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Biomedical subjects

L M Weiss

Publications and source records attributed to L M Weiss.

At least 181 records · Page 10Linked to original sources
PubMed1994

Detection of Epstein-Barr viral RNA in sinonasal undifferentiated carcinoma from Western and Asian patients.

Undifferentiated carcinoma of the nasopharynx has a well-known association with Epstein-Barr virus (EBV), but only an inconsistent relationship has been identified in undifferentiated carcinomas occurring at other sites. We investigated 22 formalin-fixed, paraffin-embedded cases of sinonasal undifferentiated carcinomas (SNUCs) occurring in Western and Asian patients. A highly sensitive in situ hybridization method was performed using an antisense oligonucleotide probe to the EBER1 gene of EBV. We identified EBV RNA in seven of 11 SNUCs from Asian patients, but in none of the Western SNUC patients (0/11). The EBER1 signal was present in all or virtually all of the tumor cell nuclei in the seven EBV-RNA-positive Asian SNUCs. The latent membrane protein-1 (LMP1) of EBV was not identified in any of the five positive cases tested. Our results suggest that genetic predisposition or environmental/geographical cofactors play an important role in determining the strength of the association of SNUC with EBV.

Adult↗
PubMed1994

Primary cutaneous immunocytoma. A B-cell lymphoma that can easily be mistaken for cutaneous lymphoid hyperplasia.

It has been estimated that immunocytomas comprise roughly 2% of all cutaneous lymphomas. We studied five patients with primary cutaneous immunocytomas who presented with cutaneous nodules or plaques. Many of the infiltrates were "top-heavy" and polymorphous with admixed eosinophils, macrophages, lymphoid follicles, and non-neoplastic lymphocytes. Other potentially confusing findings were one case each of spongiotic dermatitis and leukocytoclastic vasculitis. The neoplastic cells were often situated at the peripheries of nodules and ranged from those with nuclei that resembled small lymphocytes to others that resembled immunoblasts. Most had eccentrically placed nuclei and fan-shaped cytoplasm. Monotypic kappa-light chain was found in all five cases, accompanied by gamma-heavy chain in two cases, and mu-heavy chain in one. In situ hybridization detected only kappa-mRNA in the four cases that yielded technically satisfactory results. The neoplastic cells did not express the B-cell antigen CD20; T-cells formed the centers of many nodules. Inappropriate staining for CD43 was evident in the neoplastic cells of one case. Because of reports of immunocytomas complicating acrodermatitis chronica atrophicans, we stained sections with an antiserum to Borrelia burgdorferi, which did not detect that organism. In situ hybridization did not detect EBER-1 RNA of the Epstein-Barr virus, which can be present in immunocytomas in immunocompromised patients. One patient died of disease after failing chemotherapy; another is alive with disseminated disease, and three are in remission following excision of lesions alone in two patients and chemotherapy in one patient who had relapsed following both excision and radiation therapy.

Adult↗
PubMed1994

Follicular small lymphocytic lymphoma.

We herein provide evidence for the existence of a distinct morphologic form of small lymphocytic lymphoma (SLL) that we term follicular small lymphocytic lymphoma (FSLL). Nine specimens of FSLL from eight patients were studied. The lymphomas in this study showed a true follicular pattern that was independent of tissue planes; the cytologic composition was identical to that seen in SLL. All six of the specimens (from five patients) for which paraffin tissue was available marked as B cell phenotype and were positive for bcl-2 protein. Polymerase chain reaction studies performed on deparaffinized tissue sections showed bcl-2 major breakpoint region rearrangements in four of five cases for which study tissue was available. Clinical information was available for all eight patients. All patients presented with lymph node disease, and three patients also had extranodal involvement at the time of presentation. Three of the patients had a relapse of disease after 33-95 months, and two of these patients died soon after relapse. Another two of the eight patients never responded to chemotherapy and died of their disease after 2 and 8 months, respectively. Two patients died of causes unrelated to their lymphoma and unrelated to any lymphoma therapy. Only one patient remains disease-free, after 65 months; this patient had a relapse at 44 months. The finding of bcl-2 rearrangements suggests that the pathogenesis of FSLL is more closely related to follicular small cleaved cell lymphoma than to classic SLL.

