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R Lagacé

Publications and source records attributed to R Lagacé.

At least 19 recordsLinked to original sources
PubMed2001

Fine-needle sampling of primary neuroendocrine carcinomas of salivary glands: cytohistological correlations and clinical analysis.

Fine-needle samplings of nine examples of primary neuroendocrine carcinoma of salivary glands were evaluated for their cytologic characteristics and were correlated with the corresponding histological sections. Consistent cytological findings were dispersed or loose clusters of poorly differentiated small- to intermediate-sized cells and occasional smudged nuclei. Mild to moderate nuclear pleomorphism, scant or absent cytoplasm, and nuclear molding were also observed. Rosette-like patterns and multinucleated cells were occasionally seen. Immunostaining of one recent case showed positivity for chromogranin and keratin. The differential diagnosis of primary and metastatic tumors with neuroendocrine features of the salivary glands is discussed.

Adult↗
PubMed2001

Consistent DNA losses on the short arm of chromosome 1 in a series of malignant gastrointestinal stromal tumors.

Fourteen malignant gastrointestinal stromal tumors (GISTs), characterized by immunohistochemistry, were analyzed by comparative genomic hybridization (CGH). The most striking feature was the detection of consistent DNA losses on the short arm of chromosome 1 in these 14 malignant tumors. Additional recurrent imbalances were also found: significant gains, which could be indicative of tumor progression, were frequent on the long arm of chromosome 1, as were losses of DNA copy number detected in chromosomes 13, 14, 15 and 22.

Adult↗
PubMed2001

Leiomyosarcomas and most malignant fibrous histiocytomas share very similar comparative genomic hybridization imbalances: an analysis of a series of 27 leiomyosarcomas.

Twenty-seven tumor samples with a diagnosis of leiomyosarcomas (LMS) were characterized by comparative genomic hybridization. The results were compared with immunohistochemical analysis of the smooth muscle profile of the tumors and expression of the RB1 gene protein. The comparative genomic hybridization profiles suggested that 7 of the 27 tumors might have been misclassified. High levels of DNA amplification were detected in 20 different small regions and recurrently involved bands 1p34, q21, 12q13-15, 17p, and 22q. Most recurrent simple gains were noted at sites such as 1p3, 1q21, 15q12-15, 16p, 17p and 17q, 19, 20q, 22q, and Xp. Significant losses of chromosome 13 were detected in 19 of the 27 tumors with a putative common region of loss in bands 13q14-21. Losses of chromosomes 1q, 2p and 2q, 4q, 9p, 10p and 10q, 11p and 11q23, and 16q were also highly recurrent. A comparative analysis between the most frequent genomic imbalances observed in this study of LMS and the genomic imbalances observed in a large proportion of malignant fibrous histiocytomas (MFH) from a previous study demonstrated that both types of tumors had similar recurrent imbalances. Although MFH were once thought to be a separate member of the soft tissue sarcoma family, our observations support the hypothesis that MFH are a morphologic modulation in the tumoral progression of other sarcomas, particularly LMS.

Adult↗
PubMed1996

Pleomorphic soft tissue myogenic sarcomas of adulthood. A reappraisal in the mid-1990s.

