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Biomedical subjects

L J Rubinstein

Publications and source records attributed to L J Rubinstein.

At least 73 records · Page 4Linked to original sources
PubMed1985

Immunohistochemical recognition of human nerve sheath tumors by anti-Leu 7 (HNK-1) monoclonal antibody.

Using relatively high dilutions of anti-Leu 7 monoclonal antibody and a four-step peroxidase-antiperoxidase (PAP) reaction in paraffin-embedded tissues, we tested the affinity of this antibody to the cells of 47 human nerve sheath tumors and 22 other tumors in which the differential diagnosis with nerve sheath neoplasms is known to arise. Of all the nerve sheath tumors studied 68%, including 80% of the schwannomas, contained anti-Leu 7-positive cells. All 22 non-schwannian neoplasms were entirely negative. Specimens of eight experimental malignant rat schwannomas were also negative for anti-Leu 7 antibody. Our findings suggest that anti-Leu 7 monoclonal antibody is a promising marker that may facilitate the differential diagnosis between human Schwann cell and non-Schwann cell neoplasms.

Amputation Stumps↗
PubMed1985

The time development of direct hemolytic plaques: implications for the binding of IgM to cell surface haptens.

We studied the time development of direct hemolytic plaques in thin layers containing either sheep red blood cells (SRBC) directly haptenated (DH) with trinitrophenyl, or SRBC indirectly haptenated (IH) with dinitrophenyl coupled to human serum albumin. The DH-SRBC tend to be sparsely haptenated while the IH-SRBC tend to have very high local hapten densities. We observed marked differences in the growth of plaques for the two differently haptenated SRBC. Plots of the plaque radius squared vs time show that the slope of those curves that developed in a lawn of DH-SRBC tended to be constant while the slope of those curves that developed in a lawn of IH-SRBC tended to decrease with time. These results are what is predicted from theory if: IgM binds to DH-SRBC through attachments that rapidly dissociate, if IgM binds to IH-SRBC through attachments that very slowly dissociate, and if (3) both types of bound IgM can fix and activate complement.

Animals↗
PubMed1985

Embryonal central neuroepithelial tumors and their differentiating potential. A cytogenetic view of a complex neuro-oncological problem.

The embryonal central nervous system (CNS) neoplasms are reviewed with special reference to their differentiating potential and in the light of current neuro-oncogenetic concepts partly derived from the experimental induction of neural tumors. The conceptual (and, occasionally, practical) distinction between adult-type and embryonal CNS tumors raises a complex problem, because neoplastic transformation essentially involves replicating stem cells in tissues of renewal and because in the human brain such cells are found mostly in the course of CNS development. A cytogenetic scheme is therefore needed to serve as a frame of reference for a classification of embryonal CNS tumors that will account for the different histological entities documented so far and for the range and the restrictions of their differentiating capabilities. Most embryonal CNS tumors can be fitted into such a scheme. The cerebral medulloepithelioma, the cerebral and cerebellar neuroblastomas, the primitive polar spongioblastoma, and the ependymoblastoma show characteristic morphological features and a correspondingly distinctive cellular differentiating potential. The differentiating capabilities of the cerebellar medulloblastoma, the pineoblastoma, and the retinoblastoma are also distinctive, and are apparently determined by the cytogenesis of the area of the CNS in which the tumors originate. The indiscriminate application of a simplistic concept that would include all the so-called "primitive neuroectodermal tumors" into a single neuroepithelial tumor entity is unlikely to bring further understanding to the problem.

Age Factors↗
PubMed1984

The association of embryonal tumors originating in the kidney and in the brain. A report of seven cases.

This report documents, in seven infants younger than 2 years of age, a previously unrecognized association of a renal embryonal neoplasm (malignant rhabdoid tumor in six patients and a Wilms' tumor in one) with an embryonal primary tumor originating in the central nervous system. The neuroepithelial tumors included three cerebellar medulloblastomas, one pineoblastoma, one primitive neuroepithelial tumor (probably cerebral neuroblastoma), one malignant subependymal giant cell astrocytoma, and one cerebellar medulloepithelioma with divergent glial and neuronal differentiation. There is no evidence that this association is based on the selective neoplastic transformation of embryonal cells of similar histogenetic or cytogenetic origin. The relationship between these dissimilar, embryologically unrelated tumors remains enigmatic.

Astrocytoma↗
PubMed1984

The biological behavior of primary cerebral neuroblastoma: a reappraisal of the clinical course in a series of 70 cases.

