Galectins are proteins with high-affinity β-galactoside-binding sites that function in a variety of signaling pathways through interactions with glycoproteins. The known contributions of galectins-1, -3, -7, -8, and -9 to angiogenesis, metastasis, cell division, and evasion of immune destruction led us to investigate the circulating levels of these galectins in cancer patients. This study compares galectin concentrations by enzyme-linked immunosorbent assay (ELISA) from each stage of breast, lung, and colon cancer. Galectins-1 and -7, which share a prototype structure, were found to have statistically significant increases in breast and lung cancer. Of the tandem-repeat galectins, galectin-8 showed no statistically significant change in these cancer types, but galectin-9 was increased in colon and lung cancer. Galectin-3 is the only chimera-type galectin and was increased in all stages of breast, colon, and lung cancer. In conclusion, there were significant differences in the galectin levels in patients with these cancers compared with healthy controls, and galectin levels did not significantly change from stage to stage. These findings suggest that further research on the roles of galectins early in disease pathogenesis may lead to novel indications for galectin inhibitors.

To investigate a potential role for galectins as biomarkers that enable diagnosis or prognostication of breast or non-small cell lung cancer, the serum levels of galectins -1, -3, -7, -8, and -9 of cancer patients determined by ELISA assays were compared to the mutation status of 50 known cancer-critical genes, which were determined using multiplex PCR in tumors of the same patients. Mutations in the KIT proto-oncogene, which codes for the c-Kit protein, a receptor tyrosine kinase, correlated with higher levels of galectins -1, -3, -8, and -9 in breast cancer patients and galectin-1 in non-small cell lung cancer patients. Mutations in the KIT gene were more likely found in brain metastases from both of these primary cancers. The most common KIT mutation in our panel was p.M541L, a missense mutation in the transmembrane domain of the c-Kit protein. These results demonstrate an association between KIT oncogenic signaling and elevated serum galectins in patients with metastatic disease. Changes in protein trafficking and the glycocalyx composition of cancer cells may explain the observed alterations in galectin expression. This study can be useful for the targeted selection of receptor tyrosine kinase and galectin inhibitor anti-cancer treatments.

Background: Precision medicine holds promise of being a more effective method for treating complex diseases such as cancer. Nuanced care is needed, as the development and clinical course of cancer is multifactorial with influences from the general health status of the patient, germline and neoplastic mutations, co-morbidities, and environment including "lifestyle". To tailor an individualized treatment to the patient, such multifactorial data must be presented in an easy-to-use, easy-to-analyze fashion for providers to use effectively. Purpose: To address the need, we have built a searchable database integrating cancer-critical gene mutation status, serum galectin protein markers, serum and tumor glycomic profiles, with clinical, demographic, and lifestyle data points of individual patients. Methods: The initial data was acquired from breast, colon, and lung cancer patients’ serum and biopsy samples from the Prisma Health Cancer Institute Biorepository. The acquired data contains the status of 2,800 COSMIC cancer-critical gene mutations, individual patient profiles of five serum galectins, and serum and biopsy glycan structures from each patient’s glycomic profile. DNA from tumor cells was used to screen the regions frequently mutated in human cancer genes. Multiplex PCR using Ion AmpliSeq࣪ Cancer Hotspot panel v2 was performed by Precision Genetics. Enzyme-linked immunosorbent assay was employed to perform galectin profiling of cancer patient serum samples. Glycomic profiling of serum and biopsy samples was performed by the Emory Comprehensive Glycomic Core. In addition, healthy control values for galectin and glycomic profiles were obtained and added to the patient database for reference. The data is being stored using Microsoft SQL servers and is fed into an interactive web application using RStudio. Results: Our interactive database allows care providers to amalgamate cohorts from these groups to find correlations between different data types with the possibility of finding a "stage signature" based upon a combination of genetic mutations, galectin serum levels, glycan signatures, and patient clinical data and lifestyle choices. Conclusion: Our project provides a framework for an integrated interactive database to analyze molecular and clinical patterns across cancer stages and provides opportunities for increased diagnostic and prognostic power. Citation Format: Basil H. Chaballout, Avery T. Funkhouser, Bailey B. Blair, Jane L. Goodwin, Alexander M. Strigenz, Connie M. Arthur, Julie C. Martin, W. Jeffery Edenfield, Anna V. Blenda. Integration of molecular data into cancer patient database [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5028.