Related Experiment Video

Updated: Oct 9, 2026

Zebrafish Model of Neuroblastoma Metastasis
05:20

Zebrafish Model of Neuroblastoma Metastasis

Published on: March 14, 2021

Amplification and rearrangement of L-myc in human small-cell lung cancer

T P Mäkelä1, K Saksela, K Alitalo

  • 1Department of Virology, University of Helsinki, Finland.

Mutation Research
|May 1, 1992
PubMed

Insights

DNA amplification and rearrangements involving the L-myc gene are common in small-cell lung cancer (SCLC). A specific rlf-L-myc fusion protein may drive tumor growth, offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • DNA amplification of proto-oncogenes is a key mechanism for oncogene activation in human cancers.
  • Small-cell lung cancer (SCLC) frequently exhibits amplified myc proto-oncogenes, with approximately 25% of tumors showing this alteration.

Purpose of the Study:

  • To investigate the role of DNA rearrangements in oncogene activation within SCLC.
  • To identify specific genetic alterations associated with L-myc in SCLC.

Main Methods:

  • Analysis of DNA amplification and rearrangements in primary SCLC tumors.
  • Characterization of the L-myc gene locus and its involvement in genomic alterations.

Main Results:

  • A novel locus, rlf, is frequently involved in intrachromosomal L-myc rearrangements in SCLC.
  • These rearrangements, likely driven by repetitive DNA regions, lead to the formation of a chimeric rlf-L-myc fusion protein.

Conclusions:

  • The consistent rlf-L-myc rearrangement in SCLC suggests it confers a selective growth advantage to cancer cells.
  • This specific fusion protein represents a potential target for SCLC therapies.

More Related Videos

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Genome-Wide Mapping of Histone Modifications and Transcription Factor Binding Sites in Neuroendocrine Small Cell Lung Cancer Cell Lines Using CUT&RUN11:50

Genome-Wide Mapping of Histone Modifications and Transcription Factor Binding Sites in Neuroendocrine Small Cell Lung Cancer Cell Lines Using CUT&RUN

Published on: April 3, 2026

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...