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While superficial masses are usually apparent and easily palpated, it is sometimes difficult to determine whether they are cystic, solid, or mixed. Ultrasound was used to evaluate superficial masses determining their size, relationship to other structures and internal characteristics. In a series of 34 patients, ultrasound was able to differentiate among cystic, solid, or complex masses with a 94% accuracy.
Despite interest in the use of nuclear morphometry for cancer diagnosis and prognosis as well as to monitor changes in cancer risk, no generally accepted statistical method has emerged for the analysis of these data. To evaluate different statistical approaches, Feulgen-stained nuclei from a human lung epithelial cell line, BEAS-2B, and a human lung adenocarcinoma (non-small cell) cancer cell line, NCI-H522, were subjected to morphometric analysis using a CAS-200 imaging system. The morphometric characteristics of these two cell lines differed significantly. Therefore, we proceeded to address the question of which statistical approach was most effective in classifying individual cells into the cell lines from which they were derived. The statistical techniques evaluated ranged from simple, traditional, parametric approaches to newer machine learning techniques. The multivariate techniques were compared based on a systematic cross-validation approach using 10 fixed partitions of the data to compute the misclassification rate for each method. For comparisons across cell lines at the level of each morphometric feature, we found little to distinguish nonparametric from parametric approaches. Among the linear models applied, logistic regression had the highest percentage of correct classifications; among the nonlinear and nonparametric methods applied, the Classification and Regression Trees model provided the highest percentage of correct classifications. Classification and Regression Trees has appealing characteristics: there are no assumptions about the distribution of the variables to be used, there is no need to specify which interactions to test, and there is no difficulty in handling complex, high-dimensional data sets containing mixed data types.
Amperometric methods were used to study reaction kinetics of 2, 6-dichlorophenolindophenol (DCPIP) with NADH in the homogeneous phase. The second-order rate constant of the reaction was calculated to be 2.4 M-1 . s-1 at 37 degrees C. The reoxidation of the reduced form of DCPIP in air-saturated phosphate-buffered saline was found to follow pseudo-first-order reaction kinetics with rate constant of 5.9 X 10(-4) s-1. These data were compared to the reduction of DCPIP in suspensions of normal and neoplastic hepatocytes, in the absence and presence of oxygen. The reduction of DCPIP by intracellular NAD(P)H was shown to follow mixed-type reaction kinetics different from those of the homogeneous phase. From this, the conclusion was drawn that complexes of enzymes transferring electrons to and from NAD(P)H are involved in intracellular reduction of DCPIP.
Electron-microscopy of tumours, diagnosed by light optics as ependymoastrocytomas, helped to ascertain the common features in the ultrastructural organization of their tumorous tissue: a complex of organ-specific signs of ependymomas is constantly manifested in all the scrutinized parts of the tumorous nodes. This makes it possible to regard ependymoastrocytomas as a variant of ependymomas and not tumours of a mixed origin.
We report a case of a 14-year-old girl with papillary glioneuronal tumor (PGNT) in right parietal lobe. On MRI the tumor presented as a contrast enhancing mass with small central hypodense area and consisted of areas similar to central neurocytoma intermixed with vessels surrounded with glial cells. There were also small loose areas superficially reminding DNT. Neurocytic component presented strong synaptophysin immunostaining, while intermixed glial element presented GFAP-immunopositivity. Our case is similar to previously reported PGNT, but an important difference lies in not distinct cystic formation and a presence of loose, edematous tissue. PGNT may be regarded as a variant of ganglioglioma or as a complex variant of extraventricular neurocytoma and belongs to a wide group of benign, dysembryoplastic or even hamartomatous neuroepithelial tumors, which may differentiate into both, glial or neuronal direction: pleomorphic astrocytoma may posses neurocytic differentiation, desmoplastic infantile ganglioglioma may be regarded as complex superficial dural astrocytoma and DNT may present gliomatous areas (complex DNT). Also other rare tumors reminding DNT have been reported: DNT-like neoplasm of septum pellucidum and rosetted glioneuronal tumor. From this point of view it is important to remember that such a wide spectrum may be difficult to discriminate into very narrow clinico-pathological entities.
