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. 2023 Jun 14;3(5):100212.
doi: 10.1016/j.xjidi.2023.100212. eCollection 2023 Sep.

FISH Panel for Leukemic Cutaneous T-Cell Lymphoma: Extended Patient Cohort Correlation with Blood Involvement and Clinical Outcomes

Jonathan Avery  1 , Sa Rang Kim  2 , Wei Cheng  3 , Francine Foss  4 , Michael Girardi  2
Affiliations

FISH Panel for Leukemic Cutaneous T-Cell Lymphoma: Extended Patient Cohort Correlation with Blood Involvement and Clinical Outcomes

Jonathan Avery et al. JID Innov. .

Abstract

The genomic basis of cutaneous T-cell lymphoma has been characterized by gene copy number alterations and genomic sequencing, but there are few clinical tests that are being widely used to inform the diagnosis and prognosis of leukemic cutaneous T-cell lymphoma that may arise as a progression from mycosis fungoides or de novo as Sézary syndrome. An 11-gene FISH panel of TP53, RB1, DNMT3A, FAS, ZEB1, ARID1A, ATM, and CDKN2A deletions and MYC, signal transducer and activator of transcription gene (STAT)3/5B, and CARD11 amplifications was previously found to encapsulate >95% of gene copy number variations in leukemic cutaneous T-cell lymphoma. Through a retrospective analysis of patients with leukemic cutaneous T-cell lymphoma seen at the Yale Cancer Center from 2014 to 2020, we gathered the relevant genes as they became available and correlated them to factors with prognostic relevance as a proof of concept to show the potential utility in further developing a limited gene panel for prognosis. In this study, we show that the abnormal FISH results show an association with clinically relevant factors (blood stage, CD4:8 ratio, and percentage blood involvement) and have a nonsignificant statistical trend (>90%) toward correlation with overall survival. In addition, the previous cost-effective panels were signal transducer and activator of transcription (STAT)3/5B, MYC, TP53, and ARID1A. We now suggest adding RB1 and ZEB1 on the basis of our findings.

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Figures

Figure 1
Figure 1
Overall survival from the date of diagnosis. Kaplan–Meier analysis stratified by the presence of multiple TSG deletions is shown. The restricted mean survival time was 97.6 (95% CI = 89.2–106.0) months and 77.5 (95% CI = 61.8–93.2) months for those with and without multiple TSG deletions for the span of 102 months from diagnosis (P = 0.027), respectively, whereas the log-rank test for difference in survival produced a P = 0.069. TSG, tumor suppressor gene.
Figure 2
Figure 2
Patient GCNVs count for the most common mutations (TP53, MYC, DNMT3A, and STAT3) against the total abnormal count, defined as the total number of tumor suppressor gene deletions or oncogenic amplifications. Patient location on the Y-axis is maintained throughout every graph. The 11-gene FISH panel was incomplete during early development, which accounts for the no deletion data or no duplication data that are shown as yellow dots. GCNV, gene copy number variation; STAT, signal transducer and activator of transcription.
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