Clinicopathological Significance of Stromal Myofibroblasts in Invasive Ductal Carcinoma of the Breast

Abstract

The purpose of this study was to investigate the distribution of CD34-positive fibroblasts and α-smooth muscle actin (α-SMA)-reactive myofibroblasts in the stroma of benign and malignant breast lesions and, secondly, to determine whether the presence of stromal myofibroblasts is associated with some of the clinicopathological characteristics of patients with invasive ductal carcinoma. The presence of stromal CD34-positive fibroblasts and myofibroblasts was investigated (as defined immunohistochemically) in 8 normal breast tissue samples, 58 invasive ductal carcinomas, 9 ductal carcinomas in situ and 16 specimens with benign lesions of the breast (fibroadenomas, ductal hyperplasias). We further studied the correlations between the presence of stromal myofibroblasts with 7 clinicopathological parameters in 58 invasive ductal carcinomas. The results indicated that the stroma of normal breast tissues contained CD34-positive fibroblasts. All benign breast lesions exhibited stromal CD34-positive fibroblasts. In contrast, the stroma of ductal carcinomas showed a complete loss of CD34-positive fibroblasts. α-SMA expression in stromal fibroblasts (myofibroblasts) was not detected in normal tissue samples or benign lesions except in 1 case of fibroadenoma, whereas positive myofibroblasts were found in 44.4% of ductal carcinomas in situ and 56.9% of invasive breast carcinomas. Comparison of clinicopathological parameters between invasive ductal carcinomas with and without stromal myofibroblasts revealed significant differences in lymph node metastasis, high histological grade and high microvessel density. These results suggest that CD34 loss and the presence of myofibroblasts favor the diagnosis of breast carcinoma. In invasive ductal carcinoma, the presence of stromal myofibroblasts correlated significantly with pathological parameters associated with a poor prognosis.

SPARC enhances tumor stroma formation and prevents fibroblast activation

“…A poorer prognosis has been associated with carcinomas with desmoplastic stroma (Maeshima et al, 2002;Yazhou et al, 2004), and laboratory studies support the concept that myofibroblasts are capable of enhancing tumor progression. Activated fibroblasts explanted from human prostate carcinomas can promote epithelialmesenchymal transition of SV40-transformed prostate epithelial cell lines (Olumi et al, 1999).…”

In Vitro Evidence of the Presence of Mesenchymal Stromal Cells in Cervical Cancer and Their Role in Protecting Cancer Cells from Cytotoxic T Cell Activity

“…Such processes have been implicated in several aspects of epithelial tumor biology, such as tumor growth, neoplastic progression, angiogenesis, and metastasis [6,7]. MSCs have been isolated from different tumor types such as ovarian carcinomas [8], giant cell tumors of bone [9], neuroblastomas [10], osteosarcomas [11], lipomas [12], and gastric cancer [13]; however, the presence of MSCs in cervical cancer (CeCa) and their possible role in such tumor growth have not been documented.…”

Comparison of Myofibroblasts Expression in Oral Squamous Cell Carcinoma, Verrucous Carcinoma, High Risk Epithelial Dysplasia, Low Risk Epithelial Dysplasia and Normal Oral Mucosa

“…As there is conversion of nondiseased epithelial tissue to pre-cancerous epithelium to carcinoma, the stroma also changes from normal to ''primed'' to activated or ''tumor associated'' [19,20]. Various studies reported the presence of stromal myofibroblasts in invasive breast, throat, and larynx cancers [21][22][23]. Recently, several studies [24][25][26][27][28] have investigated myofibroblast expression in oral squamous cell carcinoma (OSCC) and few studies [26,27] have investigated myofibroblast expression in oral premalignant lesions (oral epithelial dysplasia).…”