325 diverse sarcomas, 39 rhabdomyosarcomas (RMS), including all histologic variants, and 135 leiomyosarcomas (LMS) were identified. Within these two groups, 18 (46%) of the RMS and 14 (10%) of the LMS represented pleomorphic variants. These neoplasms were studied by morphology (histology and ultrastructure) and by immunohistochemical methods employing antibodies to intermediate filaments (vimentin and desmin) and actin isoforms [alpha-smooth (sm) and alpha-sarcomeric (sr) actins]. Twenty-four pleomorphic malignant fibrous histiocytomas (MFH) and eight pleomorphic liposarcomas (LS) were examined in a similar fashion. By light microscopy, the pleomorphic RMS, LMS, and MFH were indistinguishable, as each was dominated by pleomorphic cells disposed in a haphazard growth pattern; moreover, many featured fascicular, storiform, and sclerotic zones. The distinction between these neoplasms became apparent only following immunohistochemistry and/or ultrastructural study. All pleomorphic RMS disclosed rudimentary sarcomeres and exhibited the following cytoskeletal profile: vimentin (+) (18 of 18), desmin (+) (14 of 18), alpha-sr actin (+) (18 of 18) and alpha-sm actin (+) (five of 18). All the pleomorphic LMS featured smooth-muscle differentiation of variable degrees in the form of cytoplasmic bundles of microfilaments and associated dense bodies; their cytoskeletal profile was vimentin (+) (14 of 14), desmin (+) (seven of 14), alpha-sr actin (+) (none of 14), and alpha-sm actin (+) (eight of 14). The latter was demonstrated in all moderately differentiated, but absent or only focally expressed in poorly differentiated variants. All pleomorphic MFH and LS were devoid of myogenic (skeletal or smooth) ultrastructural features and expressed vimentin solely. This combined morphological and immunohistochemical study illustrates the following: First, these pleomorphic sarcomas are often indistinguishable by histologic growth pattern alone; thus, an accurate diagnosis requires study with all of these techniques. Second, pleomorphic myogenic sarcomas are restricted to adults and are not uncommon neoplasms among pleomorphic sarcomas: RMS (28%), LMS (21%), MFH (38%), and LS (13%). Third, the study defines desmin-negative and alpha-sm actin-positive pleomorphic RMS, and desmin-negative and alpha-sm-actin-negative pleomorphic LMS.

Actins↗
PubMed1994

Isolation of yeast artificial chromosome clones from 54 polymorphic loci mapped with high odds on human chromosome 4.

We constructed a yeast artificial chromosome (YAC) framework map of human chromosome 4 by screening a YAC library with 63 polymorphic DNA markers located on the chromosome. These genetic markers are from two framework meiotic maps that had previously been constructed by two research groups, and are placed on the two maps with odds for their order of 1000:1 or greater. In addition to isolating and determining the sizes of 141 YAC clones for 54 of these markers, we combined the two framework meiotic maps to produce a single integrated map. These combined maps and the YAC clones provide a set of extended DNA loci ordered at high odds that can be used to isolate additional polymorphic loci and genes, and to serve as a framework for obtaining a higher resolution physical map of the chromosome.

Chromosome Mapping↗
PubMed1992

Prognostic influence of HSP-27 expression in malignant fibrous histiocytoma: a clinicopathological and immunohistochemical study.

Malignant fibrous histiocytoma is a very aggressive sarcoma. After the tumor has disseminated, chemotherapy is of little influence on the course of the disease because of the resistance to most chemotherapy regimens. We evaluated by immunohistochemistry the prognostic influence of the expression of a member of the stress polypeptides family, the heat-shock protein of 27 KDa (HSP-27). HSP-27 was found to be associated with an aggressive behavior in breast carcinoma and was related to chemoresistance in cell cultures. Forty-three malignant fibrous histiocytomas with no evidence of metastases at the time of diagnosis and resected between 1974 and 1985 were retrieved from the files of the Pathology Department of L'Hôtel-Dieu de Québec hospital. The immunostaining was performed on Bouin-fixed, paraffin-embedded tissue. Regardless of the percentage of positive cells, HSP-27 was expressed in the cytoplasm of 25 (58.1%) cases. HSP-27 expression was associated with a more favorable prognosis, and a significant correlation was observed with overall survival (P less than 0.025) and metastasis-free survival (P less than 0.05). HSP-27 expression was found to be the strongest prognostic factor, and multivariate analysis revealed that it was independent of tumor size, necrosis, and histological subtype. However, in the 13 patients with recurrent disease who underwent chemotherapy, the antigenic expression did not help to predict the treatment response. HSP-27 expression is one of the rare prognostic markers in this tumor type.

