Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Variable FHIT transcripts in non-neoplastic tissues

I Panagopoulos1, S Thelin, F Mertens

  • 1Department of Clinical Genetics, University Hospital, Lund, Sweden.

Genes, Chromosomes & Cancer
|August 1, 1997
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Ultrafast Amplification and Nonlinear Magnetoelastic Coupling of Coherent Magnon Modes in an Antiferromagnet.

Physical review letters·2021
Same author

Virtual pollination trade uncovers global dependence on biodiversity of developing countries.

Science advances·2021
Same author

Wide spectral range ultrafast pump-probe magneto-optical spectrometer at low temperature, high-magnetic and electric fields.

The Review of scientific instruments·2020
Same author

Smooth muscle actin expression in primary bone tumours.

Virchows Archiv : an international journal of pathology·2012
Same author

Nonrandom secondary chromosome-aberrations in liposarcomas with t(12, 16).

International journal of oncology·2011
Same author

Cytogenetic findings in pediatric germ-cell tumors.

International journal of oncology·2011
Same journal

Biphenotypic Sinonasal Sarcoma With a Novel PAX3::MAML2 Fusion.

Genes, chromosomes & cancer·2026
Same journal

An Affordable and Efficient In-House Approach for Detecting Gene Fusions in Bone and Soft Tissue Tumors Using a Custom Capture Panel and Nanopore Sequencing.

Genes, chromosomes & cancer·2026
Same journal

PKMYT1 in Cancer: Beyond Cell Cycle Checkpoints to Context-Dependent Therapeutic Vulnerability.

Genes, chromosomes & cancer·2026
Same journal

Associations of Dietary Intake Traits and Aging Indicators With Colorectal Cancer: A Mendelian Randomization Study.

Genes, chromosomes & cancer·2026
Same journal

Primary Tumor-Associated Loss of the Y Chromosome and Clinical Outcome in Metastatic Colorectal Cancer.

Genes, chromosomes & cancer·2026
Same journal

Cytogenetic and Molecular Analysis of a "Double-Hit" RUNX1 Including a RUNX1 p.Trp279* and a Cryptic Novel t(6;21)(q25;q22)/RUNX1::ARID1B in Acute Myeloid Leukemia.

Genes, chromosomes & cancer·2026
See all related articles

The FHIT gene, a potential tumor suppressor, shows multiple transcripts in healthy tissues. These variations are not specific to cancer and cannot serve as a reliable neoplasia marker.

Area of Science:

  • Molecular biology
  • Genetics
  • Cancer research

Background:

  • The FHIT gene, located at chromosomal band 3p14.2, is considered a presumptive tumor suppressor.
  • Altered expression of FHIT has been implicated in various neoplastic diseases.

Purpose of the Study:

  • To investigate the expression patterns of the FHIT gene in non-neoplastic human tissues.
  • To determine if aberrant FHIT gene transcripts are specific to cancerous conditions.

Main Methods:

  • Nested reverse transcriptase PCR was employed to analyze FHIT gene expression.
  • Samples included peripheral blood lymphocytes, skeletal muscle, liver, and an isynovial tissue cell line.

Main Results:

  • Multiple FHIT gene transcripts were detected in all non-neoplastic tissues examined.

Related Experiment Videos

  • Variable splicing of FHIT transcripts, resulting in exon deletions and nonfunctional protein, was frequently observed.

    • Conclusions:

    • The presence of multiple, potentially nonfunctional FHIT transcripts is common in non-neoplastic tissues.
    • These findings indicate that FHIT transcript anomalies are not tumor-specific and cannot be utilized as a genetic marker for neoplasia.