Profiling of oligosaccharides and p53 gene mutation in Filipino breast tumors

• Main Authors: Deocaris, Custer C., Magno, Jose Donato A., Cruz, Michael Joseph B., Prodigalidad, Abelardo-Alan T., De Vera, Azucena C., Jacinto, Sonia D.
• Format: text
• Published: Animo Repository 2022
• Subjects: Tumor proteins; Oligosaccharides; Breast—Cancer; Histochemistry; Glycoproteins; Glycoconjugates; Biochemistry, Biophysics, and Structural Biology; Genetics
• Online Access: https://animorepository.dlsu.edu.ph/faculty_research/5460
• Institution: De La Salle University

Majority of patients are diagnosed with benign tumors, however, such benign tumors can progress to an invasive disease. Since carbohydrate-mediated cell-cell adhesion and proliferative potential play crucial roles in tumorigenesis and tumor aggressive behavior, we analyzed the qualitative changes in oligosaccharide expression and analyzed for presence of mutation in the tumor suppressor p53 gene, the most mutated gene in all human cancers. Forty-three (43) breast tumors were screened for p53 mutation in exons 2-11 using polymerase chain reaction (PCR)-amplification coupled to temporal temperature gradient electrophoresis (TTGE). Paraffin-embedded tissues were stained with biotinylated-glycoproteins containing the following sugar groups: mannose (Man), lactose (Lac), fucoidan (Fuc), N-acetyl-glucosamine (GlcNac), N-acetyl-b-galactosamine (GalNAc) and hyaluronic acid (Hya). Expression of carbohydrate receptors was significantly elevated (p=0.003) in malignant compared with benign tumors, particularly at receptors for GalNAc, lac and Fuc. No change in overall glycan signatures using our panel of neoglycoconjugates was noted when grouped according to p53 mutation status in both benign and malignant cases. Although the prognostic value of carbohydrate-receptors in breast cancer has not been validated to date, our results indicate that benign and malignant tumors can be defined by their affinities to our battery of neoglyconjugates. However, result from our reverse lectin histochemistry failed to correlated glycan signature with presence of p53 mutations