Adolescent↗
PubMed1990

Intermediate filament proteins and actin isoforms as markers for soft-tissue tumor differentiation and origin. III. Hemangiopericytomas and glomus tumors.

Intermediate filament proteins and actin isoforms of a series of 12 malignant hemangiopericytomas and five glomus tumors were examined by light microscopy, transmission electron microscopy, two-dimensional gel electrophoresis (2D-GE), and by immunohistochemistry, the latter using monoclonal or affinity-purified polyclonal antibodies to desmin, vimentin, cytokeratins, alpha-smooth muscle, and alpha-sarcomeric actins. By light microscopy, all hemangiopericytomas disclosed a predominant vascular pattern with scant storiform, myxoid and spindle cell areas, and with variable degrees of perivascular fibrosis. By ultrastructure, smooth muscle differentiation was observed in each hemangiopericytoma. Immunohistochemically, neoplastic cells of hemangiopericytomas expressed vimentin as the sole intermediate filament protein and lacked alpha-smooth muscle or alpha-sarcomeric actins. 2D-GE revealed only beta and gamma actins, in proportions typical for fibroblastic tissues. Glomus tumors revealed vimentin and alpha-smooth muscle actin within glomus cells by immunohistochemical techniques and disclosed ultrastructurally distinct smooth muscle differentiation. Therefore hemangiopericytomas represent a distinct soft-tissue neoplasm with uniform morphologic, immunohistochemical, and biochemical features most likely related to glomus tumors, the former representing an aggressive and potentially malignant neoplasm of vascular smooth muscle cells and the latter a well-differentiated neoplasm of vascular smooth muscle cells. Because malignant hemangiopericytomas disclose smooth muscle differentiation by ultrastructure, but do not express alpha-smooth muscle actin, as normal pericytes and glomus cells, it is suggested that these neoplasms represent highly vascularized smooth muscle neoplasms, ie, poorly differentiated leiomyosarcomas derived from vascular smooth muscle cells or their equivalent, the pericytes, which have lost alpha-smooth muscle actin as a differentiation marker that is similar to many conventional poorly differentiated leiomyosarcomas.

Actins↗
PubMed1989

Myofibroblasts from diverse pathologic settings are heterogeneous in their content of actin isoforms and intermediate filament proteins.

We examined by immunofluorescence the distribution of vimentin, desmin, alpha-smooth muscle actin and alpha-sarcomeric actin in normal human soft tissues and in pathologic tissues containing myofibroblasts, including normally healing granulation tissue, hypertrophic scar, and fibromatosis. The pattern of actin isoforms was also documented biochemically by two-dimensional gel electrophoresis. Fibroblastic and/or myofibroblastic cells in each setting always expressed vimentin and never alpha-sarcomeric actin. Moreover, these cells showed an heterogeneous cytoskeletal composition which defined four phenotypes: (a) cells expressing only vimentin; (b) cells expressing vimentin, alpha-smooth muscle actin and desmin; (c) cells expressing vimentin and alpha-smooth muscle actin; and (d) cells expressing vimentin and desmin. Given this, two groups of lesions are distinguished: the first contains only vimentin cells and consists of normally healing granulation tissue, eschars and normally healed scars; the second contains vimentin cells admixed with variable proportions of vimentin, alpha-smooth muscle actin and desmin, vimentin and alpha-smooth muscle actin, and vimentin and desmin cells and consists of hypertrophic scars and fibromatoses. Immunogold electron microscopy showed that alpha-smooth muscle actin was present in a proportion of cells with ultrastructural features of myofibroblasts. Our findings suggest that contrary to myofibroblasts of normally healing granulation tissue and normally healed scars, myofibroblasts of pathologic conditions characterized by chronic retraction express always immunochemical features indicative of smooth muscle differentiation.

Actins↗
PubMed1988

Adult celiac sprue: changes in the pattern of clinical recognition.

