DCIS-IDC less aggressive than IDC alone
MedWire News: Invasive ductal carcinoma (IDC) co-existing with ductal carcinoma in situ (DCIS) is characterized by lower proliferation and metastatic potential than size-matched pure IDC, study findings indicate.
This is especially true when the ratio of DCIS to IDC size is high, say Richard Epstein (The University of Hong Kong, China) and colleagues.
“The metastatic propensity of IDC of the breast correlates with axillary node involvement and with expression of the proliferation antigen Ki-67, whereas DCIS is non-metastasizing,” explain Epstein and team.
To clarify whether concomitant DCIS affects IDC prognosis, the researchers compared Ki-67 expression and node status in women with size-matched IDC, either with DCIS (IDC-DCIS) or without DCIS (pure IDC).
The cohort included 1355 women with breast cancer (median age 48 years), of whom 616 (45.5%) had IDC-DCIS, 543 (40.1%) had pure IDC, and the remaining 196 (14.4%) had pure DCIS.
Epstein and team found that IDC-DCIS was significantly more likely than size-matched pure IDC to be screen detected, to occur in premenopausal women, and to be either estrogen receptor-positive or human epidermal growth factor receptor-positive, but less likely to be treated with breast-conserving surgery.
“These IDC-DCIS trends were similar in pure DCIS, supporting the view that the IDC-DCIS phenotype reflects that of the associated (presumably precursor) DCIS,” the authors remark in the British Journal of Cancer.
Of note, grade and Ki-67 levels were significantly lower in IDC-DCIS than in pure IDC, and declined significantly as the DCIS enlarged. Furthermore, node involvement and lymphovascular invasion in IDC-DCIS increased significantly with the size ratio of IDC to DCIS.
After a median follow- up of 29.3 months, the 5-year disease free survival rates favored IDC-DCIS, at 97.4%, over IDC, at 96.0%, but the difference between the groups was not statistically significant.
Epstein et al suggest “IDC-DCIS is biologically distinct from pure IDC,” and they propose “an incremental molecular pathogenesis of IDC-DCIS evolution involving an intermediate DCIS precursor that remains dependent for replication on upstream mitogens.”
The team concludes: “Future work is needed to test the observations noted here, and to explore molecular explanations for the putative differences in natural history.”
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By Laura Dean