Breast cancer is essentially the appearance of malignant new cell growth, most commonly originating in the lining of the breast ducts. But it is quite common for many women to experience benign neoplastic cell growth in the breast. The issue is really whether there is anything 'atypical' about the new cell growth. There are also ongoing discussions in the breast cancer research literature about discovering breast cancer at the earliest possible stage, even before it evoles into a conventional 'breast carcinoma' staging category. There is a strong but inconclusive link between atypical ductal hyperplasia and ductal carcinoma in situ, and it should be remembered that any breast cancer or potential breast cancer discovered and treated at the DCIS stage has a cure rate of close to 100%.
Ductal hyperplasia without atypia,(or DH) mplies a kind of 'lesion' or cellular irregularity in which there is a proliferation of ductal cells. These new cells are either purely epithelial, or, a mixture of epithelial, myo-epithelial, and metaplastic apocrine cells but without any significant irregularities.
Myoepithelial cells are usually found in-between the epithelium and basement membranes, of various body glands, including the mammory glands. They resemble smooth muscle. If these cells are present, 'where they should be', then everything is fine. ( benign ), but if they are starting to show up where they 'ought not to be', such as actually 'in' the epithelium, then it may possibly, but unlikely, indicate cancer. (note: 'epithelium' is the lining material of a body organ or feature, in this case the breast ducts) 'Metaplastic' means 'changed in form' and here means that cells which 'ought to be' occuring in a certain place are 'replaced' by cells that 'ought not' to be there. 'Apocrine glands' are sweat glands, and they are not usually found in breast tissue. One has to ask, 'why are apocrine-gland cells showing up within the epithelial lining of breast ducts'? All this means, is that there is a 'noted irregularity' and proliferation of curious cells, but nothing to cause any particular alarm, and certainly nothing yet to assert that it is cancer. So, it is called Ductal Hyperplasia.
Atypical Ductal Hyperplasia demonstrates basically the same kinds of cellular activies as DH, but there are changes in the cytologic appearance of the cells themselves. Cells may demonstrate 'anisocytosis', which is an unexpected variation in shape and size of the cell, or 'anisokaryosis', which refers to a change in the density of the chromatin in the nucleus of the cell.
In order to 'escalate' the grading of the 'lesion' to DCIS, it would have to measure more than 2mm, or be present in more than one duct. That is to say, DCIS may be flagged based upon other histological features, discussed below, but if what is viewed in the microscope already shows new cell growth in more than one duct and greater than 2mm, then it will likely be termed ductal carcinoma in situ or DCIS.
As noted elsewhere, it is hard to pin-down what people are calling 'DCIS', but in terms of an escalating situation with regards to the seriousness of the lesion, the benchmark indicator will be the crossing-over or invasion of these unusual and irregular cells and their unusual properties, into the 'stroma' or supporting-framework cells of the epithelium (lining ), but without destroying the 'basal membrane' or ('lowest possible level') of the epithelium.
To clarify, the transcendence of the 'hyperplasia' or 'large new group of abnormal cells' will have to go through TWO levels. First, it must cross into the 'stroma' of duct-lining epithelium , without destroying the basal membrane beneath and around it. Secondly, it has to move beyond even this, right into the duct itself, and of course corrupting the basal membrane of the duct-lining epithelium in the process. If and when this happens the situation may now be termed 'infiltrating ductal carcinoma'.
As mentioned above, infiltrating ductal carcinoma, which really implies outright 'breast cancer', means that the corrupted cells are now showing up within the stroma materials of the duct lining, and have destroyed the lowest or 'basal' layer of the lining, and may now or in the very near future attack the cells of the duct itself.
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