We report the clinical, laboratory, and pathological findings in a series of 52 consecutive patients with adult celiac sprue observed over a 20-year period. The frequency of that diagnosis increased from an average of 0.7 case/year during the period 1966-1975 to 5.8 cases/year during the period 1981-1985. Apart from two patients with dermatitis herpetiformis, nonclassical clinical presentations were observed in 16 of 50 (32%) patients overall and in 13 of 28 (46%) patients diagnosed since 1981. Diarrhea was the most common complaint leading to the diagnosis; since 1981, hematologic abnormalities warranted investigation in 38% of the patients. Decreased iron stores (88%), decreased red cell folate (82%), or both (74%), and abnormal radiographic studies of the small bowel (83%) were the most sensitive tests in the diagnostic investigation. We conclude that atypical or nonclassical presentations of adult celiac sprue, mostly with hematologic abnormalities, are not uncommon.

Abdomen↗
PubMed1985

Myofibroblastic stromal reaction in carcinoma of the breast: variations of collagenous matrix and structural glycoproteins.

The matrix of mammary dysplasia, noninvasive ductal carcinoma, and invasive lobular and ductal carcinoma was analyzed by indirect immunofluorescence using antibodies to types I, proIII, III, and IV collagens, and laminin and fibronectin. Types proIII and III collagens were present in increased amounts in invasive carcinomas and were most abundant in the "young" edematous mesenchyme, areas corresponding to the peripheral invasive cellular front. Type I collagen was distributed throughout the matrix of invasive carcinomas but was most prominent within the central sclerotic zone of the neoplasms. Mammary dysplasia and noninvasive ductal carcinomas showed a uniform fibrillar and granular distribution of all types of collagen. In all but two cases of invasive carcinoma, staining with anti-laminin and anti-type IV collagen demonstrated the loss of basement membranes around tumor cells. In contrast, fluorescence pattern in noninvasive ductal carcinoma and dysplasia revealed an intact basement membrane. The distribution of fibronectin was similar to types proIII and III collagen. These findings support and extend our previous studies which suggested an analogy between the dynamics of matrix changes in granulation tissue and invasive carcinomas. These data also strengthen the concept that the myofibroblast could be a pivotal cell involved in the synthesis and redistribution of matricial proteins. The loss of basement membrane in invasive carcinomas appears to be an initial step for inducing the matricial alterations.

Basement Membrane↗
PubMed1984

The intermediate filament cytoskeleton of myofibroblasts: an immunofluorescence and ultrastructural study.

The intermediate filament cytoskeleton of stromal myofibroblasts from a series of twenty-eight infiltrating ductal breast carcinomas was examined by transmission electron microscopy (TEM) and indirect immunofluorescence (IF), the latter using antibodies to desmin, vimentin and prekeratin. Three cases of fibromatoses, selected as an additional source of myofibroblasts, were processed in the same manner. Stromal myofibroblasts from invasive ductal breast carcinomas rich in actin and readily identified by IF, were most numerous in the "young" edematous mesenchyme, areas corresponding to early stromal invasion or the peripheral invasive cellular front. Within the central sclerotic zone wherein clusters of neoplastic epithelial cells were surrounded by abundant collagen, most stromal cells corresponded by TEM to fibroblasts. In like fashion, myofibroblasts were most numerous in cellular, poorly collagenized portions of fibromatoses. By IF the only detectable intermediate filament protein of myofibroblasts in these two settings was vimentin. Since the appearance of stromal myofibroblasts appears to be associated with stromal invasion by malignant epithelium, their development by modulation of pre-existent periductal fibroblasts is postulated. With the exception of vascular smooth muscle cells and endothelial cells, the only periductal mesenchymal cells shown to contain vimentin were fibroblasts. The lack of desmin in myofibroblasts constitutes evidence against an origin from vascular smooth muscle cells. Because the molecular markers (intermediate filament proteins) of stromal cell differentiation presented quantitative but not qualitative modifications, the transformation of fibroblasts into myofibroblasts is quite likely, suggesting that myofibroblasts may be more closely related to fibroblasts than to smooth muscle cells.

Breast↗