The outcome in 70 patients with primary cerebral neuroblastoma was evaluated in light of their age incidence, histological subtypes, and modes of treatment. In more than 80% of the patients, primary cerebral neuroblastoma occurred in the first decade, most often before the age of 2 years (26%). Over half of the tumors were histologically of the classic variant, the remainder showing varying degrees of mesenchymal stromal response (desmoplastic or transitional variants). Patients with a tumor of the desmoplastic or transitional variant without ganglionic differentiation had a lower mean age at the time of diagnosis than those harboring a tumor of the classic variant. Age could not be correlated with the presence of ganglionic differentiation. The overall 3-year survival rate was 60%. At least 30% of patients have a 5-year postoperative survival. Eight patients survived 7 years after diagnosis, and 3 for more than 10 years. The period of risk for tumor recurrence or death was a function of the initial age at diagnosis (Collins's law). Most deaths or fatal recurrences occurred within the first 3 years after operation. No correlation could be made between survival times and histological variant of the tumor or the presence of ganglionic differentiation. Our data do not indicate that, overall, postoperative irradiation with or without chemotherapy improved length of survival, but an occasional favorable clinical response to chemotherapy did occur. Because of the high incidence of local recurrence and the relative frequency of cerebrospinal metastasis, prophylactic whole brain and spinal irradiation is probably justified.

Adolescent↗
PubMed1984

Divergent glial and neuronal differentiation in a cerebellar medulloblastoma in an organ culture system: in vitro occurrence of synaptic ribbons.

A cerebellar medulloblastoma from a 2-year-old boy was maintained in vitro in an organ culture system for 6.5 months, and the explants studied by light and electron microscopy at different time intervals. The tumor cells progressively demonstrated divergent differentiation into astrocytes and neuroblasts. Astrocytic differentiation, confirmed by immunohistochemistry for GFA protein, became maximal after about 7 weeks in vitro and was thereafter maintained in different areas of the explants. Concomitantly, neuroblastic differentiation was expressed in other cells, with the progressive development of cell processes filled with many microtubules, of neuroblastic rosettes, of increased numbers of dense-core and clear-centered vesicles, of occasional 9 + 0 cilia, and of synaptic ribbons appearing in vitro. Neuroblastic differentiation was most pronounced in 4- and 6-month-old explants, but synapses were not found. The differentiating features reported are in contrast to those of the original tumor, which was largely undifferentiated. The alternative interpretation of a divergent glial and pineocytic differentiation is also considered. These findings support the concept of the differentiating bipotential of the cerebellar medulloblastoma.

Cell Transformation, Neoplastic↗
PubMed1984

Subependymal giant cell astrocytoma. Significance and possible cytogenetic implications of an immunohistochemical study.

Twenty-two cases of subependymal giant cell astrocytoma (SGCA), five of which associated with tuberous sclerosis, were reviewed by conventional neurohistological stains and by peroxidase-antiperoxidase (PAP) immunohistochemistry for glial fibrillary acidic (GFA) protein, the 68 Kd neurofilament subunit (68 Kd-NF), and neuron-specific enolase (NSE). Neurohistological stains confirmed the presence of PTAH-positive fibrils and the absence of Nissl bodies and of neurites originating from the tumor cells. GFA protein-positive cells were present in all tumors not associated with tuberous sclerosis. However, the number of positive cells in each tumor was highly variable. GFA protein-positive cells were rare in the two SGCA accompanying tuberous sclerosis and absent in the remaining three. Neurohistological stains showed no differences between GFA protein-positive and negative cells. 68 Kd-NF-positive cells were found in six tumors. In one tumor, associated with tuberous sclerosis, it was present in the large ganglion-like cells only. NSE-positive cells were found in 13 of 18 tumors examined, including four of the five SGCA associated with tuberous sclerosis. The significance of NSE-positivity in central neuroepithelial neoplasms in respect of their possible neuronal origin remains open. This study suggests that the SGCA, especially those associated with tuberous sclerosis, include cells that are apparently unable to express GFA protein. Some of the tumor cells express the 68 Kd-NF, but this expression falls short of the complete expression of neuronal differentiation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Electron microscopic localization of neuron-specific enolase in rat and mouse brain.

The cellular distribution and intracellular localization of neuron-specific enolase (NSE) has been studied by electron microscopic immunocytochemistry in the brain of the rat and of the mouse. Although the intensity of staining was less in the mouse, the same structures were positive in both species. In the cerebrum, the neuronal perikarya and dendrites were intensely stained, but staining was almost entirely absent in the presynaptic terminals. The deep neurons of the brain stem were also positive. In the cerebellum, perikarya, axons, and parallel fibers of the granule cell neurons were stained as were the synaptic vesicles and presynaptic membranes of the synapses between the parallel fibers and the Purkinje cell dendrites. Golgi cell dendrites, basket cells and their axons, and mossy fibers were also positive. In contrast, the Purkinje cells including their dendrites, and the climbing fibers that formed synapses with the Purkinje cell dendrites were not stained. The majority of the myelinated axons in both the cerebrum and the cerebellum did not stain, but the fibrillary astrocytic processes between myelinated axons in the white matter did. Oligodendroglia, protoplasmic astrocytes, Bergmann glia, astrocytes investing capillaries, and vascular endothelial cells were negative for reaction product. In the positively staining cells and their processes, the positivity was dispersed throughout the cytoplasm and corresponded most closely to the distribution of ribosomes, the granular endoplasmic reticulum, and microtubules. Nuclei, mitochondria, the cisternae of the Golgi complex, myelin lamellae, and most membranes were not stained.