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The oligonucleotide primers synthesized by a highly purified KB fraction containing DNA primase and DNA polymerase-alpha activities display reproducible alterations of structure and composition in response to dNTPs. These observations are sufficiently explained by a novel model of primase catalysis that defines the primase as a complex enzyme with distinct catalytic properties that are regulated by mechanisms exquisitely sensitive to dNTP concentration. The enzyme performs the template-directed, de novo synthesis of 1 unit of oligoribonucleotide (canonical priming reaction) and then elongates that moiety to a limited extent by several cycles of addition of short tracts of homogeneous oligoribonucleotide or oligodeoxynucleotide. The oligomeric units have modal lengths of approximately 11- to 14- nucleotides that are postulated to reflect the inherent processivity of the catalytic mechanisms. Elongation is accomplished by two catalytic centers, or conformers of a single center, that are synchronously coupled, mutually exclusive, and extremely stringent for respective rNTP and dNTP substrates. Transitions between these two catalytic modes are regulated by dNTPs and demonstrable at dNTP:rNTP concentrations of less than or equal to 10(-4). In the absence of dNTPs, the primase produces a family of oligoribonucleotides, approximately 24- to 36- nucleotides long; at dNTP levels between 0.08 and 0.80 micron, the primase synthesizes mixed oligomers composed of strictly alternating tandem arrays of oligoribo- and oligodeoxynucleotide units; and at dNTP levels greater than or equal to 4.8 micron, the primase becomes stabilized in the deoxy mode after the initial oligoribo leads to oligodeoxy transition and products contain only a single 5' -terminal unit of oligoribonucleotide. The model predicts that the physiologically significant primer for DNA polymerase-alpha is a mixed 5' -oligoribo-3' -oligodeoxynucleotide and the signal which governs the switch from RNA leads to DNA synthesis is intrinsic in the primase mechanism and is generated by ambient dNTPs.
Intestinal tissue samples were examined from 32 cats in which a histopathological diagnosis of alimentary lymphoma or multicentric lymphoma affecting the gastrointestinal tract had been made. These samples were re-evaluated histopathologically and serial sections were examined immunohistochemically with antisera specific for the lymphoid markers CD3, CD79a and BLA-36 and for class II molecules of the major histocompatability complex. The cats ranged in age from 4-16 years (median 10.5 years). The main presenting clinical signs were vomiting, diarrhoea and weight loss. The majority of alimentary lymphomas were of the B-cell type (n=15), whereas cases of T-cell lymphoma were fewer in number (n=8). Four cats had lymphoma of a mixed T-and B-cell phenotype. In five of the cats, immunohistochemistry suggested an inflammatory process, in contradiction to the original histopathological diagnosis of lymphoma. Immunolabelling would appear to be a useful adjunct to histopathology in classifying cases of feline alimentary lymphoma, and may help in distinguishing lymphoma from severe intestinal inflammation.
Sera from Fischer rats 3 to 13 days after i.p. injection of syngeneic 13762A mammary adenocarcinoma contain three factors specifically blocking cell-mediated cytotoxicity (CMC). The major blocking factor is a 160,000-dalton IgG that combines specifically to cytolytic lymphocytes but not to tumor cells or tumor antigen, and that is not dissociated after treatment with 8 M urea. The other factors have been putatively identified as tumor antigen (less than 70,000 daltons) and as soluble antigen-antibody complexes (greater than 200,000 daltons). Injecting the tumor antigen into tumor-free rats induced spleen cells specifically cytotoxic to the 13762A tumor and provided partial protection to challenge with live tumor cells. Treating soluble antigen-antibody complexes with 8 M urea decreased the size of the blocking activity from greater than 200,000 to less than 70,000 daltons. Although the IgG fraction dissociated from the complex did not block CMC, it did recombine with the tumor antigen fraction to transfer activity to the greater than 200,000-dalton fraction. In contrast, mixing tumor antigen with the IgG fraction that did block CMC did not alter the size of the blocking activities.
