Related Experiment Video

Updated: May 10, 2026

An Orthotopic Model of Serous Ovarian Cancer in Immunocompetent Mice for in vivo Tumor Imaging and Monitoring of Tumor Immune Responses
10:35

An Orthotopic Model of Serous Ovarian Cancer in Immunocompetent Mice for in vivo Tumor Imaging and Monitoring of Tumor Immune Responses

Published on: November 28, 2010

Conditional inactivation of p53 in mouse ovarian surface epithelium does not alter MIS driven Smad2-dominant negative

Suzanne M Quartuccio1, Daniel D Lantvit, Maarten C Bosland

  • 1Department of Medicinal Chemistry and Pharmacognosy, University of Illinois at Chicago, Chicago, Illinois, United States of America.

Plos One
|June 7, 2013
PubMed

Insights

This study investigated ovarian cancer precursors in mice. Disrupting the TGFβ pathway caused cyst formation, a potential early lesion, and high Smad2DN expression led to teratomas.

Area of Science:

  • Gynecologic Oncology
  • Cancer Etiology
  • Translational Research

Background:

  • Epithelial ovarian cancer is a lethal gynecological malignancy with poorly understood origins.
  • The transforming growth factor beta (TGFβ) pathway and p53 are frequently disrupted in chemotherapy-resistant serous ovarian tumors.
  • Ovarian surface epithelium and fallopian tube fimbriae are potential progenitor cells for ovarian cancer.

Purpose of the Study:

  • To investigate the role of the TGFβ signaling pathway and p53 in ovarian cancer development using a mouse model.
  • To create transgenic mice with disruptions in the TGFβ pathway and p53 to identify potential precursor lesions.
  • To evaluate the efficacy of adenovirus-mediated gene deletion in the reproductive tract for future ovarian cancer modeling.

Main Methods:

  • Created transgenic mice expressing a dominant-negative Smad2 (Smad2DN) in the reproductive tract.
  • Administered Cre-recombinase expressing adenovirus (AdCreGFP) to induce p53 deletion in p53 (flox/flox) mice.
  • Analyzed phenotypes including cyst formation, protein expression, and teratoma development via qPCR and morphological assessment.

Main Results:

  • Transgenic mice expressing Smad2DN developed epithelium-lined inclusion cysts resembling oviductal epithelium but with ovarian surface epithelium-like protein expression.
  • Intrabursal AdCreGFP injection in p53 (flox/flox) mice led to ovarian bursal cysts, while intraoviductal injection did not yield pathological abnormalities.
  • Bitransgenic mice (Smad2DN and p53 flox/flox) exposed to AdCreGFP did not develop additional phenotypes, indicating AdCreGFP is ineffective for oviductal epithelium gene deletion.
  • High Smad2DN expression correlated with teratoma-like lesions, suggesting a role for Smad signaling in teratoma development.

Conclusions:

  • Disruptions in TGFβ signaling can lead to ovarian cyst formation, a potential precursor lesion for ovarian cancer.
  • Adenovirus-mediated gene deletion is inefficient in the oviductal epithelium, necessitating alternative strategies like tissue-specific promoters for future models.
  • Smad signaling may play a role in the development of teratomas.

More Related Videos

Non-Invasive Ultrasound Assessment of Endometrial Cancer Progression in Pax8-Directed Deletion of the Tumor Suppressors Arid1a and Pten in Mice07:44

Non-Invasive Ultrasound Assessment of Endometrial Cancer Progression in Pax8-Directed Deletion of the Tumor Suppressors Arid1a and Pten in Mice

Published on: February 17, 2023

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice10:13

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Published on: August 12, 2014

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...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Oogenesis02:07

Oogenesis

In human women, oogenesis produces one mature egg cell or ovum for every precursor cell that enters meiosis. This process differs in two unique ways from the equivalent procedure of spermatogenesis in males. First, meiotic divisions during oogenesis are asymmetric, meaning that a large oocyte (containing most of the cytoplasm) and minor polar body are produced as a result of meiosis I, and again following meiosis II. Since only oocytes will go on to form embryos if fertilized, this unequal...