Animals↗
PubMed1984

Immunohistochemistry of central nervous system tumors. Its contributions to neurosurgical diagnosis.

Immunofluorescence and immunoperoxidase (peroxidase-antiperoxidase, PAP) techniques for the demonstration of neural and non-neural cell markers are contributing greatly to increase the diagnostic accuracy of difficult tumors of the central nervous system. Well characterized nervous system markers include glial fibrillary acidic (GFA) protein, the three protein subunits of neurofilaments, neuron-specific enolase (NSE), myelin basic protein, and S-100 protein. The most important and reliable of these is GFA protein, which is widely in use for the immunohistochemical diagnosis of tumors of the glioma group. Its many practical applications are reviewed and illustrated. Other neural markers, in particular the specificity of NSE and S-100 protein, need to be critically evaluated. Problems related to the immunohistochemical diagnosis of central neuroepithelial tumors of putative neuroblastic origin remain complex and still need to be resolved. Non-neural markers, such as vimentin, desmin, cytokeratins, Factor VIII, alpha-fetoprotein, human chorionic gonadotropin, and immunoglobulins have well defined, although more restricted, applications in surgical neuropathology.

Antibodies, Monoclonal↗
PubMed1984

The role of astrocytes in the formation of cartilage in gliomas. An immunohistochemical study of four cases.

The occasional presence of focal cartilage in gliomas is generally attributed to metaplasia of the mesenchymal supportive elements. While this mechanism undoubtedly exists, the present report describes a different mode of development of cartilage in four gliomas occurring in young individuals. Two of the tumors were pontine astrocytomas, one was a mixed ependymoma and astrocytoma involving the fourth ventricle and the brainstem, and one was an extraspinal malignant astrocytoma in the lumbar region of a young boy who earlier had been diagnosed as having a pontine glioma for which he received radiation treatment. In all four tumors, transitions from astrocytic to cartilaginous elements were seen, characterized by an increasing deposition of chondroid ground substance between the astrocytes and a gradual morphologic changes of the glial cells to more rounded forms with a vacuolated cytoplasm, indistinguishable from chondrocytes of mesenchymal origin. Many of these cells retained positive staining for glial fibrillary acidic protein by the immunoperoxidase method, attesting to their astrocytic nature. The production of cartilage by neoplastic astrocytes may be related to their ability to secrete, in certain circumstances and occasionally in large amounts, basement membrane material and other forms of mucopolysaccharides, which may become condensed to form a chondroid ground substance. The process appears analogous to that of cartilage formation by epithelial cells in pleomorphic adenomas of the salivary glands.

Adolescent↗
PubMed1984

Leukoencephalopathy in Waldenström's macroglobulinemia. Immunohistochemical and electron microscopic observations.

The clinical and pathologic features of a case of Waldenström's macroglobulinemia with leukoencephalopathy are reported. Multiple cerebral foci of demyelination, accompanied to a lesser extent by axonal degeneration, were associated with perivascular infiltrates of plasmacytoid lymphocytes and with permeation of the white matter by macroglobulins. Immunohistochemical studies demonstrated a predominance of IgM kappa within the blood plasma, in cerebral blood vessel walls, in the foci of demyelination, and within perivascular histiocytes. Electron microscopy disclosed the presence, in macrophages and pericytes, of membrane-bound cytoplasmic inclusions consisting of tubular arrays, suggestive of cryoglobulin deposits. We hypothesize that the high serum levels of macroglobulins accompanied by lymphoplasmocytic infiltrates may, either by way of viscosity-related ischemia, or by a direct toxic effect, have caused abnormal vascular permeability, infiltration of the cerebral parenchyma by paraproteins, and, ultimately, focal degeneration of the white matter.

Demyelinating Diseases↗
PubMed1984

Immunohistochemical demonstration of neuron-specific enolase in neoplasms of the CNS and other tissues.

