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A A Howeedy

Publications and source records attributed to A A Howeedy.

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Distribution of tenascin, cellular fibronectins and integrins in the normal, hyperplastic and neoplastic breast.

We present immunolocalization data on tenascin (Ten), and extradomains A and B (EDA-, EDB-) and oncofetal (Onc-) isoforms of cellular fibronectin (cFn), and alpha 1-6 and alpha v and beta 1-4 integrin subunits on cryosections of normal human breast, the spectrum of fibrocystic disease (FCD), and benign and malignant breast neoplasms. Fetal breast ducts were surrounded by broad Ten bands; adult breast ducts and acini were encompassed by thin continuous rims. In FCD, Ten was detectable and was clearly enhanced around hyperplastic ducts. Fibroadenomas showed uneven Ten periductal reactions while in all carcinomas, the stroma showed extensive and strong reactions that were most intense at the tumors' invasive edge. EDA-cFn's distribution was similar to Ten's but the staining was stronger while EDB- and Onc-cFn were virtually restricted to fetal breasts and carcinomas. In the normal adult breast, alpha 1,2,3 and alpha 6, and B1 and beta 4 integrins were detected in myoepithelial cells; weaker staining was also noted in the basolateral aspect of luminal cells; this profile was retained--and at times enhanced--in FCD, fibroadenomas and in situ carcinomas in which myoepithelial elements were present. In carcinomas, particularly in those of high grade, integrins tended to be reduced. However, mucinous carcinomas showed enhanced expression and the emergence of alpha 5 integrin that was not in the normal repertory; also a subset of infiltrating lobular carcinomas showed prominent alpha 1 and alpha 6 and beta 1 and--rarely--beta 4 staining distributed in delicate cytoplasmic processes (kinetopodia). These data indicate that the complex cell-matrix and cell-cell interactions of the normal breast are slightly altered in hyperplastic processes and benign neoplasms whereas profound chances occur in carcinomas. The latter display enhanced Ten and EDA- and Onc-cFn expression in particular, while most integrins appear decreased. Notably, mucinous and some lobular carcinomas display enhancement of certain integrins. The conspicuous localization of integrins in kinetopodia may be significant in relation to the invasive behavior of lobular carcinomas.

Breast↗

Giant benign mesenchymoma of the breast.

The term mesenchymoma refers to a group of mixed tumors that are composed of two or more mesenchymal elements, excluding fibrous tissue, not ordinarily found together within the same tumor. Mesenchymomas occur most commonly in the renal and perirenal regions with rare occurrence in the breast. We describe what to our knowledge is the first report of a giant benign mesenchymoma of the breast. The clinical presentation, course, and treatment of a patient with this condition is discussed. Clinicians should be aware that benign mesenchymomas may involve the breast and simulate a malignant breast neoplasm.

Aged↗

Differential distribution of tenascin in the normal, hyperplastic, and neoplastic breast.

We studied by immunohistochemistry the distribution of tenascin with the monoclonal antibody 100EB2, and compared it with that of laminin in breast tissue samples from fetal, adult resting, lactating, and aging parenchyma, variants of fibrocystic disease, fibroadenomas, cystosarcoma phylloides, and ductal and lobular carcinomas. Monoclonal antibodies were applied to cryosections by the avidin-biotin-complex method; selected samples were studied by double immunofluorescence, and by Western blot analysis. In adult resting and aging breasts, tenascin immunoreactivity was noted in the periductal and periacinar stromal regions as thin irregular bands; in the lactating breast, broader periductal bands were observed. In these samples, laminin immunoreactivity was a single continuous line around ducts, acini, and vessels. In fetal breasts, tenascin appeared as thick periductal bands, whereas laminin remained as a delicate single line. In FCD, tenascin increased around ducts showing hyperplasia, papillomas and apocrine metaplasia, whereas laminin retained its delicate linear pattern. Similar patterns were seen in fibroadenomas and cystosarcoma phylloides with variable tenascin reactivity in the stroma beyond the ducts. Tenascin immunoreactivity was markedly increased around ducts containing in situ carcinoma appearing as broad bands, whereas that of laminin showed a linear, frequently discontinuous appearance. Prominent stromal tenascin immunoreactivity was seen in infiltrating ductal and lobular carcinomas, whereas laminin was virtually absent save for scattered lines. The abundance of tenascin in the carcinomatous stroma contrasted with its scarcity in the non-neoplastic stromal regions. By Western blotting, both chains of tenascin with molecular weights 250,000 and 180,000 were shown in ductal and lobular carcinomas as well as in normal breast. Tenascin immunoreactivity was noted in the periepithelial stromal regions of adult resting and aging breast ducts and acini. The amount of tenascin was moderately enhanced in certain physiologic conditions (fetal growth, gestation), as well as hyperplasias, dysplasias (fibrocystic disease) and benign tumors, whereas it was markedly enhanced in intraductal and infiltrating carcinomas. During fetal mammary development, adult physiologic and pathologic hyperplasias, and in carcinomas, the increasing tenascin reactivity contrasted with the stable or decreasing laminin reactivity.

Adult↗