---
title: "Human-like sialome (CMAH loss) links hyperglycemia to accelerated colorectal cancer progression"
id: "biorxiv-0-human-like-sialome-remodeling-links-hyperglycemia-to-colorectal-cancer"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-0-human-like-sialome-remodeling-links-hyperglycemia-to-colorectal-cancer"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.09.04.739806v1?rss=1"
published_at: "2026-09-09T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Human-like sialome (CMAH loss) links hyperglycemia to accelerated colorectal cancer progression
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-0-human-like-sialome-remodeling-links-hyperglycemia-to-colorectal-cancer
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.09.04.739806v1?rss=1)
- **Published At:** 2026-09-09T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- The study investigates how a **human-like sialome** (loss of CMAH and absence of Neu5Gc synthesis) modifies colorectal cancer (CRC) progression under metabolic stress. - Researchers used a spontaneous CRC mouse model combining conditional **Apc** mutation with **Cmah** deficiency (CPC-Apc Cmah -/-) to mimic the human sialic acid repertoire. - Under normal glycemia, CPC-Apc Cmah -/- mice had fewer polyps and lower tumor burden than wild-type controls, indicating that CMAH loss alters baseline tumor development. - Tumors from Cmah -/- mice under euglycemia showed remodeling of the tumor immune microenvironment: increased tumor-infiltrating leukocytes, enrichment of **B cells**, and reduced PD-1 expression on B cells and cytotoxic CD8+ T cells. - When chronic hyperglycemia was induced with low-dose streptozotocin, tumor progression was dramatically worsened only in Cmah -/- mice despite similar blood glucose levels between genotypes. - In hyperglycemic Cmah -/- mice there was increased tumor burden, accelerated lesion development, and progression toward high-grade dysplasia. - Histopathology in hyperglycemic Cmah -/- tumors showed increased mesenchymal expansion and histological resemblance to colorectal tumors from diabetic patients. - The work identifies CPC-Apc Cmah -/- mice as a translational model for studying the interplay between diabetes and CRC and suggests that a human-like sialome increases susceptibility to metabolic stress-driven tumor progression. - Specific experimental details (exact cohort sizes, quantitative metrics, timelines, and statistical values) were not reported in the abstract and are not available in the provided source text.
## Clinical Analysis & Structured Key Points
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Santos, Giulia S. Ferreira, Ana Luiza Lopes, Vanessa H.N. Silva, Agata C. Fonseca, Miguel Fontes, [ View ORCID Profile](http://orcid.org/0000-0002-7187-6259)Cesar de Souza Bastos Jr., [ View ORCID Profile](http://orcid.org/0000-0002-8019-628X)Christina Maeda Takiya, Joao Carlos Machado, [ View ORCID Profile](http://orcid.org/0000-0003-1287-8526)Miriam B.F. Werneck, [ View ORCID Profile](http://orcid.org/0000-0002-8378-8846)Wagner Barbosa Dias, [ View ORCID Profile](http://orcid.org/0000-0001-6717-2518)Frederico Alisson-Silva, [ View ORCID Profile](http://orcid.org/0000-0002-6049-2751)Adriane Regina Todeschini doi: https://doi.org/10.64898/2026.09.04.739806 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. Ronan C.M. Santos 1 Universidade Federal do Rio de Janeiro; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Ronan%2BC.M.%2BSantos%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Santos%20RC&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ARonan%2BC.M.%2BSantos%2B) * [ORCID record for Ronan C.M. Santos](http://orcid.org/0009-0000-7604-0779 "Open in new tab") Giulia S. 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However, whether a human-like sialome modulates the impact of metabolic stress on colorectal cancer (CRC) progression remains unclear. Here, we investigated the diabetes-sialome-tumor axis using a spontaneous CRC model combining conditional _Apc_ mutation with _Cmah_ deficiency, thereby recapitulating the human sialic acid repertoire. Under euglycemic conditions, CPC-_Apc Cmah -/-_ mice exhibited reduced polyp numbers and tumor burden compared with WT mice, accompanied by remodeling of the tumor immune microenvironment, including increased tumor-infiltrating leukocytes, enrichment of B cells, and reduced PD-1 expression in B cells and cytotoxic CD8+ T cells. Induction of chronic hyperglycemia with low-dose streptozotocin revealed a striking genotype-specific effect. Despite comparable hyperglycemia between genotypes, tumor progression was dramatically exacerbated exclusively in _Cmah -/-_ mice, with increased tumor burden, accelerated lesion development, and progression toward high-grade dysplasia. Histopathological analyses further revealed increased mesenchymal expansion and close resemblance to colorectal tumors from diabetic patients. Together, these findings demonstrate that a human-like sialome increases susceptibility to metabolic stress and identify CPC-_Apc Cmah -/-_ mice as a translationally relevant model for investigating diabetes-associated colorectal carcinogenesis. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared INCT_2024: GLICOSAÚDE: Diagnóstico, Terapia Avançada e Inovação em Glicobiologia para Saúde, 408756/2024 CNPq Edital Universal 2024. Glicosilação Aberrante como Elo Molecular do Câncer Colorretal & Diabetes: Oportunidade para Novos Alvos Terapêuticos., 407826/2025-4 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. bioRxiv and medRxiv thank the following for their generous financial
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