NCOA1-ALK Fusion FISH Probe

The NCOA1-ALK Fusion FISH Probe is used to confirm a fusion of the NCOA1 and ALK genes. The fusion of the NCOA1 and ALK genes has been associated with Skin Cutaneous Melanoma. 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
NCOA1-ALK-20-ORGR (Standard Design)	20 (40 μL)	200 μL
NCOA1-ALK-20-RERE	20 (40 μL)	200 μL
NCOA1-ALK-20-REOR	20 (40 μL)	200 μL
NCOA1-ALK-20-REGO	20 (40 μL)	200 μL
NCOA1-ALK-20-REGR	20 (40 μL)	200 μL
NCOA1-ALK-20-REAQ	20 (40 μL)	200 μL
NCOA1-ALK-20-ORRE	20 (40 μL)	200 μL
NCOA1-ALK-20-OROR	20 (40 μL)	200 μL
NCOA1-ALK-20-ORGO	20 (40 μL)	200 μL
NCOA1-ALK-20-ORAQ	20 (40 μL)	200 μL
NCOA1-ALK-20-GORE	20 (40 μL)	200 μL
NCOA1-ALK-20-GOOR	20 (40 μL)	200 μL
NCOA1-ALK-20-GOGO	20 (40 μL)	200 μL
NCOA1-ALK-20-GOGR	20 (40 μL)	200 μL
NCOA1-ALK-20-GOAQ	20 (40 μL)	200 μL
NCOA1-ALK-20-GRRE	20 (40 μL)	200 μL
NCOA1-ALK-20-GROR	20 (40 μL)	200 μL
NCOA1-ALK-20-GRGO	20 (40 μL)	200 μL
NCOA1-ALK-20-GRGR	20 (40 μL)	200 μL
NCOA1-ALK-20-GRAQ	20 (40 μL)	200 μL
NCOA1-ALK-20-AQRE	20 (40 μL)	200 μL
NCOA1-ALK-20-AQOR	20 (40 μL)	200 μL
NCOA1-ALK-20-AQGO	20 (40 μL)	200 μL
NCOA1-ALK-20-AQGR	20 (40 μL)	200 μL
NCOA1-ALK-20-AQAQ	20 (40 μL)	200 μL

ALK Gene Summary

This gene encodes a receptor tyrosine kinase, which belongs to the insulin receptor superfamily. This protein comprises an extracellular domain, an hydrophobic stretch corresponding to a single pass transmembrane region, and an intracellular kinase domain. It plays an important role in the development of the brain and exerts its effects on specific neurons in the nervous system. This gene has been found to be rearranged, mutated, or amplified in a series of tumours including anaplastic large cell lymphomas, neuroblastoma, and non-small cell lung cancer. The chromosomal rearrangements are the most common genetic alterations in this gene, which result in creation of multiple fusion genes in tumourigenesis, including ALK (chromosome 2)/EML4 (chromosome 2), ALK/RANBP2 (chromosome 2), ALK/ATIC (chromosome 2), ALK/TFG (chromosome 3), ALK/NPM1 (chromosome 5), ALK/SQSTM1 (chromosome 5), ALK/KIF5B (chromosome 10), ALK/CLTC (chromosome 17), ALK/TPM4 (chromosome 19), and ALK/MSN (chromosome X).[provided by RefSeq, Jan 2011]

Gene Name: ALK Receptor Tyrosine Kinase

Chromosome: CHR2: 29415639 -30144477

Locus: 2p23.2-p23.1

NCOA1 Gene Summary

The protein encoded by this gene acts as a transcriptional coactivator for steroid and nuclear hormone receptors. It is a member of the p160/steroid receptor coactivator (SRC) family and like other family members has histone acetyltransferase activity and contains a nuclear localization signal, as well as bHLH and PAS domains. The product of this gene binds nuclear receptors directly and stimulates the transcriptional activities in a hormone-dependent fashion. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Jul 2008]

Gene Name: Nuclear Receptor Coactivator 1

Chromosome: CHR2: 24807345 -24993570

Locus: 2p23.3

Gene Diseases

The NCOA1 ALK Fusion has been associated with the following diseases:

Disease Name
Skin Cutaneous Melanoma

FISH Probe Protocols

Protocol, Procedure, or Form Name	Last Modified	Download

Atypical Spitzoid Neoplasms in Childhood: A Molecular and Outcome Study

Atypical spitzoid neoplasms (APNs) are primarily pediatric lesions characterized by their intermediate features; clinically and histopathologically, they fall somewhere between benign spitz nevi and malignant melanoma. The genetics of these tumors are still poorly understood. In this study, 34 APNs were analyzed using FISH and IHC. Our ALK, BRAF, and NTRK1 break-apart FISH probes were used to detect rearrangements of the genes .

Alterations in ALK/ROS1/NTRK/MET drive a group of infantile hemispheric gliomas

While studies are plentiful on adult gliomas, infant cases are historically understudied. This team sought to account for that lack of data by analyzing glioma biopsies from 150 infants. As part of genetic profiling, our ALK break apart probe was used to detect ALK rearrangements. The team was able to divide the tumors into three genetic subtypes that were tightly tied to clinical outcome. They also found that many of the tumors harbored just a single oncogene, evidence that infant gliomas are usually single driver tumors.

ALK-rearranged renal cell carcinomas in Polish population

Since the first report 2010, 22 cases of ALK-rearranged renal cell carcinoma (RCC) have been described. This study screened over 1000 Polish RCC patients for ALK translocations using IHC followed by FISH with our ALK break apart FISH probe. Only 31 cases were considered potentially positive or indeterminable by IHC; of these, none tested positive for ALK rearrangement with FISH. These results suggests that the mutation might be related to ethnicity, warranting further investigation into its prevalence in other ethnicities.

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