Aged↗
PubMed1994

Utility of microsporidian rRNA in diagnosis and phylogeny: a review.

This paper summarizes work done in this laboratory over the last two years on the cloning of microsporidian rRNA by homology PCR and its subsequent use in diagnostic tests and phylogenetic studies. Using highly conserved primers in the 16S or small subunit rRNA (SSU-rRNA) these genes were cloned from human intestinal biopsies with transmission electron microscopy proven Enterocytozoon bieneusi and Septata intestinalis. The SSU-rRNA genes were then used to design and test several primer pairs for the diagnosis of microsporidian infection. Utilizing the polymerase chain reaction and primers V1 and EB450 Ent. bieneusi infected duodenal aspirates or intestinal biopsies could be detected. Using V1 and SI500 infection with S. intestinalis could be detected. In addition to diagnostic tests, phylogenetic relationships were examined using sequence data from the fragment amplified by PCR by primer 530f in the SSU-rRNA and primer 580r in the large subunit rRNA. This data supported the placement of S. intestinalis in the family Encephalitozoonidae. In addition, it confirmed that Encephalitozoon cuniculi, E. hellem and S. intestinalis are distinct organisms. These techniques have broad applications to the study of other microsporidia and the development of a molecular phylogeny.

Animals↗
PubMed1994

Mycobacterium marinum infection in a patient with the acquired immunodeficiency syndrome.

A variety of mycobacterial organisms may infect patients with acquired immunodeficiency syndrome. A patient with acquired immunodeficiency syndrome, lymphoma, and sporotrichoid Mycobacterium marinum is described. The patient responded completely to antimycobacterial therapy but relapsed when he discontinued his medications six months into his course. Disease persistence in spite of therapy had been noted in other immunocompromised states but not previously in acquired immunodeficiency syndrome. Patients with acquired immunodeficiency syndrome may require prolonged treatment or suppressive therapy for Mycobacterium marinum infections.

AIDS-Related Opportunistic Infections↗
PubMed1994

Patterns of p53 mutations in squamous cell carcinoma of the lung. Acquisition at a relatively early age.

Squamous cell carcinoma (SQCC) of the lung is thought to arise after the accumulation of multiple mutations, including p53. To better characterize when p53 mutations are acquired, 37 SQCC of the lung were examined by polymerase chain reaction and single-strand conformation polymorphism analysis. Somatic p53 mutations were detected in nine tumors (24.3%). There were no significant differences in the stage, sex, or race between patients with or without p53 mutations. However, the patients with SQCC and p53 mutations were significantly (P = 0.0006) younger (mean age, 54.3 years) compared with patients without p53 mutations (mean age, 65). The topographical tissue distributions of the p53 mutations were examined by selective ultraviolet radiation fractionation. In all nine cases, the specific p53 mutant alleles were homogeneously present throughout the primary tumors, in all three examples with in situ carcinoma, and in all four cases with metastases. In one case, squamous metaplasia contiguous with the primary tumor also contained the same p53 mutation. Normal or hyperplastic and metaplastic or dysplastic epithelium not contiguous with the primary tumors lacked the specific p53 mutations. These findings suggest that p53 mutations are commonly acquired at a relatively early age, before the bulk of clonal expansion, and usually persist throughout the progression of SQCC of the lung.

Aged↗
PubMed1994

Diagnosis and treatment of common intestinal helminths. II: Common intestinal nematodes.

