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PubMed1981

Congenital progressive muscular dystrophy of the Fukuyama type - clinical, genetic and pathological considerations.

The Fukuyama type congenital muscular dystrophy (FCMD), which was firstly described by one of the authors in 1960, is now recognized as an independent subtype of progressive muscular dystrophy in Japan. Recent advances in clinical, pathological and etiological studies of this syndrome were extensively reviewed. A long-term observation on a large number of cases revealed a wide spectrum of clinical features and courses, and comprehensive laboratory examinations including cranial computed tomography disclosed several new findings. A sharp dichotomy exists in the study of etiology; the genetic or intrauterine infection theories, with reasonable grounds for each. The most conspicuous is the fact that FCMD had been seldom described in countries other than Japan. If attention and interest on FCMD expand in a worldwide scale, the elucidation of basic pathogenesis of this disorder will be facilitated rapidly.

Central Nervous System↗

PubMed1991

Parvalbumin-immunoreactive neurons in the neocortex are resistant to degeneration in Alzheimer's disease.

Recent studies have stressed the fact that specific neuronal subtypes may display a differential sensitivity to degeneration in Alzheimer's disease. For example, large pyramidal neurons have been shown to be vulnerable, whereas smaller neurons are resistant to pathology. Using a monoclonal antibody against the calcium-binding protein parvalbumin, we investigated the possible changes in a subpopulation of interneurons in two cortical areas known to be strongly damaged in Alzheimer's disease. In the prefrontal cortex as well as in the inferior temporal cortex, we observed no differences in parvalbumin-immunoreactive cell counts or cell size in Alzheimer's disease brains as compared to control cases. Moreover, the general cellular morphology of these neurons was preserved in the Alzheimer's disease cases, in that their perikarya and dendritic arborizations were intact. These results suggest that paravalbumin-immunoreactive cells represent a neuronal subset resistant to degeneration, and further support the hypothesis that the pathological process in Alzheimer's disease involves specific neuronal subtypes with particular morphological and molecular characteristics.

Aged↗

PubMed1996

Differential expression of CD44 variants among meningioma subtypes.

Aims/background-CD44 is a widely distributed cell surface molecule which has numerous isoforms generated by alternative splicing. The diverse functions related to the CD44 variants (CD44v) have been reported in various physiological and pathological conditions. The pattern of expression of CD44v among meningioma subtypes was investigated to ascertain whether CD44 variants play a role in a variety of biological processes, such as epithelial differentiation and extracranial metastasis.Methods-Twenty three meningiomas were studied immunohistochemically using novel antibodies directed against CD44 isoforms. Six of the 23 samples were analysed by reverse transcription polymerase chain reaction (RT-PCR), followed by Southern blotting with CD44v specific probes.Results-In meningothelial, fibrous and anaplastic meningiomas, a standard form of CD44 was detected by RT-PCR and was homogeneously expressed in tumour cells when studied immunohistochemically. CD44v was not detected in these subtypes. In secretory meningiomas, however, CD44v isoforms were strongly expressed in the cell clusters that produce secretory granules and also accumulated in the granules. The population of tumour cells immunopositive for CD44v was similar to that which stained with antibodies directed against carcinoembryonic antigen, epithelial membrane antigen and ezrin. On RT-PCR with Southern blotting, only the secretory type showed high level expression of CD44v.Conclusions-CD44v in meningiomas is expressed in relation to tumour cell differentiation towards the epithelial type.

Journal Article↗

PubMed1992

Cardiac malignant lymphoma in acquired immune deficiency syndrome.

