Fluorescence in‐situ hybridisation for TP63 rearrangements in T cell lymphomas: single‐site experience of 470 patients and implications for clinical testing

  title={Fluorescence in‐situ hybridisation for TP63 rearrangements in T cell lymphomas: single‐site experience of 470 patients and implications for clinical testing},
  author={Jess F Peterson and Kathryn E. Pearce and Reid G. Meyer and Patricia T Greipp and Ryan A. Knudson and Linda B. Baughn and Rhett P Ketterling and Andrew L. Feldman},
  pages={481 - 485}
The aims of this study were to review our 5‐year experience with clinical FISH testing for TP63 rearrangements using both TP63 break‐apart (BAP) and TBL1XR1/TP63 dual‐fusion (D‐FISH) probes to evaluate the frequency of TP63 rearrangements and the distribution of TBL1XR1 vs. alternate partner loci, and to assess whether both probe sets are necessary in all cases undergoing FISH testing. 
2 Citations


DUSP22 and TP63 rearrangements predict outcome of ALK-negative anaplastic large cell lymphoma: a Danish cohort study.
To the editor: Peripheral T-cell lymphomas (PTCLs) represent a group of rare hematological cancers of mature T-cell or natural killer cell origin accounting for 10% to 15% of all lymphomas.[1][1]
TBL1XR1/TP63: a novel recurrent gene fusion in B-cell non-Hodgkin lymphoma.
The discovery of a gene fusion between TBL1XR1 and TP63, the only recurrent somatic novel gene fusion identified in DLBCL cases, suggests an important functional role in the lymphomas that harbor this event.
Genome-wide analysis reveals recurrent structural abnormalities of TP63 and other p53-related genes in peripheral T-cell lymphomas.
It is suggested that a constellation of alternate genetic abnormalities may contribute to disruption of p53-associated tumor suppressor function in PTCL.
The heterogeneous landscape of ALK negative ALCL
A further understanding of the genetic landscape of ALK negative ALCL is required to dictate more effective therapeutic strategies specifically tailored for each subgroup of patients.
Targetable vulnerabilities in T- and NK-cell lymphomas identified through preclinical models
AlRN-6924 induced a complete remission in a patient with TP53-wild-type angioimmunoblastic T-cell lymphoma, demonstrating the potential for rapid translation of discoveries from subtype-specific preclinical models.
Discovery of recurrent t(6;7)(p25.3;q32.3) translocations in ALK-negative anaplastic large cell lymphomas by massively parallel genomic sequencing.
These findings represent the first recurrent translocation reported in ALK-negative ALCL and highlight the utility of massively parallel genomic sequencing to discover novel translocations in lymphoma and other cancers.
ALK-negative anaplastic large cell lymphoma is a genetically heterogeneous disease with widely disparate clinical outcomes.
ALK-negative ALCL is a genetically heterogeneous disease with widely disparate outcomes following standard therapy, and DUSP22 and TP63 rearrangements may serve as predictive biomarkers to help guide patient management.
Chromosomal rearrangements and copy number abnormalities of TP63 correlate with p63 protein expression in lung adenocarcinoma
A novel chromosomal rearrangement involving TP63 in a p63+/p40− lung adenocarcinoma is identified and correlated with immunohistochemistry positivity for p63.
Targeting ALK With Crizotinib in Pediatric Anaplastic Large Cell Lymphoma and Inflammatory Myofibroblastic Tumor: A Children's Oncology Group Study.
  • Y. Mossé, S. Voss, B. Weigel
  • Medicine
    Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • 2017
The robust and sustained clinical responses to crizotinib therapy in patients with relapsed ALCL and metastatic or unresectable IMT highlight the importance of the ALK pathway in these diseases.