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

p53 and lung cancer

E Brambilla1, C Brambilla

  • 1Lung Cancer Research Group, Institut Albert Bonniot, Faculté de Médecine, La Tronche, France.

Pathologie-Biologie
|October 14, 1998
PubMed
Summary
This summary is machine-generated.

Lung cancer arises from genetic changes in lung cells, often driven by tobacco carcinogens. The p53 tumor suppressor gene

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

A personalized clinical assessment: multi-sensor approach for understanding musculoskeletal health in the frail population.

Biomedical engineering online·2024
Same author

Robot-assisted laparoscopic gastrectomy with D2 dissection for adenocarcinoma: initial experience with 17 patients.

Journal of robotic surgery·2016
Same author

Endobronchial tumours in a campaign for early detection of bronchial cancer: Computed tomography versus endoscopy.

Diagnostic and interventional imaging·2012
Same author

Imaging of a case of extramedullary solitary plasmacytoma of the trachea.

Case reports in radiology·2012
Same author

Smoking history and lung carcinoma: KRAS mutation is an early hit in lung adenocarcinoma development.

Lung cancer (Amsterdam, Netherlands)·2011
Same author

Primary lung adenocarcinoma: characteristics by smoking habit and sex.

The European respiratory journal·2011
Same journal

Pathologie-biologie·2020
Same journal

Antibacterial and antibiofilm activities of Laurus nobilis L. essential oil against Staphylococcus aureus strains associated with oral infections.

Pathologie-biologie·2015
Same journal

[Not Available].

Pathologie-biologie·2015
Same journal

Oxidative damage and histopathological changes in lung of rat chronically exposed to nicotine alone or associated to ethanol.

Pathologie-biologie·2015
Same journal

Biological diagnosis of diabetes mellitus.

Pathologie-biologie·2015
Same journal

Association of CagPAI integrity with severeness of Helicobacter pylori infection in patients with gastritis.

Pathologie-biologie·2015
See all related articles

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Malignant transformation of pulmonary epithelial cells involves genetic and molecular alterations linked to tobacco carcinogens.
  • Key mechanisms include uncontrolled proliferation and inhibited apoptosis, leading to clonal expansion.
  • Oncogene activation and tumor suppressor gene inactivation drive cell division and bypass growth constraints.

Purpose of the Study:

  • To investigate the role of p53 gene alterations in lung cancer development and progression.
  • To analyze the p53 mutational spectrum and its concordance with protein stabilization and immunoreactivity.
  • To explore the prognostic significance of p53 stabilization and its downstream targets for therapeutic interventions.

Main Methods:

  • Analysis of genetic and molecular alterations in pulmonary epithelial cells.

Related Experiment Videos

  • Evaluation of p53 gene mutations, stabilization, and immunoreactivity using immunohistochemistry.
  • Examination of p53 mutational spectrum, including hot spot codons and their relation to carcinogens.
  • Assessment of p53 auto-antibody secretion and T-cell cytotoxicity in patients.
  • Investigation of downstream p53 pathway components such as Rb, Bax-Bcl2 balance, and matrix degrading enzymes.

    • Main Results:

    • p53 inactivation is the most frequent genetic alteration in lung cancer (70%), affecting G1-checkpoint control and apoptosis.
    • p53 missense mutations correlate with stabilization and immunoreactivity, but immunohistochemistry can yield false negatives.
    • Specific p53 codons are hot spots for carcinogen adduct formation; stabilized mutants trigger immune responses.
    • p53 stabilization predicts progression of preneoplastic lesions, though not tumor prognosis.
    • Deregulation of downstream p53 pathway genes (Rb, Bax-Bcl2, MMPs) contributes to uncontrolled growth and dissemination.

    Conclusions:

    • The p53 pathway is critically involved in lung cancer pathogenesis, offering potential therapeutic targets.
    • Understanding p53 alterations and downstream effects is crucial for developing novel gene therapies and modulations.
    • Targeting p53 pathway components presents a promising strategy for future lung cancer treatment.