BACKGROUND: Extranodal malignant lymphomas (ML) are known to occur with increased frequency in patients with human immunodeficiency virus infection. The authors report a 30-year-old man with acquired immune deficiency syndrome (AIDS) with ML primarily involving the heart and compare the clinical and pathologic features to those of previously reported patients. METHODS: The patient's hospital record was reviewed and pertinent clinical data were abstracted. Tissue obtained at autopsy was processed for routine light microscopic study and immunohistochemistry. A computer-assisted search of the medical literature for patients with malignant cardiac lymphoma was performed. RESULTS: The patient's initial signs and symptoms were nonspecific, and an abnormal gallium scan suggested pericarditis. Clinically, the course was characterized by progressive heart failure. Autopsy disclosed a diffuse large cell non-Hodgkin lymphoma of B-cell phenotype with massive involvement of the pericardium and extension into the myocardium. A literature search revealed 22 patients with cardiac lymphoma associated with AIDS. Clinical findings were nonspecific, but rapid progression of cardiac dysfunction was common after symptoms appeared. Pathologically, most lymphomas were of diffuse aggressive subtypes. CONCLUSIONS: ML of the heart is extremely rare but is being encountered with increasing frequency in patients with AIDS. The diagnosis should be considered in such patients in whom cardiovascular symptoms develop suddenly and progress rapidly.

Adult↗

PubMed2001

DNA mismatch repair genes hMLH1, hMSH2, and hMSH6 are not inactivated in bronchioloalveolar carcinomas of the lung.

BACKGROUND: Defective DNA mismatch repair (MMR) appears to be rare in nonsmall cell carcinomas of the lung. Defective DNA MMR results from genetic or epigenetic alterations that inactivate the DNA MMR genes hMLH1 or hMSH2, and rarely hMSH6. The loss of normal DNA MMR is thought to promote tumorigenesis by accelerating the accumulation of mutations in oncogenes and tumor suppressor genes. Inactivation of hMLH1, hMSH2, and hMSH6 is observed as a loss of expression of these proteins by immunohistochemistry. Bronchioloalveolar carcinoma is a subtype of adenocarcinoma with distinctive clinical and pathologic features. MATERIALS AND METHODS: An immunohistochemical study was performed on paraffin embedded sections of 33 bronchioloalveolar carcinomas (20 nonmucinous and 13 mucinous) for hmlh1, hmsh2, and hmsh6 proteins. RESULTS All the tumors showed normal expression of hmlh1, hmsh2, and hmsh6. CONCLUSIONS: These findings suggest that defective DNA MMR due to inactivation of hMLH1, hMSH2, or hMSH6 does not play a significant role in the pathogenesis of bronchioloalveolar carcinomas.

Adaptor Proteins, Signal Transducing↗

PubMed1991

Neocortical neuronal subpopulations labeled by a monoclonal antibody to calbindin exhibit differential vulnerability in Alzheimer's disease.

Numerous studies have demonstrated that specific neuronal subtypes display a differential vulnerability to the pathological process in Alzheimer's disease. Large pyramidal neurons are likely to be highly vulnerable, whereas smaller neurons are more resistant to pathology. Using a monoclonal antibody to the calcium-binding protein calbindin, we observed in the human prefrontal cortex distinct populations of labeled cells. First, a subset of heavily stained interneurons was located in layers II and superficial III and in layers V-VI. Second, a subpopulation of pyramidal neurons in the mid and deep parts of layer III displayed a less intense, punctate staining pattern. The interneurons in the superficial layers were unaffected in the Alzheimer's disease cases. Interestingly, in layers V-VI, there was significant cell loss in the interneuron population, but only in the Alzheimer's disease cases with high neurofibrillary tangle densities. The calbindin-immunoreactive pyramidal neurons of layer III were dramatically affected in the disease. Moreover, there was a strong correlation between the extent of the loss of these cells and neurofibrillary tangle counts. These data suggest that calbindin is present in multiple neuronal subpopulations that exhibit a differential vulnerability in Alzheimer's disease and support the hypothesis that the degenerative process involves specific neuronal subsets with particular anatomical and molecular profiles.

Aged↗

PubMed1993

In rats, the metabotropic glutamate receptor-triggered hippocampal neuronal damage is strain-dependent.

The effect of intrahippocampal (i.h.) and intraocular (i.o.) administration of the selective metabotropic glutamate receptor (mGluR) agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) was studied in different rat strains. A massive hippocampal damage was observed in CD/SD and Fischer 344 but not in SD/Rij and Brown Norway rats 7 days following the i.h. injection of 1S,3R-ACPD, while no retinal damage was observed following its i.o. administration. Moreover, 1S,3R-ACPD reduced the N-methyl-D-aspartate (NMDA) toxicity in the retina of both CD/SD and SD/Rij rats. Regardless of its toxic action on hippocampal neurons the i.h. injection of 1S,3R-ACPD caused an acute stimulation of motor activity in both CD/SD and SD/Rij rats. This effect was blocked by the intracerebroventricular (i.c.v.) administration of the putative mGluR antagonist L-2-amino-3-phosphono-propionic acid (L-AP3). It is suggested that the differential expression of mGluR subtypes might determine their role in brain pathology.