In the second article of this series, we discuss the diagnosis and treatment of some important intestinal nematodes. Common parasites discussed in detail include Ascaris lumbricoides, Trichuris trichiura, hookworm, and Enterobius vermicularis (pinworm). In addition, Strongyloides stercoralis has emerged as an important pathogen in immunocompromised patients, and Capillaria philippinensis is now recognized as an important cause of diarrhea in Asia. Finally, anisakiasis and other illnesses due to parasitic nematodes are discussed.

Adult↗
PubMed1994

c-k-ras and p53 mutations occur very early in adenocarcinoma of the lung.

The topographical distribution of a mutation provides insight into past patterns of tumor evolution. This approach was applied to two loci commonly mutated in adenocarcinoma of the lung--p53 and c-K-ras. In 41 primary adenocarcinomas, c-K-ras codon 12 point mutations were detected in 8 (19.5%) tumors and p53 point mutations were detected in 10 (24.4%) tumors, with one tumor harboring both mutations. These mutations were only detected in malignant cells and with a homogeneous topographical distribution throughout 16 tumors, including metastasis. Intratumor heterogeneity was detected in only one tumor in which a small portion lacked the specific p53 mutation. Based on this topographical analysis, it is likely that when these mutations occur in adenocarcinoma of the lung, they are usually acquired during the very earliest phases of tumor formation before the bulk of clonal expansion, and in very small precursor lesions.

Adenocarcinoma↗
PubMed1994

An investigation of the viral pathogenesis of Kikuchi-Fujimoto disease. Lack of evidence for Epstein-Barr virus or human herpesvirus type 6 as the causative agents.

Histiocytic necrotizing lymphadenitis of Kikuchi and Fujimoto is a well-defined clinicopathologic entity of unknown cause. Both the Epstein-Barr virus (EBV) and human herpesvirus type 6 (HHV-6) have been suggested as potential etiologic agents. Twenty cases of Kikuchi-Fujimoto disease were studied for the presence of EBV DNA and HHV-6 DNA by the polymerase chain reaction (PCR), and in situ hybridization in the case of EBV. Cellular DNA from sections of formalin-fixed, paraffin-embedded lymph node tissue was amplified using the PCR technique and oligonucleotide primers to the EBV BamH1 W, lymphocyte-determined membrane antigen, or the EBNA-1 region. These studies were performed in three separate laboratories. In addition, 12 cases were examined by in situ hybridization, eight of which had shown at least one positive PCR signal for EBV. The presence of HHV-6 was assessed by PCR using primers to part of the pZVH14 sequence. Biopsy specimens from eight patients (40%) showed a strong positive signal for EBV in at least one laboratory, while an additional three specimens (15%) showed a weaker positive signal. Five cases studied showed rare positive cells by in situ hybridization, and one case had scattered positive cells. All samples lacked HHV-6 genomic templates. These findings indicate that HHV-6 does not play a role in the pathogenesis of Kikuchi-Fujimoto disease and do not implicate EBV as a causal agent for Kikuchi-Fujimoto disease, since EBV was detected in only a fraction of cases with a low number of positive cells detected by in situ hybridization. Further, some discrepancies were identified in the positive results for EBV in samples studied by multiple laboratories. These results indicate that inconsistent results by PCR may occur with very low levels of viral genomes and that different laboratories perform DNA amplification at different efficiencies. Alternatively, laboratory contamination may give rise to false-positive results. Therefore, a positive result for EBV should be interpreted with caution and should be confirmed by repeated study (PCR) or by independent methodology (in situ hybridization).

Adolescent↗
PubMed1993

Epstein-Barr virus-containing T-cell lymphoma presents with hemophagocytic syndrome mimicking malignant histiocytosis.

