The obese inflammatory microenvironment may promote breast DCIS progression

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Introduction Ductal carcinoma in situ (DCIS), characterized by a proliferation of neoplastic cells confined within the mammary ducts, is distinctly isolated from the surrounding stroma by an almost uninterrupted layer of myoepithelial cells (MECs) and by the basement membrane. Heightened interactions within the adipose microenvironment, particularly in obese patients, may play a key role in the transition from DCIS to invasive ductal carcinoma (IDC), which is attracting growing interest in scientific research. Adipose tissue undergoes metabolic changes in obesity, impacting adipokine secretion and promoting chronic inflammation. This study aimed to assess the interactions between DCIS, including in situ cancer cells and MECs, and the various components of its inflammatory adipose microenvironment (adipocytes and macrophages). Methods To this end, a 3D co-culture model was developed using bicellular bi-fluorescent DCIS-like tumoroids, adipose cells, and macrophages to investigate the influence of the inflammatory adipose microenvironment on DCIS progression. Results The 3D co-culture model demonstrated an inhibition of the expression of genes involved in apoptosis ( BAX, BAG1, BCL2, CASP3, CASP8 , and CASP9 ), and an increase in genes related to cell survival ( TP53 , JUN , and TGFB1 ), inflammation ( TNF-α, PTGS2, IL-6R ), invasion and metastasis (TIMP1 and MMP-9) in cancer cel

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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