Animals↗

PubMed1990

Neurophysiological heterogeneity and the definition of dyslexia: preliminary evidence for plasticity.

Developments in the field of quantified electroencephalography have enhanced visualization of brain function in the learning disabilities. Optimal utilization of these techniques requires that populations under study be unambiguously defined. Evidence from the literature demonstrates that brain electrical activity of children with reading disability is more extensive and differs from that seen in children with "dyslexia-pure". Preliminary data are presented demonstrating that electrophysiological change seen in children with dyslexia-plus (dyslexia and attentional deficit disorder) could not be predicted by knowledge of electrophysiologic change in children with dyslexia-pure alone and attentional deficit disorder alone. Data from our laboratory are summarized to show that within dyslexia-pure the anomic, dysphonemic and global Denckla subtypes differ electrophysiologically from one another. Of particular interest is the demonstration that regions of electrophysiological difference among these subtypes may reflect compensatory mechanisms rather than pathological change. Finally, a case study is presented demonstrating advantageous effects of remediation upon brain electrical function. As both spontaneous and environmentally induced change in brain function can be documented, developmental dyslexia in its broadest terms appears to represent a more dynamic or plastic process than previously appreciated.

Anomia↗

PubMed1996

Psychobiologic correlates of treatment response in schizophrenia.

In studies conducted on largely treatment naive patients in their first episode of psychosis, we have found that treatment outcome is quite good and that most patients recover or at least achieve a substantial degree of symptom remission. However, over the course of their illness and in the context of subsequent psychotic episodes, they may experience some decrease in their treatment response from illness progression. In addition, the heterogeneity of treatment outcome is associated with specific clinical (gender, primary negative symptoms of the deficit state, duration of psychosis) and biological variables (pHVA, ventricular volume). It is unclear whether these variables represent aspects of discrete subtypes of schizophrenia or dimensional measures of pathology within the broad context of a unitary disease entity.

Follow-Up Studies↗

PubMed2006

Does adjuvant radiation therapy improve disease-free survival in completely resected Masaoka stage II thymoma?

OBJECTIVE: To determine whether or not patients with completely resected Masaoka stage II thymoma benefit from postoperative radiotherapy (RT). METHODS: We retrospectively review the case records and compared the long-term outcomes of patients affected by Masaoka stage II thymoma treated by resection alone with same stage thymoma patients submitted to resection and RT. Surgical specimens were reviewed to confirm pathological stage, negative resection margins and histological subtype. RESULTS: Between 1988 and 2000, we performed 197 resections for thymoma; 58 patients resulted to be affected by completely resected tumours with microscopic transcapsular invasion (stage IIA, n=25) or macroscopic invasion into the surrounding fatty tissue with or without adhesion to the mediastinal pleura (stage IIB, n=33). Thirty-two patients underwent only complete surgical resection (14 stage IIA and 18 stage IIB); 26 patients underwent complete resection and subsequent mediastinal RT (11 stage IIA and 15 stage IIB). RT dosages were 45-54grays (Gy), in 25-30 fractions. Histological subtypes were similarly represented in both groups. Median follow-up was 91 months (range 9-170). Five intrathoracic recurrences occurred: three radiated patients (2 stage IIB - 1 AB and 1 B2 thymoma; 1 stage IIA B1 thymoma) and two not-radiated patients (1 stage IIA AB thymoma and 1 stage IIB B1 thymoma). Disease-free survival rate at 5- and 10-year were 94% and 87%, respectively. Log-rank test showed no difference in Kaplan-Meier survival curves (p=0.432) between radiated and not-radiated patients. CONCLUSIONS: These data support the concept that radical surgical resection alone should be considered a sufficient treatment for stage II thymoma.

Adult↗

PubMed2005

Maspin nuclear localization is linked to favorable morphological features in pulmonary adenocarcinoma.

