Non-invasive Breast Cancer

Non-invasive Breast Cancer

Non-invasive breast cancer (NIBC) is a type of breast cancer that has not spread beyond the milk ducts or lobules where it originated. This form of breast cancer is considered a pre-cancerous condition, as it has the potential to develop into invasive breast cancer (IBC) if left untreated. At Alfa Cytology, our team of experienced biologists work with you to develop non-invasive breast cancer therapeutics.

Introduction to Non-invasive Breast Cancer

The progression from non-invasive to invasive breast cancer is a complex and multifaceted process that requires a comprehensive understanding of the underlying biological mechanisms. The transition from NIBC to IBC is a complex and multifaceted process that involves various genetic and molecular alterations within the affected cells.

Fig.1 Proposed models of DCIS progression. (Wang J., et al. 2024)Fig.1 Proposed models of DCIS progression. (Wang J., et al. 2024)

Studies have shown that certain molecular signatures, such as the overexpression of specific oncogenes or the loss of tumor suppressor genes, can increase the likelihood of non-invasive breast cancer progressing to an invasive form. Understanding these molecular and cellular underlying mechanisms in the transition from NIBC to IBC is critical for developing therapeutic and personalized strategies.

Therapeutic Development for Non-invasive Breast Cancer

The current treatment of NIBC remains controversial due to uncertainty about the risk of progression to IBC or recurrence. The main goal of treatment is to prevent the development of potentially progressive non-invasive breast cancer into malignant IBC and future recurrence.

We summarize here all current treatments and relevant clinical trials for NIBC.

NCT Therapy Trial Name NIBC Feature Phase
NCT00072462 Endocrine Therapy IBIS II DCIS HR-positive DCIS
NCT02005887 TREND NIBC
NCT02926911 Active Surveillance COMET Low risk DCIS Not Applicable

Our Services

At Alfa Cytology, we are committed to advancing the field of non-invasive breast cancer research. Our comprehensive suite of services encompasses the full spectrum of preclinical research, from target identification and validation to the evaluation of novel therapeutic strategies. Ductal carcinoma in situ (DCIS) is a non-invasive form of breast cancer that is considered a precursor to IBC. We also provide one-stop solutions for ductal carcinoma in situ (DCIS).

Small Molecule Drug Development

Therapeutic Antibody Development

Gene Therapy Development

Cell Therapy Development

Peptidomimetic Development

Cancer Vaccine Development

Modeling Services for Non-invasive Breast Cancer

In Vitro Models Animal Models
  • MCF10 series
  • HMT-3522 series
  • 21T series
  • SUM225CWN
  • SUM102PT
  • h.DCIS.01

Case Study

A MIN-O DCIS Transplant Model for Assessing Chemopreventive Efficacy of SERMs

  • Model Introduction

The MIN-O (Mouse Intraepithelial Neoplasia-Outgrowth) transplant model is a critical preclinical tool for studying ductal carcinoma in situ (DCIS), a non-invasive precursor to invasive breast cancer. It recapitulates key features of human DCIS progression, including estrogen receptor (ER) positivity and ovarian hormone dependence, providing a biologically relevant platform for evaluating chemopreventive agents like selective estrogen receptor modulators (SERMs).

  • Model Information
  • Model: MIN-O DCIS Transplant Model
  • Cancer Type: Non Invasive Breast Cancer, Ductal Carcinoma In Situ (DCIS)
  • Host Mouse Strain: FVB/N Mice
  • Age: 5 Weeks
  • Tissue Origin: Dysplastic foci from MMTV-PyV-mT transgenic mice
  • Molecular Profile: ER-positive; PyV-mT driven (activates Ras/Shc/PI3K pathways).
  • Weight: 15-20 g
  • Model Construction

The MIN-O model was established by orthotopically transplanting 1 mm3 MIN-O tissue fragments into the cleared mammary fat pads of female FVB/N mice. Selective estrogen receptor modulators treatments (Drug A or Drug B at 50 mg/kg) or vehicle control were administered daily via oral gavage, starting one week prior to transplantation. MIN-O growth and tumor development were assessed at 3 and 10 weeks post-transplantation.

  • In Vivo Efficacy Evaluation

This case utilized the MIN-O DCIS transplant model to evaluate the chemopreventive efficacy of drugs A and B systematically.

  • Inhibition of MIN-O Growth: Both drug A and drug B significantly reduced MIN-O growth in mammary fat pads compared to controls at 3 weeks post-transplantation (p < 0.0001), with no statistical difference between the two SERMs.
  • Suppression of Tumor Incidence: Long-term SERM treatment (10 weeks) significantly reduced tumor incidence in MIN-O transplants. Tumor-bearing fat pads decreased from 84% in controls to 35% with drug A (p = 0.0008) and 33% with drug B (p = 0.0011).

Fig. 2 Effect of the selective estrogen receptor modulator (SERM) treatments. (A) The amount of MIN-O tissue treated with drug A or drug B was significantly less than that of untreated mice (p < 0.0001). (B) p = 0.0008 for drug A and p = 0.0011 for drug B. (C) The drug A-treated and drug B-treated MIN-Os were significantly smaller than the untreated MIN-Os (p < 0.0001). (Source: Alfa Cytology)

If you are interested in learning more about Alfa Cytology's services or our ongoing research in non-invasive breast cancer, please don't hesitate to contact us. Our team of experts is dedicated to providing personalized solutions and support to help you achieve your research and development goals. We look forward to the opportunity to discuss how we can collaborate to advance the field of non-invasive breast cancer research.

Reference

  1. Wang J., Li B., and et al. Progression from ductal carcinoma in situ to invasive breast cancer: molecular features and clinical significance. Sig Transduct Target Ther. 2024, 9, 83.
All our services are exclusively intended for preclinical research purposes. They are not intended for diagnostic, therapeutic, or patient management applications.