Esophageal cancer ranks as the seventh leading cause of cancer death globally, with esophageal squamous cell carcinoma (ESCC) accounting for about 85% of new cases.

Recent gene expression analysis has led to the development of a prognostic test indicating that patients with elevated levels of desmoplastic cancer-associated fibroblasts (dCAFs) are at a higher risk of cancer mortality under current treatments.

CAFs are heterogeneous, originating from various cell types including resting fibroblasts, muscle cells, and stem cells, and they vary in their differentiation status.

Researchers have categorized cancer-associated fibroblasts into three types: myofibroblastic (myCAFs), inflammatory (iCAFs), and desmoplastic (dCAFs), with dCAFs being particularly associated with poor patient prognoses.

Tumors characterized by high levels of dCAFs tend to be stiffer, richer in collagen, and exhibit increased expression of genes linked to drug resistance.

ASCs can transdifferentiate into CAFs under the influence of tumor-derived signals, which enhances their secretion of extracellular matrix components and pro-inflammatory cytokines that promote tumorigenesis.

These fibroblasts play a crucial role in remodeling the extracellular matrix (ECM) surrounding tumors, which complicates drug delivery and can diminish the effectiveness of immunotherapies.

Potential therapeutic strategies may involve disrupting the interactions between adipose-derived stem cells (ASCs), CAFs, and tumor cells, as well as targeting key signaling pathways and exploring immunotherapy options.

Research indicates that epigenetic modifications can impact the functionality of ASCs and CAFs, with ongoing studies focusing on targeting these changes to inhibit their pro-tumorigenic effects.

Adipose-derived stem cells (ASCs) are identified by specific surface markers such as CD34, CD90, and CD105, which indicate their mesenchymal stem cell properties and plasticity.

Ovarian cancer is notably aggressive, exhibiting high mortality rates and recurrence, and often develops resistance to platinum-based treatments.

In co-culture studies, ESCC cells showed increased expression and secretion of amphiregulin (AREG) when interacting with CAFs, along with activation of its receptor, EGFR.