AIMS AND BACKGROUND: Various histogenetic mechanisms have been postulated to explain the biphasic carcinomatous-sarcomatous appearance of malignant mixed mullerian tumors (MMMTs), but the nature of these uncommon neoplasms is still unclear. Some evidence would suggest that MMMT displays similarities with sarcomatoid carcinoma, a tumor arising in extragenital sites that also features a mixed appearance. To gain further insight into the histogenesis of this tumor, we have studied by immunohistochemistry a case of uterine MMMT showing an extensive rhabdomyosarcomatous component. METHODS: A panel of antibodies including reactivity for p53, cytokeratin, vimentin, desmin, muscle actin, epithelial membrane antigen (EMA), myoglobin, type IV collagen, laminin, and tenascin was applied to paraffin tumor sections by means of the avidin-biotin complex technique. RESULTS: p53 immunoreactivity was observed in approximately the same number of cells in carcinomatous and sarcomatous tissue. The former stained for vimentin, cytokeratin and EMA, while the latter, in addition to expressing vimentin, desmin, muscle actin and myoglobin, also exhibited immunoreactivity for epithelial markers such as cytokeratin and EMA. At the borders between carcinoma and sarcoma the basement membrane pattern, as seen by staining for type IV collagen and laminin, showed interruptions in correspondence with areas of transition between the two tissues. Antibody to tenascin strongly labeled the sarcomatous tissue immediately around carcinomatous elements. CONCLUSIONS: A similar immunoreactivity for p53 in both carcinomatous and sarcomatous components, expression of epithelial markers in the sarcomatous cells, and disruption of the basement membrane profile in areas of transition between carcinomatous and sarcomatous tissue, would all suggest, as has been postulated for extragenital sarcomatoid carcinomas, an origin from a common epithelial clone and an epithelial-to-mesenchymal transformation-based mechanism of development for this MMMT. In addition, these findings provide further analogies between these categories of tumors, supporting a unifying nosological concept for MMMTs and sarcomatoid carcinomas of non-genital tract origin.
A 39-year-old woman had mixed IgM/IgG cryoglobulinemia, but was later found to have a lymphoma that produced an IgM kappa paraprotein with rheumatoid factor activity. With intermittent chlorambucil and prednisone therapy, the lymphoma was controlled for five years and she had no evidence of cryoglobulinemia. Because of the presence of intractable pulmonary infection and hypogammaglobulinemia G, she was given an intravenous infusion of gamma globulin. Within 72 hours, renal failure and a sustained decrease in serum concentrations of IgM and IgG began concurrently. A kidney biopsy specimen obtained five days after the infusion showed hyaline "thrombi" in numerous glomerular capillaries and glomerular necrosis, consistent with acute, severe mixed cryoglobulinemic nephropathy. Immunostaining showed strong positivity for IgM, IgG, and light chains in glomerular capillary lumina and subendothelial sites; immunostaining with a monoclonal antiidiotypic antibody specific for the patient's paraprotein established the presence of the rheumatoid factor paraprotein in the deposits. These observations strongly suggest that complexes consisting of IgM kappa rheumatoid factor, IgG, and complement initiated the renal damage. Therefore, demonstrable serum rheumatoid factor activity in patients with B cell neoplasms should be considered a contraindication to the administration of intravenous gamma globulin.
Seventy-three mammary tumors and three mammary tissue specimens were examined to elucidate the expression of bone morphogenetic protein (BMP)-6 in the myoepithelial cells of canine mammary gland tumors. Morphologically, the myoepithelial cells were classified into four types: resting and proliferating cells inside the basement membrane, and spindle- and star-shaped cells proliferating in the outer area of the basement membrane. The characteristics of these myoepithelial cells were confirmed by immunohistochemistry using antibodies raised against keratin, cytokeratin 19, alpha-smooth muscle actin, and vimentin. In simple adenoma, a small number of resting myoepithelial cells was immunopositive for BMP-6. In complex adenomas and benign mixed tumors, all types of myoepithelial cells, depending in some cases on their specific location within the tumor, were immunopositive for BMP-6, but almost all of the tubular epithelial cells were immunonegative. Foci consisting of a proliferation of BMP-6-positive star- and spindle-shaped cells had mucinous stroma with marked hyaline and chondroid changes. In contrast, the foci with BMP-6-negative spindle- and star-shaped cells tended to have mucinous stroma without chondroid change. Several types of mesenchymal cells including chondrocytes, osteoblasts, and fibroblastlike cells in the mixed tumors, showed an intense immunopositive reaction for the BMP-6 antibody, and were located close to the ectopic cartilage and bone matrix. No significant immunoreactivity for BMP-6 was observed in most of the malignant mammary tumors; only one malignant mixed tumor was examined. All of these findings indicate that BMP-6 expression in myoepithelial cells may increase in complex adenomas and benign mixed tumors in canine mammary glands, and that BMP-6 expression is most intense in the vicinity of chondroid matrix in these tumors.