In normal conditions, neuron-specific enolase (NSE) is histochemically demonstrable only in neurons and cells of the amine precursor uptake and decarboxylation (APUD) system. This has been found not to be true for neoplastic cells. Several types of CNS tumors, including glioblastoma, astrocytoma, oligodendroglioma, ependymoma, medulloblastoma, pineocytoma , meningioma, and choroid plexus papilloma, focally stained positively for NSE. Reactive astrocytes were also frequently positive. In the peripheral nervous system, neuroblastoma, ganglioneuroma, and paraganglioma stained positively for NSE. A number of non-APUD tumors were focally positive. These included schwannoma, carcinoma and fibroadenoma of the breast, renal cell carcinoma, giant cell tumor of the tendon sheath, and chordoma. Caution should be exercised in relying on the immunohistochemical demonstration of NSE as a diagnostic marker in those tumors that do not belong to the APUD cell system. It seems of little value as evidence of differentiation in CNS tumors.

14-3-3 Proteins↗
PubMed1984

Immunoradiometric and immunohistochemical demonstration of neuron-specific enolase in experimental rat gliomas.

A number of neural and nonneural tumor cell lines of rat and human origin were assayed for neuron-specific enolase (NSE) by radioimmunoassay. Most neural tumor cell lines had appreciably higher levels of NSE than did the nonneural tumor cell lines, the highest levels being found in two anaplastic rat glioma lines ( F98 and T24). These two lines contained more than twice the amount of NSE found in a rat pheochromocytoma line (PC12) and in neuroblastoma lines derived from rats ( B35 and B50 ) or humans (IMR-32 and SHSY - 5Y ). Several of the rat glioma and schwannoma lines were inoculated intracerebrally into syngeneic rats. In the resulting tumors, NSE was demonstrable by immunohistochemistry only in those from the F98 and T24 cell lines. A number of ethylnitrosourea-induced rat tumors were also examined immunohistochemically for NSE: NSE was demonstrated in three anaplastic gliomas; three astrocytomas; and two mixed gliomas. Reactive astrocytes were also positive. Fibroadenomas of apocrine and mammary glands in rats were weakly positive, but other extraneural tumors tested were negative. Since normal neuronal elements, axonal swellings, and amine precursor uptake and decarboxylation cells are strongly positive for NSE, whereas glia and most other normal cells are negative, we hypothesize that the elevated metabolic demands imposed on neoplastic and reactive glial cells and on some extraneural tumors necessitate the opening up of metabolic pathways that are normally operative only in neurons and neuroendocrine cells, therefore resulting in the synthesis of the more stable neuron-specific form of enolase.

Animals↗
PubMed1983

Idiotype-antiidiotype regulation. V. The requirement for immunization with antigen or monoclonal antiidiotypic antibodies for the activation of beta 2 leads to 6 and beta 2 leads to 1 polyfructosan-reactive clones in BALB/c mice treated at birth with minute amounts of anti-A48 idiotype antibodies.

The anti-beta 2 leads to 6 fructosan antibodies sharing the idiotypes (Id) of ABPC48 (A48) monoclonal protein represent a silent fraction of the anti-beta 2 leads to 6 fructosan repertoire, since these antibodies cannot be detected during a conventional immune response elicited by bacterial levan (BL). However, the administration at birth of minute amounts of anti-A48 Id antibodies causes a long-lasting activation of A48 Id+-bearing clones. This activation is related to direct interaction of anti-A48 Id antibodies with precursors bearing the A48 Id+ immunoglobulin receptor, since an A48 Id+ response can be transferred with highly purified B cells in lethally irradiated mice. The maturation of these precursors into A48 Id+ anti-beta 2 leads to 6 fructosan antibody-secreting cells requires challenge by the antigen. Isoelectric focusing (IEF) data showed that in 1-mo-old mice an UPC10 (U10)-like spectrotype was observed, whereas in 3-mo-old mice, a new spectrotype binding BL rather than inulin (In) was identified. This spectrotype was observed only in CXBJ mice, the single strain in which an A48 Id+ response was observed. The antigenic challenge can be replaced by a monoclonal anti-A48 Id antibody (i.e., 17-38). Interestingly, in 1-mo-old BALB/c mice treated with anti-A48 Id antibodies, the challenge with 17-38 monoclonal antibody led to the activation of A48 Id- anti-beta 2 leads to 6 fructosan-reactive clones with BALB/c type IEF spectrotypes, whereas in 3-mo-old BALB/c mice treated with anti-A48 Id antibodies, the challenge with 17-38 monoclonal antibody led to the activation of W3082 IdX+ anti-beta 2 leads to 6 and beta 2 leads to 1 fructosan-reactive clones. In these animals, inhibition of A48 Id+ anti-beta 2 leads to 6 fructosan clones was observed. This antibody probably represents a homobody carrying the internal image of the antigen, which through its paratope suppresses the A48 Id+ response and through its Id activates an A48 Id- anti-beta 2 leads to 6 fructosan response in 1-mo-old mice and in 3-mo-old mice leads to an anti-beta 2 leads to 6 and beta 2 leads to 1 fructosan response dominated by the W3082 IdX.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