differences in bacterial abundances or metabolite levels were observed across BMI subgroups.
Conclusions: This study identifies differences in the abundance of specific bacterial genera and metabolite levels between breast cancer patients and healthy controls, independent of BMI. These findings provide preliminary evidence of microbial and metabolic alterations associated with breast cancer. However, due to methodological limitations including the targeted analysis of only three bacterial genera and the absence of dietary data, these results should be considered hypothesis-generating rather than conclusive. Further studies with comprehensive metagenomic and metabolomic profiling, along with dietary assessment, are needed to validate and extend these observations.
Methods: In a case-control study, stool and breast tissue samples from 137 newly diagnosed, treatment-naive breast cancer patients and 57 healthy controls were analyzed. Bacterial abundance was quantified using real-time PCR with genus-specific primers targeting the 16S rRNA gene. Levels of seven metabolites (estradiol, cadaverine, propionic acid, isobutyric acid, isovaleric acid, caproic acid, and heptanoic acid) were measured using liquid chromatography-mass spectrometry. Statistical analyses included Mann-Whitney U tests, Wilcoxon signed-rank tests, and Spearman correlations.
Results: Breast cancer patients showed significantly lower abundances of Lactobacillus and Bifidobacterium in both stool and breast tissue samples compared to controls (p < 0.05 for all comparisons). Within the patient group, stool samples showed higher concentrations of Lactobacillus and Bifidobacterium than matched breast tissue samples (p < 0.001). Streptococcus abundance did not differ between groups or sample types. Levels of estradiol, cadaverine, propionic acid, isovaleric acid, and caproic acid were significantly elevated in patient stool samples compared to controls (p < 0.01 for all). A weak negative correlation was observed between tissue Bifidobacterium concentration and caproic acid levels (r = -0.254, p = 0.003). No significant differences in bacterial abundances or metabolite levels were observed across BMI subgroups.
Conclusions: This study identifies differences in the abundance of specific bacterial genera and metabolite levels between breast cancer patients and healthy controls, independent of BMI. These findings provide preliminary evidence of microbial and metabolic alterations associated with breast cancer. However, due to methodological limitations including the targeted analysis of only three bacterial genera and the absence of dietary data, these results should be considered hypothesis-generating rather than conclusive. Further studies with comprehensive metagenomic and metabolomic profiling, along with dietary assessment, are needed to validate and extend these observations.
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