Maspin, a mammary homologue of Serine Protease Inhibitors, has been shown to inhibit tumor progression and metastasis. Recently, its biological functions have been linked to its subcellular localization. Specifically, a nuclear, opposed to a combined nuclear and cytoplasmic localization has been associated with increased survival in human malignancies, including non-small cell lung cancer (NSCLC). However, it is not known whether transformation affects maspin expression during lung carcinogenesis, and whether its subcellular localization correlates with the morphological features of NSCLC. To address these questions, we studied maspin expression in a model of transformation of bronchial epithelial cells and in resected NSCLC. We found that decreased maspin accompanied chemical transformation of normal immortalized bronchial epithelial cells BEAS 2B. Immunohistochemistry revealed maspin expression to be virtually universal in NSCLC, occurring in 72/77 Adenocarcinoma (ACa), and 46/46 squamous cell carcinoma (SqCCa). SqCCa showed almost exclusively a combined nuclear-cytosolic stain. In contrast, nuclear maspin, but not combined nuclear-cytoplasmic maspin significantly correlated with low histological grade, lower proliferative rate, absence of invasion, and negative p53 stain in ACa. These data support the hypothesis that nuclear localization of maspin may stratify subtypes of NSCLC with favorable clinical-pathological features.

Adenocarcinoma↗

PubMed2006

KRAS and BRAF mutations in ovarian tumors: a comprehensive study of invasive carcinomas, borderline tumors and extraovarian implants.

OBJECTIVE: Mutations of BRAF, a downstream mediator of K-RAS, have been described in serous borderline tumors of the ovary. Data concerning other types of ovarian tumors are scarce. Therefore, we assessed KRAS and BRAF mutation in a series of more than 100 different ovarian tumors. METHODS: Paraffin-embedded material, including invasive carcinomas, borderline tumors, benign lesions and implants, was used. BRAF codon 600 in exon 15 and K-RAS codon 12 in exon 2 were analysed. RESULTS: 92 cases (92%), including all serous carcinomas (100%), did not show a mutation of BRAF. Eight cases (8.0%), including five serous borderline tumors (31.25%), contained a mutation. In all serous borderline tumors, codon 600 was affected. The remaining three cases were invasive carcinomas of endometrioid (mutation on codon 600), mucinous (mutation on codon 600) and clear cell (mutation on codon 615) subtype. There was no BRAF mutation in mucinous borderline tumors. Regarding K-RAS, 89 cases (87.25%) did not show an aberration. The 11 positive borderline tumors (10.7%) were of serous (22.2%) and of mucinous type (46.6%). There was a KRAS mutation in a serous and a mucinous invasive carcinoma each. BRAF and K-RAS mutations were mutually exclusive and not seen in implants. CONCLUSION: Mutation of either K-RAS or BRAF is frequent in borderline tumors but is not found in invasive serous carcinomas and is very rare in other invasive subtypes. This supports the notion of different pathological pathways. For the development of extraovarian implants, further studies are observed.

Adenocarcinoma, Clear Cell↗

PubMedDate not supplied

[Nonspecific interstitial pneumonitis: a clinicopathologic entity, histologic pattern or unclassified group of heterogeneous interstitial pneumonitis?].

Nonspecific interstitial pneumonitis (NSIP) initially described by Katzenstein and Fiorelli in 1994, seems to be a distinct clinicopathologic entity among idiopathic interstitial pneumonitis (IIP). Besides different histologic features from other IIP, NSIP is characterized by a better long-term outcome, associated with a better steroids responsiveness than idiopathic pulmonar fibrosis (IPF), where usually were included. Thus, differentiating NSIP from other IIP, namely IPF is very significant, since it has important therapeutic and prognostic implications. NSIP encloses different pathologies, namely those with inflammatory predominance (cellular subtype) or fibrous predominance (fibrosing subtype). NSIP is reviewed and discussed by the authors, after two clinical cases description.

Adult↗

PubMed2001

From genomics to proteomics: techniques and applications in cancer research.

