Induction of remission in a patient with end-stage cutaneous T-cell lymphoma by concurrent use of radiation therapy, gentian violet, and mogamulizumab

Westergaard, Sarah A.; Lechowicz, Mary Jo; Harrington, Maggie; Elsey, Justin; Arbiser, Jack L.

doi:10.1016/j.jdcr.2020.05.035

Cited by 5 publications

(6 citation statements)

References 19 publications

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“… 6 In addition, we and others have demonstrated antitumor activity of gentian violet against cutaneous lymphomas. 7 , 8 Chemical peeling allows the removal of excess stratum corneum, and we have not observed Koebnerization as a result of the chemical peel.…”

Section: Discussionmentioning

confidence: 64%

Successful treatment of palmoplantar psoriasis with chemical peeling and gentian violet

2021

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Section: Discussionmentioning

confidence: 64%

Successful treatment of palmoplantar psoriasis with chemical peeling and gentian violet

2021

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“…We found that bortezomib induced potent malignant cell death that could not be rescued by SE ( Figure 3 I-J). Similarly, SE did not confer resistance to crystal violet (gentian violet, 54 which has been shown to inhibit NF-κB in CTCL 55 ) ( supplemental Figure 4 G). These findings suggests that SE-induced drug resistance may be driven by enhanced NF-κB-mediated cell survival of malignant cells.…”

Section: Resultsmentioning

confidence: 96%

“…However, the protective effect was not universal and unspecific, because SE could not rescue malignant cells from cell death induced by bortezomib and crystal violet, which have also been used for the treatment of CTCL. 52 , 54 Importantly, the induction of drug resistance was dependent on continuous presence of SE, implying that drug resistance may also subside after eradication of S aureus in patients. This points to a possible beneficial clinical effect of a persistent control and prevention of skin colonization by S aureus in these patients.…”

Section: Discussionmentioning

confidence: 99%

Staphylococcus aureus induces drug resistance in cancer T cells in Sézary syndrome

Vadivel,

Willerslev-Olsen,

Namini

et al. 2024

Blood

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Patients with Sézary syndrome (SS), a leukemic variant of cutaneous T cell lymphoma (CTCL), are prone to Staphylococcus aureus (S. aureus) infections and have a poor prognosis due to treatment-resistance. Here, we report that S. aureus and staphylococcal enterotoxins (SE) induce drug resistance in malignant T-cells against therapeutics commonly used in CTCL. Supernatant from patient-derived, SE-producing S. aureus and recombinant SE significantly inhibit cell death induced by HDAC inhibitor romidepsin in primary malignant T-cells from SS patients. Bacterial killing by engineered, bacteriophage-derived, S. aureus-specific endolysin (XZ.700) abrogates the effect of S. aureus supernatant. Likewise, mutations in MHC Class II binding sites of SE type-A (SEA) and anti-SEA antibody block induction of resistance. Importantly, SE also triggers resistance to other HDAC inhibitors (vorinostat and resminostat) and chemotherapeutic drugs (doxorubicin and etoposide). Multimodal single-cell sequencing indicates TCR, NFB, and JAK/STAT signaling pathways (previously associated with drug-resistance) as putative mediators of SE-induced drug resistance. In support, inhibition of TCR-signaling and Protein Kinase C (upstream of NFB) counteracts SE-induced rescue from drug-induced cell death. Inversely, SE cannot rescue from cell death induced by proteasome/NFB inhibitor bortezomib. Inhibition of JAK/STAT only blocks SE-induced rescue of malignant T-cells in some but not all patients, suggesting two distinct ways SE can induce drug resistance. In conclusion, we show that S. aureus enterotoxins induce drug-resistance in primary malignant T-cells. These findings suggest that S. aureus enterotoxins cause clinical treatment-resistance in SS patients and that anti-bacterial measures may improve the outcome of cancer-directed therapy in patients harboring S. aureus.

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“…Since the ORR of mogamulizumab monotherapy for relapsed CTCL is 28%, several mogamulizumab-based combination therapies have been reported recently [ 27 , 28 , 29 , 30 ]. For example, the combined administration of etoposide and mogamulizumab was shown to be useful for the treatment of mogamulizumab-resistant MF [ 28 , 29 ].…”

Section: Systemic Treatment Options For Advanced Ctclsmentioning

confidence: 99%

“…Those researchers concluded that CCR4+ CTCL cells, as well as CXCR3+ effector cells and CXCR2+ monocytes, accumulate in tumor sites, leading to potentiation of the ADCC activities of mogamulizumab [ 28 ]. Other reports have suggested that mogamulizumab monotherapy may be augmented by the concurrent use of radiation therapy [ 27 , 30 ]. Although mogamulizumab has been approved by the FDA for the treatment of CTCL since 2018, the use of mogamulizumab in clinical practice is still limited.…”

Section: Systemic Treatment Options For Advanced Ctclsmentioning

confidence: 99%

Topical and Systemic Formulation Options for Cutaneous T Cell Lymphomas

et al. 2021

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Although various anti-cutaneous T-cell lymphoma (CTCL) therapies are available for clinical use, appropriate chemotherapy lines for the treatment of CTCLs have yet to be established. Therefore, to date, various clinical trials for the treatment of advanced CTCLs are ongoing. In this review, we evaluate the therapeutic options that are available in clinical practice for treatment of early- and advanced-stage CTCLs (targeted therapies, histone deacetylase (HDAC) inhibitors, retinoids, interferons, cytotoxic drugs, etc.). We also examine clinical trials of novel regimens for the treatment of CTCLs.

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Induction of remission in a patient with end-stage cutaneous T-cell lymphoma by concurrent use of radiation therapy, gentian violet, and mogamulizumab

Cited by 5 publications

References 19 publications

Successful treatment of palmoplantar psoriasis with chemical peeling and gentian violet

Successful treatment of palmoplantar psoriasis with chemical peeling and gentian violet

Staphylococcus aureus induces drug resistance in cancer T cells in Sézary syndrome

Topical and Systemic Formulation Options for Cutaneous T Cell Lymphomas

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