2026-06-26 | Follicular Mucinosis Associated with Adult T-Cell Leukemia-Lymphoma.

Follicular mucinosis is characterized by deposits of mucin in the sebaceous gland and outer root sheath of hair follicles. The diagnosis may occur without another cutaneous disease ("idiopathic" follicular mucinosis) or in association with hematologic malignancies, most often cutaneous T-cell lymphoma, and other skin conditions. We present a case of follicular mucinosis occurring in an African male with adult T-cell leukemia-lymphoma. Four cases of follicular mucinosis in the setting of adult T-cell leukemia-lymphoma have been reported previously in the literature. It is important to consider that not all lymphoma related follicular mucinosis is associated with cutaneous T-cell lymphoma.

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2026-06-24 | Closing the Mechanism Loop: A Unified Mechanistic Framework for Parasite-Associated Carcinogenesis

Background. Six parasite–cancer associations are supported by IARC carcinogen classification or strong mechanistic and epidemiological evidence: Schistosoma haematobium → bladder cancer (Group 1); Opisthorchis viverrini and Clonorchis sinensis → cholangiocarcinoma (Group 1); Schistosoma japonicum → colorectal cancer (Group 2B, priority reclassification); Plasmodium falciparum → endemic Burkitt lymphoma (Group 2A, reclassification evidence reviewed in Study 8 ([10.5281/zenodo.20402639](https://doi.org/10.5281/zenodo.20402639))); and Strongyloides stercoralis × HTLV-1 → adult T-cell leukemia/lymphoma (mechanistic evidence reviewed in Study 9 ([10.5281/zenodo.20402641](https://doi.org/10.5281/zenodo.20402641))). These associations span five parasite taxa, four cancer types, and four continents. No synthesis has mapped their underlying mechanisms onto a common framework. Methods. Narrative mechanistic synthesis. PubMed and Google Scholar were searched for publications on: (1) parasite-induced inflammation and genotoxicity; (2) helminth-driven immune polarisation; (3) parasite extracellular vesicles and epigenetic reprogramming; (4) parasite–oncovirus amplification systems. Results are...

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2026-06-17 | Loss of HTLV-1-specific CD8+ T-cell immunity in virus carriers predisposed to adult T-cell leukemia/lymphoma.

Adult T-cell leukemia/lymphoma (ATL) is caused by chronic infection with human T-lymphotropic virus type 1 (HTLV-1). HTLV-1 contains highly immunogenic CD8 + T-cell epitopes that elicit high frequencies of virus-specific CD8 + T cells in most virus carriers. Despite the virus being present in the tumor, HTLV-1-specific CD8 + cells are often undetectable in ATL. To characterize HTLV-1-specific CD8 + T cells during ATL development, we studied a subgroup of people living with asymptomatic HTLV-1 infection at very high risk of developing ATL. These so-called "high-risk" carriers have suspected premalignant lesions: expanded, HTLV-1-infected "ATL-like" clones circulating in their peripheral blood. Compared to viral antigen-burden matched controls, high-risk carriers had significantly fewer Tax-specific IFN-γ + CD8 + cells in peripheral blood. Furthermore, ex vivo CD8 + T cells from high-risk carriers did not efficiently kill autologous HTLV-1-infected T cells, including premalignant ATL-like clones. We stained Tax11-19/HLA-A∗0201 pentamer + CD8 + T cells to test whether the low frequencies of functional CD8+ T cells resulted from phenotype or absolute frequency of HTLV-1-specific CD8 + T cells. High-risk carriers had significantly lower frequencies of Tax11-19/HLA-A∗0201 pentamer + CD8 + T cells than controls, but we observed no difference in effector function, memory phenotype, or expression of checkpoint control molecules. In contrast, there was no difference in the frequency of CD8 + T cells specific for other viruses (cytomegalovirus, Epstein-Barr virus, influenza virus) between high-risk carriers and controls. This is the first report of HTLV-1-specific immune dysregulation in the premalignant stage of ATL. Low frequencies of HTLV-1-specific CD8 + T cells may contribute to ATL development and may be a novel therapeutic target for ATL prevention.

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