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LEPREL1-TP63 Fusion FISH Probe

The LEPREL1-TP63 Fusion FISH Probe is used to confirm a fusion of the LEPREL1 and TP63 genes. The fusion of the LEPREL1 and TP63 genes has been associated with Brain Lower Grade Glioma. These probes are FISH confirmed on normal peripheral blood in both interphase nuclei and metaphase spreads before shipment. Typical turnaround time for this product is 7-14 days after purchase.

** This product is for in vitro and research use only. This product is not intended for diagnostic use. Please note that both genes fall on the same chromosome and inter-chromosomal detection may be difficult to detect depending on the genes proximity to one another. Please consult our support staff before ordering this product to ensure that the probe can be designed to meet your specific needs.

Turnaround Time: 7-10 Business Days    Shipping Time: 1-2 Day Expedited Shipping
Download Datasheet Download FISH Protocol Download Material Safety Data Sheet

SKU Test Kits Buffer Dye Color Order Now
LEPREL1-TP63-20-ORGR  (Standard Design) 20 (40 μL) 200 μL
LEPREL1-TP63-20-RERE 20 (40 μL) 200 μL
LEPREL1-TP63-20-REOR 20 (40 μL) 200 μL
LEPREL1-TP63-20-REGO 20 (40 μL) 200 μL
LEPREL1-TP63-20-REGR 20 (40 μL) 200 μL
LEPREL1-TP63-20-REAQ 20 (40 μL) 200 μL
LEPREL1-TP63-20-ORRE 20 (40 μL) 200 μL
LEPREL1-TP63-20-OROR 20 (40 μL) 200 μL
LEPREL1-TP63-20-ORGO 20 (40 μL) 200 μL
LEPREL1-TP63-20-ORAQ 20 (40 μL) 200 μL
LEPREL1-TP63-20-GORE 20 (40 μL) 200 μL
LEPREL1-TP63-20-GOOR 20 (40 μL) 200 μL
LEPREL1-TP63-20-GOGO 20 (40 μL) 200 μL
LEPREL1-TP63-20-GOGR 20 (40 μL) 200 μL
LEPREL1-TP63-20-GOAQ 20 (40 μL) 200 μL
LEPREL1-TP63-20-GRRE 20 (40 μL) 200 μL
LEPREL1-TP63-20-GROR 20 (40 μL) 200 μL
LEPREL1-TP63-20-GRGO 20 (40 μL) 200 μL
LEPREL1-TP63-20-GRGR 20 (40 μL) 200 μL
LEPREL1-TP63-20-GRAQ 20 (40 μL) 200 μL
LEPREL1-TP63-20-AQRE 20 (40 μL) 200 μL
LEPREL1-TP63-20-AQOR 20 (40 μL) 200 μL
LEPREL1-TP63-20-AQGO 20 (40 μL) 200 μL
LEPREL1-TP63-20-AQGR 20 (40 μL) 200 μL
LEPREL1-TP63-20-AQAQ 20 (40 μL) 200 μL

TP63 Gene Summary

This gene encodes a member of the p53 family of transcription factors. The functional domains of p53 family proteins include an N-terminal transactivation domain, a central DNA-binding domain and an oligomerization domain. Alternative splicing of this gene and the use of alternative promoters results in multiple transcript variants encoding different isoforms that vary in their functional properties. These isoforms function during skin development and maintenance, adult stem/progenitor cell regulation, heart development and premature aging. Some isoforms have been found to protect the germline by eliminating oocytes or testicular germ cells that have suffered DNA damage. Mutations in this gene are associated with ectodermal dysplasia, and cleft lip/palate syndrome 3 (EEC3); split-hand/foot malformation 4 (SHFM4); ankyloblepharon-ectodermal defects-cleft lip/palate; ADULT syndrome (acro-dermato-ungual-lacrimal-tooth); limb-mammary syndrome; Rap-Hodgkin syndrome (RHS); and orofacial cleft 8. [provided by RefSeq, Aug 2016]

Gene Name: Tumor Protein P63

Chromosome: CHR3: 189349215 -189615068

Locus: 3q28

Gene Diseases

The LEPREL1 TP63 Fusion has been associated with the following diseases:

Disease Name
Brain Lower Grade Glioma

FISH Probe Protocols

Protocol, Procedure, or Form Name Last Modified Download

Anaplastic large cell lymphoma with TP63 rearrangement: A dismal prognosis

Anaplastic large cell lymphoma (ALCL) is a rare form of T-cell lymphoma that makes up about 3% of adult non-Hodgkin lymphoma. Recently, TP63 translocations have emerged as a new class of biomarkers in ALCL. This study examined two cases of TP63-rearranged ALCL, using Empire Genomics’ TP63 break apart probe to detect translocations of the gene. Although the effects of TP63 rearrangement still aren’t clear, results suggest that the N-terminal domain of the protein, which is truncated as a result of gene rearrangement, may act as a tumor suppressor.
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Systemic, primary cutaneous, and breast implant-associated ALK-negative anaplastic large-cell lymphomas present similar biologic features despite distinct clinical behavior

Systemic, primary cutaneous, and breast implant-associated ALK-negative anaplastic large cell lymphomas, although diverse in their clinical features, can be difficult to distinguish histopathologically. This study sought to cytogenetically discern between these lymphoma 3 subtypes using IHC and FISH. Twenty-two S-ALCL ALK?, 13 PC-ALCL, and 2 BI-ALCL were analyzed. Empire Genomics' PD-L1 and TP63 break apart probes were used to detect PD-L1 and TP63 rearrangements.
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Genetic Subtypes of Systemic Anaplastic Large Cell Lymphoma Show Distinct Differences in PD-L1 Expression and Regulatory and Cytotoxic T Cells in the Tumor Microenvironment

This publication looked at 4 different ALCL subtypes to determine whether a correlation existed between several tumor microenvironment factors (PDL1 expression, FOXP3+ regulatory cell density, and CD8+ tumor-infiltrating lymphocyte density) and ALCL subtype. Our break apart probes for DUSP22/IRF4 and TP63 were used to determine which patients fell into 2 of the 4 ALCL subtypes under analysis: DUSP22/IRF-rearranged ALCL and TP63-rearranged-ALCL.
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