BACKGROUND: The previously designated malignant histiocytosis (MH) may include lymphoid neoplasms of T-cell lineage as well as patients with benign virus-associated hemophagocytic syndrome (VAHS). In this study, the association of Epstein-Barr virus (EBV) with T cell lymphomas which present with clinicopathologic features indistinguishable from malignant histiocytosis (MH) was investigated further. METHODS: Four adult patients, three women and one man, were admitted because of fever, cutaneous lesions, hepatosplenomegaly, and jaundice. Laboratory examinations revealed pancytopenia, abnormal liver functions and coagulopathy. All patients ran a fulminant course terminating in a hemophagocytic syndrome within 1 month. Immunophenotypic study, Southern blot analysis, and in situ hybridization were performed on the specimens obtained from the four patients. RESULTS: The biopsy-necropsy specimens from skin, liver, spleen, and bone marrow showed infiltration of atypical large cells with reactive histiocytosis and florid hemophagocytosis activity. Based on the clinical and histologic findings, these cases would have been designated as MH by previous criteria. Immunophenotypic, Southern blot, and in situ hybridization studies, however, showed clonotypic proliferation of EBV genomes in the nuclei of the large atypical cells that expressed T-cell antigens. Therefore, these patients should be diagnosed as a recently described EBV-associated peripheral T-cell lymphoma (EBV-PTCL). CONCLUSIONS: EBV-PTCL may present with a fulminant hemophagocytic syndrome indistinguishable from the previously designated MH. This finding represents a step forward in our changing concept regarding MH, some of which only recently has been suggested to be of T-cell lymphoma origin. Differentiation from benign VAHS is clinically important. Features useful in this distinction are tabulated and discussed.

Adult↗
PubMed1993

B-cell lymphoma after angioimmunoblastic lymphadenopathy: a case with oligoclonal gene rearrangements associated with Epstein-Barr virus.

We describe a patient with angioimmunoblastic lymphadenopathy with dysproteinemia (AILD), who subsequently developed large-cell immunoblastic lymphoma of B-cell immunophenotype. At the time of the initial diagnosis, histologic examination of an inguinal lymph node showed typical features of AILD, and there was no evidence of a monoclonal B-cell population by immunohistochemical analysis. In situ hybridization and Southern blot analysis for Epstein-Barr virus (EBV) were negative. At autopsy 2 years later, the patient had widespread lymph node and organ involvement by large-cell immunoblastic lymphoma of B-cell immunophenotype. Southern blot analysis performed on DNA extracted from lymph nodes, liver, and spleen showed two patterns of Ig heavy chain and kappa light chain gene rearrangements. The T-cell receptor beta chain gene was in the germline configuration. Analysis with an EBV terminal repeat region probe showed two clonal populations that paralleled the Ig gene rearrangement studies. Double-labeling immunohistochemistry and in situ hybridization confirmed the presence of EBV within the neoplastic B cells. The data support the hypothesis that EBV was not etiologically related to AILD in this case, and that EBV proliferation may occur after the onset of the disease. Further, the data suggest that some B-cell lymphomas that arise in the setting of AILD resemble EBV-associated B-cell lymphomas that arise in other immunodeficiency states.

Blotting, Southern↗
PubMed1993

Epstein-Barr virus-associated non-Hodgkin's lymphoma in patients infected with the human immunodeficiency virus.

Lymphoproliferations associated with Epstein-Barr virus (EBV) commonly arise in settings of immune dysfunction, including human immunodeficiency virus (HIV) infection. In this study, EBV was associated with 39 of 59 (66%) HIV-related systemic lymphomas. Unlike the lymphoproliferations that arise in the setting of transplantation, the HIV-related lymphomas were monoclonal, as evaluated by Ig heavy chain rearrangements and EBV termini analysis, and associated (40%) with c-MYC rearrangements. Furthermore, analysis of multiple lymphoma tissues from one autopsy showed evidence that a single lymphoma clone was responsible for dissemination. The latent EBV nuclear antigen (EBNA-1) transcripts detected in the HIV-related lymphomas were characteristic of the pattern found in Burkitt lymphoma (g1 EBNA1) and not in transplant-related lymphoproliferations. However, unlike Burkitt lymphoma, EBV latent membrane-associated protein (LMP) transcripts were also detected, thereby constituting an EBV expression pattern (g1 EBNA1+, LMP+) not previously observed in B-cell lymphomas. These findings demonstrate a high frequency of EBV-associated lymphomas in the setting of HIV infection that are distinct from the lymphoproliferations that arise during iatrogenic transplant-associated immuno-suppression or in the general population. However, it is also apparent that HIV-related lymphomas are biologically heterogeneous, which may reflect the multiple mechanisms or steps necessary for eventual malignant transformation.

