TPM1-ALK Fusion FISH Probe

The TPM1-ALK Fusion FISH Probe is used to confirm a fusion of the TPM1 and ALK genes. The fusion of the TPM1 and ALK genes has been associated with Bladder Urothelial Carcinoma. 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.

Turnaround Time: 7-10 Business Days Shipping Time: 1-2 Day Expedited Shipping

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SKU	Test Kits	Buffer
TPM1-ALK-20-ORGR (Standard Design)	20 (40 μL)	200 μL
TPM1-ALK-20-RERE	20 (40 μL)	200 μL
TPM1-ALK-20-REOR	20 (40 μL)	200 μL
TPM1-ALK-20-REGO	20 (40 μL)	200 μL
TPM1-ALK-20-REGR	20 (40 μL)	200 μL
TPM1-ALK-20-REAQ	20 (40 μL)	200 μL
TPM1-ALK-20-ORRE	20 (40 μL)	200 μL
TPM1-ALK-20-OROR	20 (40 μL)	200 μL
TPM1-ALK-20-ORGO	20 (40 μL)	200 μL
TPM1-ALK-20-ORAQ	20 (40 μL)	200 μL
TPM1-ALK-20-GORE	20 (40 μL)	200 μL
TPM1-ALK-20-GOOR	20 (40 μL)	200 μL
TPM1-ALK-20-GOGO	20 (40 μL)	200 μL
TPM1-ALK-20-GOGR	20 (40 μL)	200 μL
TPM1-ALK-20-GOAQ	20 (40 μL)	200 μL
TPM1-ALK-20-GRRE	20 (40 μL)	200 μL
TPM1-ALK-20-GROR	20 (40 μL)	200 μL
TPM1-ALK-20-GRGO	20 (40 μL)	200 μL
TPM1-ALK-20-GRGR	20 (40 μL)	200 μL
TPM1-ALK-20-GRAQ	20 (40 μL)	200 μL
TPM1-ALK-20-AQRE	20 (40 μL)	200 μL
TPM1-ALK-20-AQOR	20 (40 μL)	200 μL
TPM1-ALK-20-AQGO	20 (40 μL)	200 μL
TPM1-ALK-20-AQGR	20 (40 μL)	200 μL
TPM1-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

TPM1 Gene Summary

This gene is a member of the tropomyosin family of highly conserved, widely distributed actin-binding proteins involved in the contractile system of striated and smooth muscles and the cytoskeleton of non-muscle cells. Tropomyosin is composed of two alpha-helical chains arranged as a coiled-coil. It is polymerized end to end along the two grooves of actin filaments and provides stability to the filaments. The encoded protein is one type of alpha helical chain that forms the predominant tropomyosin of striated muscle, where it also functions in association with the troponin complex to regulate the calcium-dependent interaction of actin and myosin during muscle contraction. In smooth muscle and non-muscle cells, alternatively spliced transcript variants encoding a range of isoforms have been described. Mutations in this gene are associated with type 3 familial hypertrophic cardiomyopathy. [provided by RefSeq, Jul 2008]

Gene Name: Tropomyosin 1

Chromosome: CHR15: 63334837 -63364113

Locus: 15q22.2

Gene Diseases

The TPM1 ALK Fusion has been associated with the following diseases:

Disease Name
Bladder Urothelial Carcinoma

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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