College of American Pathologists
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  Anatomic Abstracts





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February 2002

  • Superficial cervicovaginal myofibroblastoma
  • P57KIP2 immunohistochemistry as an adjunct in diagnosing hydatidiform mole
  • Value of tissue microarray technology

    Superficial cervicovaginal myofibroblastoma
    Differentiating between the various mesenchymal proliferations in the vulvovaginal area can be difficult and is based primarily on identifying key clinical and morphologic features and immunoreactivity profiles. A review of 310 mesenchymal lesions of the vaginal area and uterine cervix from the files of the Armed Forces Institute of Pathology identified 11 cases (along with three retrieved from files at other institutions) with similar histomorphologic features that were unique and differed from mesodermal stromal polyp, angiomyofibroblastoma, aggressive angiomyxoma, and other neoplasms in this region. Salient microscopic features of this new entity include spindle and stellate mesenchymal cells of moderate to high cellularity with variegated growth patterns embedded in a finely collagenous stroma and separated from the mucosa by a layer of native stroma. These tumors are further characterized by myxoid and edematous foci, moderately increased vascularity, reactivity for vimentin, estrogen and progesterone receptors, and desmin, reactivity for CD34 in most, alpha-smooth-muscle actin and muscle-specific actin in some, and no immunoreactivity for S100 protein, epithelial membrane antigen, or keratins. Median age at incidence was 58 years (40 to 74 years), and none of the tumors recurred or metastasized following local excision (followup, one to 20 years).

    Laskin WB, Fetsch JF, Tavassoli FA. Superficial cervicovaginal myofibroblastoma: fourteen cases of distinctive mesenchymal tumor arising from the specialized subepithelial stroma of the lower female genital tract. Hum Pathol. 2001;32:715-725.

    Reprints: Dr. William B. Laskin, Dept. of Pathology, Northwestern Memorial Hospital, Feinberg Pavilion 7-325, 251 E. Huron St., Chicago, IL 60611-2908

    P57KIP2 immunohistochemistry as an adjunct in diagnosing hydatidiform mole
    It is difficult to distinguish complete hydatidiform mole (CHM) from partial hydatidiform mole (PHM) and hydropic spontaneous abortion (SA), particularly in early gestation. The distinction, however, is important due to the higher risk of persistent disease and choriocarcinoma associated with CHM as compared to PHM. The authors examined p57KIP2, a strongly paternally imprinted gene that is expressed predominantly from the maternal allele in most tissues. Using immunohistochemistry, they examined the expression of p57KIP2 in CMHs, which are derived exclusively from paternal DNA; PHMs, which contain one maternally derived and two paternally derived haploid genomes; SA; and mature and immature placentas. Gestational age of the CHMs ranged from five to 22 weeks and was less than 10 weeks in more than half the cases. In 58 of 59 CHMs, expression of p57KIP2 in cytotrophoblast and villous mesenchyme was absent or markedly decreased (focal cytotrophoblast positivity). In contrast, expression of p57KIP2 was strong in these tissues in normal placenta, PHM (39 of 39), and SA (51 of 51).

    Castrillon DH, Sun D, Weremowicz S, et al. Discrimination of complete hydatidiform mole from its mimics by immunohistochemistry of the paternally imprinted gene product p57KIP2. Am J Surg Pathol. 2001;25:1225-1230.

    Reprints: Dr. Diego H. Castrillon, Dept. of Pathology, Brigham and Women’s Hospital, 75 Francis St., Boston, MA 02115;

    Value of tissue microarray technology
    Tissue microarray technology promises to greatly expand the utility of paraffin blocks for research, but its limitations are still being addressed. Advances in genomics and proteomics are dramatically increasing the need to evaluate large numbers of molecular targets for their diagnostic, predictive, or prognostic value in clinical oncology. Conventional molecular pathology techniques are often tedious, time-consuming, and require a substantial amount of tissue, thereby limiting the number of tissues and targets that can be evaluated. The authors demonstrated the power of tissue microarray technology in analyzing prognostic markers in 553 breast carcinomas. Four independent TMAs were constructed by acquiring 0.6-mm biopsies from formalin-fixed, paraffin-embedded tumors. Immunostaining of TMA sections and conventional large sections were performed for estrogen receptor and progesterone receptor, as well as for p53, another protein for which the data on prognostic utility in breast cancer are less unequivocal. Compared with conventional large- section analysis, a single sample from each tumor identified about 95 percent of the information for estrogen receptors, 75 to 81 percent for progesterone receptors, and 70 to 74 percent for p53. All 12 TMA analyses (three antibodies on four different arrays), however, yielded as significant or more significant associations with tumor-specific survival than large-section analyses (P<0.0015 for each of the 12 comparisons). A single sample from each tumor could identify associations between molecular alterations and clinical outcome. The authors concluded that, contrary to expectations, tissue heterogeneity did not negatively influence the predictive power of TMA results. TMA technology will be of substantial value in rapidly translating genomic and proteomic information to clinical applications.

    Torhorst J, Bucher C, Kononen J, et al. Tissue microarrays for rapid linking of molecular changes to clinical endpoints. Am J Pathol. 2001;159:2249-2256.

    Reprints: Guido Sauter, Institute of Pathology, University Hospital, Schonbeinstrasse 40, 4003 Basel, Switzerland; guido.sauter@unibas.chn