Antigens, Viral↗
PubMed1993

High prevalence of Epstein-Barr virus in the Reed-Sternberg cells of Hodgkin's disease occurring in Peru.

The Epstein-Barr virus (EBV) has been implicated in the pathogenesis of Hodgkin's disease (HD). This study was undertaken to determine whether the association of EBV with HD showed geographical variation, as in Burkitt's lymphoma. We studied 32 formalin-fixed, paraffin-embedded cases of HD occurring in Peru. EBV DNA-RNA in situ hybridization was performed using a 30-base biotinylated antisense oligonucleotide complementary to the EBER1 gene of EBV. EBV immunohistochemistry was also performed, using a monoclonal antibody (MoAb) to the latent membrane protein (LMP1) of EBV. Identification of the precise cellular subset staining with EBV was accomplished via double-labeling with MoAbs directed against Reed-Sternberg cells (LeuM1/CD15) and B cells (L26/CD20). EBV RNA was identified in all or virtually all of the Reed-Sternberg cells and variants in 30 of the 32 (94%) cases of HD by in situ hybridization. LMP1 expression was identified in 83% of the EBER1-positive cases. Double-labeling studies confirmed the localization of EBV RNA to CD15-expressing Hodgkin's cells. This study found an extremely high prevalence of EBV in Peruvian HD, in contrast to the much lower percentage of EBV-associated cases of HD occurring in "Western" patients.

Adolescent↗
PubMed1993

Chromosome 11Q13 amplification in head and neck squamous cell carcinoma.

OBJECTIVE: To establish the frequency and clinicopathologic correlates of 11q13 amplification in head and neck squamous cell carcinoma. DESIGN: Retrospective clinicopathologic analysis. SETTING: University and private cancer centers. PATIENTS: Eighty-five patients with pathologically confirmed head and neck squamous cell carcinoma. MEASUREMENTS: The degree of DNA amplification in each tumor was determined using chromosome 11q13 probes for the bcl-1 major translocation cluster, PRAD1/cyclin D1 (CCND1), the fibroblast growth factor gene HST1, EMS1, and glutathione S transferase, pi-1. The presence or absence of amplification was correlated with anatomic site, tumor stage, cytologic grade, histologic pattern, and mitotic activity. RESULTS: Thirty-one patients (36%) showed a twofold to 10-fold amplification of 11q13 loci compared with the chromosome 11q23 ETS1 control probe. Twenty-nine of these encompassed bcl-1 through EMS1 loci; one sample showed only bcl-1 and PRAD1/cyclin D1 plus HST1 amplification, with another amplified at HST1 and EMS1 with minimal or no bcl-1 and PRAD1/cyclin D1 amplification. Amplification was significantly correlated with high cytologic grade, a diffusely infiltrative growth pattern, and with a hypopharyngeal primary site. CONCLUSIONS: Chromosome 11q13 amplification in head and neck squamous cell carcinoma is correlated with an aggressive histologic appearance and hypopharyngeal primary site and should be assessed in prospective clinical trials to determine its utility for treatment stratification and prognosis. Although PRAD1/cyclin D1 and EMS1 have been implicated in the pathogenesis of neoplasms with 11q13 amplification, rare cases with more limited amplicon size suggest that another relevant gene or genes may exist between these loci.

Adult↗