Histology grade changes Risk for ADH and DCIS

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 evolves 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%.

I have created a newer version of this page that is a little bit more ‘up-to-date’, however this page still has some great information.

Ductal Hyperplasia- lowest risk

Ductal hyperplasia without atypia, (or DH) implies 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.

Background on breast hyperplasia

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‘ occurring 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 – increased risk

Atypical Ductal Hyperplasia demonstrates basically the same kinds of cellular actives 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.

DCIS – high risk

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‘.

Infiltrating Ductal Carminoma – imminent risk

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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Here are a couple Q&A…

• What is DCIS grade 3 , and what does it mean? In this high-grade pattern, these DCIS tend to grow more quickly and look much different from normal, healthy breast cells. People with grade 3 have a higher risk of invasive cancer, either when the DCIS is diagnosed or at some point in the future. They also have an increased risk of the cancer coming back earlier, within the first 5 years. This is also called “comedo”.
• What is DCIS grade 2? (moderate grade) These tend to grow slowly and are sometimes described as non-comedo DCIS. People with DCIS grade 2 are less likely to have the cancer return or have a new cancer develop.

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References

1. Tavassoli F.A, Pathology of the Breast, p 254-397, 1999
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3. Kohr JR, Eby PR, Allison KH, DeMartini WB, Gutierrez RL, Peacock S, Lehman CD. Risk of upgrade of atypical ductal hyperplasia after stereotactic breast biopsy: effects of number of foci and complete removal of calcifications. Radiology. (Jun 2010) 255(3):723-30. Epub 2010 Feb 19.
4. Jackman RJ, Birdwell RL, Ikeda DM. Atypical ductal hyperplasia: can some lesions be defined as probably benign after stereotactic 11-gauge vacuum-assisted biopsy, eliminating the recommendation for surgical excision? Radiology. (Aug. 2002) 224(2):548-54.
5. Wagoner MJ, Laronga C, Acs G. Extent and histologic pattern of atypical ductal hyperplasia present on core needle biopsy specimens of the breast can predict ductal carcinoma in situ in subsequent excision. Am J Clin Pathol.(Jan 2009) 131(1):112-21.
6. Boecker, W., Buerger, H., Usual and atypical ductal hyperplasia—members of the same family? Current Diagnostic Pathology (June 2004) Volume 10, Issue 3, Pages 175-182.
7. Shaaban AM, Sloane JP, West CR, Foster CS. Breast cancer risk in usual ductal hyperplasia is defined by estrogen receptor-alpha and Ki-67 expression. Am J Pathol.(Feb 2002 ) 160(2):597-604.
8. Kerlikowske K. Epidemiology of ductal carcinoma in situ. J Natl Cancer Inst Monogr.( 2010) (41):139-41.
9. Winchester DP, Strom EA. Standards for diagnosis and management of ductal carcinoma in situ (DCIS) of the breast. American College of Radiology. American College of Surgeons. College of American Pathologists. Society of Surgical Oncology. CA Cancer J Clin. (Mar-Apr. 1998) 48(2):108-28.
10. Morrow, M. The Certainties and the Uncertainties of Ductal Carcinoma In Situ J Natl Cancer Inst, (March 17, 2004) 96(6): 424 – 425.
11. Rakovitch E, Franssen E, Kim J, Ackerman I, Pignol JP, Pazat L, et al. A comparison of risk perception and psychological morbidity in women with ductal carcinoma in situ and early invasive breast cancer. Breast Cancer Res Treat (2003); 77: 285–93.
12. Hoorntje LE, Schipper ME, Peeters PH, Bellot F, Storm RK, Borel Rinkes IH. The finding of invasive cancer after a preoperative diagnosis of ductal carcinoma-in-situ: causes of ductal carcinoma-in-situ underestimates with stereotactic 14-gauge needle biopsy. Ann Surg Oncol (2003); 10: 748–53.
13. King TA, Farr GH Jr, Cederbom GJ, et al. A mass on breast imaging predicts coexisting invasive carcinoma in patients with a core biopsy diagnosis of ductal carcinoma in situ. Am Surg (2001); 67: 907–12.
14. Dinkel HP, Gassel AM, Tschammler A. Is the appearance of microcalcifications on mammography useful in predicting histological grade of malignancy in ductal cancer in situ? Br J Radiol (2000); 73: 938–44.
15. Darling ML, Smith DN, Lester SC, et al. Atypical ductal hyperplasia and ductal carcinoma in situ as revealed by large-core needle breast biopsy: results of surgical excision. AJR Am J Roentgenol (2000); 175: 1341–6.

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