Abstract
Cutaneous T-Cell Lymphomas (CTCL) presents with substantial clinical variability and transcriptional heterogeneity. In the recent years, several studies paved the way to elucidate aetiology and pathogenesis of CTCL using sequencing methods. Several T-cell subtypes were suggested as the source of disease thereby explaining clinical and transcriptional heterogeneity of CTCL entities. Several differentially expressed pathways could explain disease progression. However, exogenous triggers in the skin microenvironment also seem to affect CTCL status. Especially Staphylococcus aureus was shown to contribute to disease progression. Only little is known about the complex microbiome patterns involved in CTCL and how microbial shifts might impact this malignancy. Nevertheless, first hints indicate that the microbiome might at least in part explain transcriptional heterogeneity and that microbial approaches could serve in diagnosis and prognosis. Shaping the microbiome could be a treatment option to maintain stable disease. Here, we review current knowledge of transcriptional heterogeneity of and microbial influences on CTCL. We discuss potential benefits of microbial applications and microbial directed therapies to aid patients with CTCL burden.
Highlights
Cutaneous T-cell lymphomas (CTCL) are a group of skin homing neoplastic malignancies comprising approximately 10% of total non-Hodgkin lymphomas (NHL) withMycosis fungoides (MF) as the most common entity [1]
High-throughput sequencing of the T-cell receptor (TCR)-beta gene showed that mycosis fungoides (MF) patients with a tumour clone frequency in lesions less than 25% have a good prognosis for overall and progression-free survival, while this is inverse for tumour clone frequencies over 25%
staphylococcal enterotoxin A (SEA) and staphylococcal enterotoxin E (SEE) were the only staphylococcal toxins to elicit disease-stimulating activity in Sézary syndrome (SS) patient-derived tumour cells in vitro [17]. This conflicting data might be caused by (i) other staphylococcal enterotoxins (SEs) than toxic shock syndrome toxin-1 (TSST-1) associating with TRBV20, (ii) specific host-pathogen interactions [104] that differed between the CTCL cohorts and/or (iii) microbe-microbe interactions leading to an altered expression of virulence factors [19]
Summary
Cutaneous T-cell lymphomas (CTCL) are a group of skin homing neoplastic malignancies comprising approximately 10% of total non-Hodgkin lymphomas (NHL) with. Several clinical variables and biological markers are discussed as prognostic factors. These parameters are partially subjective and imprecisely specified or show conflicting results across studies [5]. Interobserver variation for MF diagnosis is considerable, resulting in a median delay of 3 years before the definitive diagnosis is made since the first patient presentation [5]. These challenges underline the need for better diagnostic and prognostic tools [8]. We indicate first evidence of microbial implications on disease progression in CTCL and how differential colonization could lead to inter-patient heterogeneity.
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