Well differentiated clinging carcinoma and atypical ductal hyperplasia aresynonim.
Azzopardi in 1979 (1)described a type of in situ duct carcinoma that he
named “clinging” to indicate that neoplastic cells are “attached” to the ductwalls. One or two layers of neoplastic cells line the ducts in a mural
fashion. Azzopardi (1) stated that this form of growth constitute the firstneoplastic change that can be appreciated at light microscopy. He also
implied that the neoplastic process might figure a continuous progression
from normal epithelium to frank malignancy but most of the neoplastic
progression develops at submicroscopic level. In conclusion he stated thatclinging carcinoma was the earliest morphological recognizable sign ofmalignancy. De Potter et al.(2) later found that there are two types ofClinging Carcinoma (C.C.), i.e. one with monotonous , regular nuclei and
one with pleomorphic nuclei. This latter form displayed cells positive with
Erb-c2 and the implication was that pleomorphic C.C. was the precursor of
poorly differentiated DCIS, while the form with monotonous nuclei wasthe precursor of well differentiated DCIS. Tavassoli (4) has shown thatC.C., named DIN Ic, has the same pattern of LOH as invasive duct
carcinoma and therefore C.C. also at molecular level appears to be aneoplastic process.
Page et al. in 1985 (5) introduced the term of atypical duct
hyperplasia (ADH) , indicating a lesion that was bearing a risk ofdevelopping a duct carcinoma 4 times higher than a normal patient. The
precise morphological definition was never definetely given and it wasmodified in the years till recent times in which by admission of David Page
himself, most of the lesions regarded as atypical duct hyperplasia
recognize the phenotype of CC with monotonous nuclei.
The similarity of the two lesions is also evident at molecular level as
Lakhani et al.(3) have found similar LOH changes between ADH and insitu and invasive carcinomas.
It has also been found that the relative risk of subsequent carcinoma
is very similar between ADH and CC ,i.e. in the order of 2-4 times the riskof developping a subsequent carcinoma.

It is proposed that all these lesions (i.e. CC-ADH-DIN Ic) are
different names of the same entity , they have to be followed up and no
specific treatment is necessary.

Reference List
1. Azzopardi JG, Ahmed A, Millis RR. Problems in breast pathology.
London: W.B. Saunders Company, 1979:
2. De Potter CR, Foschini MP, Schelfhout AM, Schroeter C, Eusebi V(1993) Immunohistochemical study of neu protein overexpression
in clinging in situ duct carcinoma of the breast. Virchows Arch A
Pathol Anat 422:375-80.
3. Lakhani SR, Collins N, Stratton MR, Sloane JP (1995) Atypical ductal
hyperplasia of the breast:clonal proliferation with loss
heterozygosity on chromosomes 16q and 17p. J Clin Path
48:611-5.
4. Moinfar F, Man YG, Bratthauer GL, Ratschek M, Tavassoli FA (2000)
Genetic abnormalities in mammary ductal intraepithelial
neoplasia-flat type ("clinging ductal carcinoma in situ"). A
simulator of normal mammary epithelium. Cancer 88:2072-81.
5. Page DL, Dupont WD, Rogers LW, Rados MS (1985) Atypical
hyperplastic lesions of the female breast. A long-term follow-up
study. Cancer 55:2698-708.