Send to

Choose Destination
Mod Pathol. 2003 Feb;16(2):99-107.

Breast cancer stromal myxoid changes are associated with tumor invasion and metastasis: a central role for hyaluronan.

Author information

Department of Pathology, Hospital Italiano, Gascon 450, Buenos Aires (1181), Argentina.


The interplay between a tumor and its environment is exemplified by the morphological changes observed in the stroma of human breast cancer. These changes are evident as stromal myxoid changes. Hyaluronan, an extracellular polysaccharide that has been implicated in invasion, is one of the major constituents of the stromal myxoid changes. This study evaluated the association of these stromal changes with axillary node status, tumor grade, and mortality. The prognostic value of the stromal myxoid changes was evaluated in patients with negative axillary nodes with 10 years of follow-up. Our results showed a high level of reproducibility of our stromal myxoid changes grading system (overall kappa = 0.68). Image analysis semiquantification showed marked correlation of a strong stromal hyaluronan signal with high-grade stromal myxoid changes. In a multiple logistic regression analysis, positive nodes were associated with stromal myxoid changes, tumor size, desmoplasia, lymphocytic infiltration, high tumor grade, tumor emboli, and multifocality. Stromal myxoid changes were also associated with young age and lymphatic embolizations (P <.001). Overall, there is a weak correlation between mortality and stromal myxoid changes (P <.01). Mortality was more evident with high stromal myxoid changes grades and tumor size >2 cm (P <.008). However Cox multivariate analysis fail to show stromal myxoid changes as an independent prognostic factor. In conclusion, stromal myxoid changes with high hyaluronan concentration are strongly associated with positive nodes, tumor grade, and lymphatic emboli, thereby identifying high-risk group and reinforcing the role of hyaluronan in invasion and metastasis.

[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center