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Biomedical subjects

S Peiper

Publications and source records attributed to S Peiper.

11 recordsLinked to original sources
PubMed1999

Localization of chromogranin, synaptophysin, serotonin, and CXCR2 in neuroendocrine cells of the minor vestibular glands: an immunohistochemical study.

Sections of vulvar tissue containing minor vestibular glands (15 sections from 14 women with vulvar vestibulitis syndrome and six control sections from five asymptomatic women) were immunohistochemically stained with antibodies against chromogranin, synaptophysin, serotonin, and CXCR2. The degree of inflammation in vestibular tissue from women with and without vulvar vestibulitis syndrome was not significantly different. All vulvar minor vestibular glands contained neuroendocrine cells that expressed chromogranin to some degree. Only one case failed to express synaptophysin. The number of cells expressing chromogranin and synaptophysin was the same regardless of the degree of inflammation. However, moderate to severe inflammation was associated with a statistically significant increase in the number of cells expressing serotonin (p < 0.001) and CXCR2 (p < 0.02). It is concluded that neuroendocrine cells are present within minor vestibular glands of the vulva. The number of cells expressing the inflammatory mediator serotonin and CXCR2, the shared interleukin-8 receptor, are upregulated with inflammation. Chronic inflammation is a normal finding in vestibular tissue and does not serve as a histologic marker for vulvar vestibulitis.

Adult↗
PubMed1998

The second extracellular loop of CXCR4 determines its function as a receptor for feline immunodeficiency virus.

The feline homolog of the alpha-chemokine receptor CXCR4 has recently been shown to support cell-cell fusion mediated by CXCR4-dependent strains of human immunodeficiency virus (HIV) and strains of feline immunodeficiency virus (FIV) that have been selected for growth in the Crandell feline kidney (CrFK) cell line. In this report we demonstrate that expression of CXCR4 alone is sufficient to render cells from diverse species permissive for fusion with FIV-infected cells, suggesting that CXCR4 is the sole receptor for CrFK-tropic strains of FIV, analogous to CD4-independent strains of HIV-2. To identify the regions of CXCR4 involved in fusion mediated by FIV, we screened panels of chimeric CXCR4 molecules for the ability to support fusion with FIV-infected cells. Human CXCR4 supported fusion more efficiently than feline CXCR4 and feline/human CXCR4 chimeras, suggesting that the second and third extracellular loops of human CXCR4 contain a critical determinant for receptor function. Rat/human CXCR4 chimeras suggested that the second extracellular loop contained the principal determinant for receptor function; however, chimeras constructed between human CXCR2 and CXCR4 revealed that the first and third loops of CXCR4 contribute to the FIV Env binding site, as replacement of these domains with the corresponding domains of CXCR2 rendered the molecule nonfunctional in fusion assays. Mutation of the DRY motif and the C-terminal cytoplasmic tail of CXCR4 did not affect the ability of the molecule to support fusion, suggesting that neither signalling via G proteins nor receptor internalization was required for fusion mediated by FIV; similarly, truncation of the N terminus of CXCR4 did not affect the function of the molecule as a receptor for FIV. CXCR4-transfected feline cells were rendered permissive for infection with both the CrFK-tropic PET isolate of FIV and the CXCR4-dependent RF strain of HIV-1, and susceptibility to infection correlated well with ability to support fusion. The data suggest that the second extracellular loop of CXCR4 is the major determinant of CXCR4 usage by FIV.

3T3 Cells↗
PubMed1989

Rhabdomyosarcoma, presenting as disseminated malignancy from an unknown primary site: a retrospective study of ten pediatric cases.

From 1962-1984, ten children were referred to St. Jude Children's Hospital with a metastatic poorly differentiated malignancy; extensive diagnostic workup had failed to disclose the site of the primary tumor. Multiple skeletal metastases as well as bone marrow involvement were common findings. Erythrocytes were detected in the cytoplasm of tumor cells in several cases, and cytochemical stains confirmed that these phagocytic cells did not have features of mononuclear phagocytes. Establishing a pathologic diagnosis in these cases was difficult, and most special studies including cytochemistry and electron microscopy were not helpful in elucidating the diagnosis. A diagnosis of rhabdomyosarcoma was made at presentation in six cases. In the remaining cases, the diagnosis of rhabdomyosarcoma was subsequently made after rebiopsy of new tumor masses during the course of the illness, by ultrastructural examination of a cell line derived from the tumor or at postmortem examination. Based on initial symptoms, clinical features, and postmortem findings, the primary tumor sites were assumed to be in the middle ear, paravertebral area, base of skull, retrobulbar space, chest wall, and retropancreatic area. In four patients the disease was confined to bone marrow, lymph nodes, and meninges so that a primary site could not be assigned. The approach to pediatric patients presenting with disseminated malignancy from an occult primary site should consist of an aggressive pursuit of a specific diagnosis and establishment of a primary site to better direct therapy, particularly for those children whose tumors may be responsive to specific therapy.

Adolescent↗
PubMed1986

Shedding of the common acute lymphoblastic leukemia antigen (CALLA) by lymphoblastoid cell lines.