To date, two isoforms of estrogen receptors (ER) have been identified, cloned, and characterized from several species, estrogen receptor-alpha (ERalpha) and estrogen receptor-beta (ERbeta). Although the presence of ERalpha has been demonstrated in normal and tumoral canine mammary tissues, the issue of ERbeta expression has not been addressed in the dog. In this study, we have analyzed the expression of ERbeta in formalin-fixed, paraffin-embedded tissue samples of nonaltered mammary gland, 30 malignant (six complex carcinoma, 12 simple carcinoma, three carcinosarcoma, and nine carcinoma or sarcoma in benign tumor), and five benign (one fibroadenoma, one complex papilloma, one complex adenoma, and two benign mixed tumors) mammary tumors of the dog by using a polyclonal ERbeta antibody and the avidin-biotin-peroxidase complex immunohistochemical technique. Our results show that high numbers of normal ductal and acinar epithelium and approximately one third of canine mammary tumors express ERbeta. This expression was higher in benign than in malignant tumors. Furthermore, expression was higher in complex and mixed histologic subtypes of malignant tumors when compared with simple subtypes.
Cytogenetic analysis of short-term cultures initiated from an ovarian malignant mixed mesodermal tumor yielded the following karyotype: 59-61, XX,t(1;?)(p36;?), +t(1;9) (q43;q21), +t(2;?)(p25;?), +i(5p), +i(5p), +7, +t(7;?)(p13;?), +8,der(11) (pter----cen----q23::q13----q23::q13----q23::?), +12, + der(13)t(13;15)(q21;q15), -15,der(16) (16qter----cen----16p13::hsr::8q21----8qter), +19, + der(20)t(X;20)(q13;p13), -22, +4 - 6mar. Because the only other cytogenetically characterized ovarian neoplasm of this rare histopathologic subtype also had a small metacentric marker interpreted as an isochromosome for the short arm of a B-group chromosome, we suggest that i(5p) constitutes a nonrandom anomaly in mixed mesodermal tumors.
A method is presented for correcting distribution function estimators for distortions in the joint distribution of covariates in the subsamples receiving different treatments. This form of standardization is useful for depicting multivariate analyses and predicting population behavior. Furthermore, it also proves useful for comparing two trials which differ in patient mix and for adjusting estimates for know imbalances in patient characteristics. Standardization though important, is not often used in clinical trials because of the complexities introduced by multiple covariates. The proposed method overcomes these difficulties in a wide class of analyses.
Binding of unlabelled monoclonal antibody preparations has been assessed by competition at saturation with fluorochrome labelled homologous antibody for binding to antigen bearing target cells. The extent of competition was measured by quantitative flow cytofluorimetry, and simple mathematical procedures have been developed to allow the interpretation of competition data in terms of antibody binding activity. In the system studied, non-specific (non-competitive) fluorescence was minimal, but an iterative method to calculate its contribution to the measured signal is given. This approach has the advantage that the antibody preparation to be tested does not need to be labelled or modified; this is particularly important when evaluating the binding activity of therapeutic antibody conjugates. Comparison with a well characterized standard antibody preparation provides a rapid, sensitive and accurate quality control procedure. This test is also simple to perform, requiring only the mixing of labelled and unlabelled antibodies with target cells, a single incubation, followed by analysis without washing of the target cells.
The prevalence of recurrent fetal loss and its relationship to sharing of human leukocyte antigens within couples was examined in a large, ethnically homogeneous Chinese population in Taiwan: 91 couples with primary recurrent spontaneous abortion, 32 couples with secondary recurrent spontaneous abortion, and 51 normal fertile couples. There was an excess of human leukocyte antigen sharing in both types of recurrent aborters. The primary aborters shared human leukocyte A and DQ antigens and three or more of the human leukocyte A, B, DR, and DQ antigens. The secondary aborters did not have an excess of sharing at any one locus but they did share three or more of the human leukocyte A, B, DR, and DQ antigens. There was no excess of antipaternal cytotoxic antibodies in any group of aborters, and the primary aborters had a lower level of mixed lymphocyte reaction blocking factor than normal couples or secondary aborters. Previous studies showed that couples in whom a gestational trophoblastic tumor developed in the woman shared human leukocyte B and DQ antigens and three or more of the human leukocyte A, B, DR, and DQ antigens. These studies provide substantial support for the role of recessive genes linked to the major histocompatibility complex in the pathogenesis of recurrent spontaneous abortions and of gestational trophoblastic tumors.