New technologies designed to facilitate the comprehensive analyses of genomes, transcriptomes and proteomes in health and disease are poised to exert a dramatic change on the pace of cancer research and to impact significantly on the care of cancer patients. These approaches have already demonstrated the power of molecular medicine in discriminating among disease subtypes that are not recognizable using traditional pathological criteria and in identifying specific genetic events involved in cancer progression. This review outlines the current status of these technologies and highlights recent studies in which they have been applied in the context of carcinogenesis.

Affinity Labels↗

PubMedDate not supplied

ONCOMINE: a cancer microarray database and integrated data-mining platform.

DNA microarray technology has led to an explosion of oncogenomic analyses, generating a wealth of data and uncovering the complex gene expression patterns of cancer. Unfortunately, due to the lack of a unifying bioinformatic resource, the majority of these data sit stagnant and disjointed following publication, massively underutilized by the cancer research community. Here, we present ONCOMINE, a cancer microarray database and web-based data-mining platform aimed at facilitating discovery from genome-wide expression analyses. To date, ONCOMINE contains 65 gene expression datasets comprising nearly 48 million gene expression measurements form over 4700 microarray experiments. Differential expression analyses comparing most major types of cancer with respective normal tissues as well as a variety of cancer subtypes and clinical-based and pathology-based analyses are available for exploration. Data can be queried and visualized for a selected gene across all analyses or for multiple genes in a selected analysis. Furthermore, gene sets can be limited to clinically important annotations including secreted, kinase, membrane, and known gene-drug target pairs to facilitate the discovery of novel biomarkers and therapeutic targets.

Databases, Genetic↗

PubMed1999

Development of a calcifying fibrous pseudotumour within a lesion of Castleman disease, hyaline-vascular subtype.

A nine year old boy with localised Castleman disease of the hyaline-vascular subtype developed a calcifying fibrous pseudotumour. This pathological association does not appear to have been described before. In this case, the development of this very unusual soft tissue tumour-like process was thought to be related to a previous fine needle aspiration biopsy, which was performed because of lymphadenopathy localised to the right inguinal area. This case provides further evidence of the reactive nature of calcifying fibrous pseudotumour and also broadens the pathological spectrum of the stromal cell proliferation that occasionally supervenes within lesions of Castleman disease, hyaline-vascular type.

Biopsy, Needle↗

PubMedDate not supplied

The molecular basis of thyroid epithelial tumorigenesis.

Significant alterations in gene sequences, expression levels and protein structures have been associated with specific types of thyroid epithelial tumorigenesis. Recent revolutionary changes in molecular biology have spanned the disciplines of genomics and proteomics, which systematically generate and analyze the information about genomes, gene transcripts, proteins and their functions in a global, comprehensive manner. The application of these approaches will better discriminate between thyroid tumor subtypes that are not recognizable when traditional pathological criteria are used.

Carcinoma, Papillary↗

PubMed1999

Salivary gland P2 nucleotide receptors.

The effects of ATP on salivary glands have been recognized since 1982. Functional and pharmacological studies of the P2 nucleotide receptors that mediate the effects of ATP and other extracellular nucleotides have been supported by the cloning of receptor cDNAs, by the expression of the receptor proteins, and by the identification in salivary gland cells of multiple P2 receptor subtypes. Currently, there is evidence obtained from pharmacological and molecular biology approaches for the expression in salivary gland of two P2X ligand-gated ion channels, P2Z/P2X7 and P2X4, and two P2Y G protein-coupled receptors, P2Y1 and P2Y2. Activation of each of these receptor subtypes increases intracellular Ca2+, a second messenger with a key role in the regulation of salivary gland secretion. Through Ca2+ regulation and other mechanisms, P2 receptors appear to regulate salivary cell volume, ion and protein secretion, and increased permeability to small molecules that may be involved in cytotoxicity. Some localization of the various salivary P2 receptor subtypes to specific cells and membrane subdomains has been reported, along with evidence for the co-expression of multiple P2 receptor subtypes within specific salivary acinar or duct cells. However, additional studies in vivo and with intact organ preparations are required to define clearly the roles the various P2 receptor subtypes play in salivary gland physiology and pathology. Opportunities for eventual utilization of these receptors as pharmacotherapeutic targets in diseases involving salivary gland dysfunction appear promising.

Adenosine Triphosphate↗