The release of common acute lymphoblastic leukemia antigen (CALLA) into culture medium by lymphoblastoid cell lines was studied. CALLA release was detected using a solid phase indirect radioimmunometric assay which combines the specificity of lectins and monoclonal antibodies and using immunoadsorption of labeled CALLA in spent medium from cells incubated with 35S-methionine. No CALLA was present in the medium of cells pulse-labeled at 37 degrees C, when they were placed at 4 degrees C, thus this is an active process. Sequential analysis of soluble CALLA revealed shedding of CALLA to be associated with cell growth.

Antibodies, Monoclonal↗
PubMed1986

Nonrandom involvement of the 12p12 breakpoint in chromosome abnormalities of childhood acute lymphoblastic leukemia.

We studied the presenting clinical and biologic features of 23 children with acute lymphoblastic leukemia (ALL) whose leukemic marrow karyotypes contained abnormalities involving the short arm of chromosome 12. Nineteen of the abnormalities were assigned to the 12p12 breakpoint. The median age of the children was 5 years (range 2 to 13 years) and their initial leukocyte counts ranged from 1,800 to 424,000/microL (median 30,000/microL). Twenty-one patients (91%) had common phenotype ALL (CALLA+, HLA-DR+), including three cases with a pre-B cell phenotype (CIg+). The remaining two cases were T cell in origin. The French-American-British (FAB) morphologic type of lymphoblastic leukemia was L1 in all cases but one. With a median follow-up of 11 months, four patients have relapsed and another failed induction therapy. The modal chromosome number in all cases was less than 50. Three distinct cytogenetic patterns, with apparently similar clinical manifestations, were noted: terminal deletions of chromosome 12 in 10 cases, apparently balanced reciprocal translocations in 6, and unbalanced translocations in 7. All translocations were between the 12p arm and different donor chromosomes except for chromosomes 7, 9, and 17, which participated twice. Only two patients had identical translocations: t(7;12)(q11;p12). This unusual variation in donor chromosomes and breakpoints suggests that translocations involving the 12p are specific with respect to only one member of the translocation pair, namely chromosome 12. The relatively high frequency of the 12p abnormalities in this study (10% of all completely banded cases seen over a 35-month period) warrants further investigation.

Adolescent↗
PubMed1985

Acute megakaryoblastic leukemia. Blast cell aggregates simulating metastatic tumor.

Acute megakaryoblastic leukemia is a rare leukemia that can present diagnostic problems. We describe two children who have this disease and had clumps of blast cells in their bone marrow, a finding usually attributed to metastatic tumor. The megakaryocytic origin of the cells was supported by their cytochemical staining pattern (positive alpha-naphthyl acetate esterase resistant to sodium fluoride inhibition and negative alpha-naphthyl butyrate esterase) and by the presence of factor VIII-related antigen. Ultrastructural studies of blast cells from one patient demonstrated platelet peroxidase. The mechanism of blast cell clump formation in these cases is unknown; nevertheless, awareness that this feature can occur in acute megakaryoblastic leukemia may avoid a misdiagnosis of metastatic solid tumor.

Acute Disease↗
PubMed1984

Acute leukaemia with mixed lymphoid and myeloid phenotype.

Three children with acute leukaemia had blasts that expressed both lymphoid and myeloid markers. The blasts met immunological criteria for acute lymphoblastic leukaemia (ALL)--common ALL antigen+, HLA-DR+, terminal deoxynucleotidyl transferase+--but their cytochemical features, including positive myeloperoxidase and Sudan black B, were those of acute nonlymphoblastic leukaemia (ANLL) as defined by the French-American-British Group. 30% of the blasts from one of two patients tested reacted with a monoclonal antibody specific for nonlymphoid cells (MCS-2). The wide overlap in the percentages of blasts expressing lymphoid or myeloid markers indicates that some leukaemic cells in each child had a mixed phenotype. There were no consistent cytogenetic findings, and the Philadelphia chromosome was not present. Complete remission was induced by treatment effective for either ALL (two patients) or ANLL. These three cases appear to represent a rare leukaemia subtype that we have designated acute leukaemia with mixed lymphoid and myeloid phenotype. Its recognition may be important in treatment, since two patients achieved remission with standard therapy for ALL. These cases demonstrate further the phenotypic heterogeneity that may be seen in leukaemic cell differentiation.

Acute Disease↗
PubMed1983

Granular acute lymphoblastic leukemia.

Granules in blasts are most typical of acute myeloblastic leukemia. However, there have been scattered reports of patients with acute lymphoblastic leukemia (ALL) that have lymphoblasts with azurophilic cytoplasmic granules. These reports do not describe immunologic markers or cytogenetics. We report five additional cases with detailed cytologic, immunologic, and cytogenetic studies. At diagnosis one of these patients had central nervous system disease, while the others had no unusual features. Four of the five patients attained remission. The blasts of all five patients contained distinct cytoplasmic azurophilic granules. The granules were negative for peroxidase and chloroacetate esterase and positive for PAS, acid phosphatase, alpha-naphthyl acetate esterase incompletely fluoride inhibited, alpha-naphthyl butyrate esterase, and in one case, Sudan black B. In the one patient studied by electron microscopy, characteristic lymphoblasts contained membrane-bound electron lucent inclusions, which stained positively with non-specific esterase. Immunologic markers showed a common ALL phenotype. Different cytogenetic abnormalities were seen in all cases. It is important to recognize the characteristics of this morphologic subtype of ALL in order to avoid a misdiagnosis of acute nonlymphocytic leukemia.

Adolescent↗