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RET by FISH : 1005011
MessagePlease provide most recent Pathology report.
Test Code
MDFCPCRET or 1005011
Alias/See Also
RET (10q11); ret proto-oncogene; KIF5B-RET; Lung carcinoma;
Non-small cell lung cancer; NSCLC
Non-small cell lung cancer; NSCLC
CPT Codes
88271x2, 88275
Instructions
Tissue.
Transport Container
Paraffin embedded formalin fixed tissue that has been fixed in 10% neutral buffered formalin for at least 6 hours and no longer than 48 hours. Two unstained slides, with tissue of 4 microns in thickness are needed for processing, accompanied by a circled H & E clearly indicating the area to be examined.
Transport Temperature
Paraffin embedded tissue block: Ambient or on ice pack in summer. Slides: Ambient.
Specimen Stability
Ambient: Indefinitely; Refrigerated: Indefinitely; Frozen: Unacceptable
Methodology
Fluorescence in situ hybridization (FISH)
Setup Schedule
Monday - Friday
Report Available
Up to 7 days
Limitations
Laboratory test results should always be considered in the context of clinical observations. This test was developed and its performance characteristics determined by med fusion. It has not been cleared or approved by the U.S. Food and Drug Administration(FDA). The FDA has determined that such clearance or approval is not necessary. This test is used for clinical purposes. It should not be regarded as investigational for research. This laboratory is certified under the Clinical Laboratory Improvement Amendmentsof 1988 (CLIA) as qualified to perform high complexity clinical laboratory testing.
Reference Range
An interpretive report will be provided.
Clinical Significance
Identifies RET gene rearrangements in patients with late-stage, lung adenocarcinomas that are negative for EGFR mutations and ALK rearrangements.
The rearranged during transfection (RET) proto-oncogene encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor family of extracellular signaling molecules. RET gene rearrangements that generate a fusion gene consisting of the juxtaposition of the C-terminal region of the RET protein with the N-terminal portion of another protein can also lead to constitutive activation of the RET kinase. RET gene rearrangements have been observed in 1-2% of lung adenocarcinoma and may define a molecular subgroup mutually exclusive from EGFR, KRAS, ALK and ROS1 alternations. Recent clinical data indicate that patients harboring RET gene rearrangements may benefit from multiple kinase inhibitors such as Sorafenib, Sunitinib, Cabozantinib, Vandetanib,Ponatinib, and clinical trial opportunities that may be available for RET(+) populations.
The rearranged during transfection (RET) proto-oncogene encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor family of extracellular signaling molecules. RET gene rearrangements that generate a fusion gene consisting of the juxtaposition of the C-terminal region of the RET protein with the N-terminal portion of another protein can also lead to constitutive activation of the RET kinase. RET gene rearrangements have been observed in 1-2% of lung adenocarcinoma and may define a molecular subgroup mutually exclusive from EGFR, KRAS, ALK and ROS1 alternations. Recent clinical data indicate that patients harboring RET gene rearrangements may benefit from multiple kinase inhibitors such as Sorafenib, Sunitinib, Cabozantinib, Vandetanib,Ponatinib, and clinical trial opportunities that may be available for RET(+) populations.
Performing Laboratory
med fusion
