This histopathological slide shows enlarged breast ducts containing large pleomorphic cells. They have
irregular nuclei and are arranged in a cribriform pattern. There is no evidence of invasion of the
basement membrane. This is non-comedo ductal carcinoma in situ. Two forms of non-invasive breast
cancer exist - Ductal carcinoma in situ (DCIS) and Lobular carcinoma in situ (LCIS).
DCIS is by far the more frequently seen, accounting for approximately 4% of symptomatic and 20% of screen
detected breast cancers respectively. Symptomatic DCIS usually presents as either a lump, nipple discharge or
Paget's disease. Asymptomatic DCIS presents as either localised or widespread microcalcification seen at
screening mammography. Microcalcification is not specific for malignancy. Over 60% of localisation biopsies are
performed for microcalcification but only about 25% yield either invasive or non-invasive cancer. Malignant
microcalcification is typically heterogeneous in shape, size and density often in clusters and with a branching
The natural history of DCIS is unclear. There is no doubt that a certain proportion progress to invasive
cancer but the exact number is difficult to determine as treatment alters the natural course of the disease.
From studies in those in whom the disease was missed the risk of progression has been estimated to be about 30%
at 10 years. Some cases of DCIS have a better prognosis than others. The worst outcome is seen in those with
comedo DCIS characterised by high grade dysplasia, high mitotic activity and necrosis with intraluminal debris.
The pathological confirmation of asymptomatic DCIS detected by screening mammography has required the
development of new imaging localisation techniques. By far the most commonly used are stereotactic core biopsy
and percutaneous wire localisation methods. X-ray of the excised specimen is required to ensure that the
suspicious area of microcalcification has been identified and completely excised.
Until recently symptomatic DCIS has often been treated by mastectomy with a 98% 5-year survival rate. With
screening mammography detecting smaller areas of DCIS and the introduction of breast conserving surgery for
invasive cancer, it has been realised that mastectomy is probably over treatment of localised DCIS. The outcome
of wide local excision for DCIS is dependent on the histological type of lesion excised. Good prognosis
non-comedo DCIS is associated with a local recurrence rate of about 5% at 10 years. Poor prognosis comedo DCIS
has a local recurrence rate of up to 30% at 10 years. It should be noted that up to 50 % of recurrences of DCIS
is associated with invasive disease. Mastectomy is still appropriate for those with widespread disease. Axillary
surgery is not required for those with localised DCIS. Only 2% of those with widespread DCIS have been shown to
develop axillary metastases. These patients probably have unrecognised invasive cancer.
The role of radiotherapy in DCIS is controversial. In the American NSABP B17 and European EORTC 10853 studies
it has been shown that the local recurrence rate can be reduced by about 50% with the use of adjuvant
radiotherapy. Similar good results have been obtained in Nottingham by ensuring a 10 mm pathologically clear
margin around areas of DCIS without the use of radiotherapy. It may be that poor prognosis cases of DCIS may
benefit from radiotherapy but that those already with good prognosis will not. The importance of adequate
surgery with histologically clear resection margins should not be underestimated. The NSABP B24 study
showed a reduction in the risk of local recurrence with adjuvant tamoxifen therapy. The role of tamoxifen
in DCIS is currently being further investigated by the UK DCIS trial.
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