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

Multiple genetic alterations in malignant metastatic insulinomas

K Pavelić1, R Hrasćan, S Kapitanović

  • 1Department of Molecular Medicine, Ruder Bosković Institute, Zagreb, Croatia.

The Journal of Pathology
|December 1, 1995
PubMed
Summary

Malignant insulinomas show genetic alterations in proto-oncogenes like c-myc and c-K-ras, along with growth factors and tumor suppressors. These genetic lesions are crucial for tumor progression and metastasis.

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

TGF-β1 expression in chromophobe renal cell carcinoma and renal oncocytoma.

European journal of histochemistry : EJH·2014
Same author

miR-106a overexpression and pRB downregulation in sporadic colorectal cancer.

Experimental and molecular pathology·2012
Same author

Micropapillary urothelial carcinoma of the ureter.

Ceskoslovenska patologie·2012
Same author

Nm23-h1 protein in oligodendrogliomas.

International journal of oncology·2011
Same author

Expression of nm23-h1 gene in squamous-cell carcinoma of the cervix correlates with 5-year survival.

International journal of oncology·2011
Same author

MAGE-A3/4 and NY-ESO-1 antigens expression in metastatic esophageal squamous cell carcinoma.

European journal of histochemistry : EJH·2011

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Insulinomas are pancreatic tumors with varying degrees of malignancy.
  • Understanding the genetic underpinnings of malignant transformation is crucial for developing targeted therapies.

Purpose of the Study:

  • To analyze proto-oncogenes, growth factors/receptors, and tumor suppressor genes in malignant metastatic insulinomas.
  • To identify genetic alterations associated with malignant progression and metastasis in insulinomas.

Main Methods:

  • Immunohistochemical analysis of c-myc proto-oncogene, transforming growth factor alpha (TGF alpha), and epidermal growth factor receptor (EGF-R).
  • Analysis of c-K-ras activation and p53 protein overexpression.
  • Detection of c-K-ras point mutations at codon 12 using DNA sequencing.

Related Experiment Videos

Main Results:

  • Malignant insulinomas exhibit strong immunoreaction for c-myc and TGF alpha, with activation of c-K-ras and p53 overexpression.
  • Three out of six malignant insulinomas had a c-K-ras point mutation (guanine to cytosine transversion) at codon 12, present only in metastatic tumors.
  • Patients with mutated c-K-ras also showed overexpression of p53, c-myc, and TGF alpha.

Conclusions:

  • Malignant progression of insulinomas results from multiple genetic lesions.
  • Activation of myc, TGF alpha, and ras genes plays a significant role in the multistep process of tumor progression, potentially as initiating events.