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M Dictor

Publications and source records attributed to M Dictor.

At least 55 records · Page 3Linked to original sources

Ultrastructural development of Kaposi's sarcoma in relation to the dermal microvasculature.

Ultrastructural subtypes of endothelial cells in Kaposi's sarcoma were compared with lymphatics and the normal dermal microcirculation in different stages of lesional development. In the earliest patch stage, lymphatic channels, recognised by their dissecting growth pattern and a lack of a basal lamina and pericytes, were prominent. Venous endothelium was recognised by virtue of its multilaminated basal lamina and often showed markedly irregular luminal and abluminal cytoplasmic projections. As the histological stage progressed toward spindle cells, venous endothelium showed a tetrad of changes: dissolution of the basal lamina; fragmentation and disappearance of the pericyte sheath, decreased and often rudimentary intercellular junctions and markedly reduced numbers of Weibel-Palade bodies. These were also features of spindle cells, which were rarely seen to emerge from narrow vascular channels of indeterminate type. Spindle cells showed sparse intercellular junctions and minimal basal lamina but no Weibel-Palade bodies. These progressive venous alterations thus resulted in a mixed intermediate subtype of endothelium with the morphological traits resembling lymphatics as well as venous blood vessels. The mixed subtype included endothelial tubes surrounded by a complete basal lamina but lacking pericytes, and much more commonly, tubes with pericytes but a scanty basal lamina. Both forms had remarkably few or no Weibel-Palade bodies. In the spindle cell stage, normal vessels were largely replaced by the mixed subtype and an indeterminate type of frequently disrupted endothelial tube which lacked a basal lamina as well as a pericytic investment. Dissecting lymphatic channels could not be confidently distinguished from the latter vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Flow cytometric DNA content in Kaposi's sarcoma by histologic stage. Comparison with angiosarcoma.

Kaposi's sarcoma occurs as a multicentric proliferation of endothelial cells. A lesion may progress through several histologic stages, culminating in a lesion consisting of spindle cells with marked nuclear atypia that may be indistinguishable from angiosarcoma. To assess the relationship between the nuclear DNA content and the stage, 29 paraffin-embedded biopsy specimens from 25 cases of Kaposi's sarcoma were classified according to their histologic stage and flow cytometric DNA ploidy status. The findings were compared with those in 14 angiosarcomas (5 postmastectomy angiosarcomas, 6 other cutaneous angiosarcomas and 3 angiosarcomas of deep tissues). The Kaposi's sarcoma specimens studied included samples with irregular lymphatic-like channels (stage 1), transition to spindle cells (stage 1t2), nodular spindle-cell aggregates (stage 2), scattered atypical spindle cells (stage 2t3) and histologic features indistinguishable from those of angiosarcoma (stage 3). Of the 25 Kaposi's sarcoma specimens of stage 2 or less, 17 had a diploid DNA distribution while an additional 8 had broad diploid G0G1 peaks (peridiploid, with a coefficient of variation greater than 7.5%, present in similar proportions in stages 1, 1t2 and 2). One of three stage 2t3 lesions showed tetraploidy while the single stage 3 specimen (from the leg) was aneuploid, with a DNA index (DI = 1.16) similar to that of four of the five postmastectomy angiosarcomas (DI = 1.14 to 1.20). An additional three angiosarcomas also showed nondiploid distributions (DI = 1.16, 1.98 and 2.13, respectively); the remainder were diploid or peridiploid. These results support previous cytogenetic data suggesting a normal karyotype in Kaposi's sarcoma up to stage 2, with atypia beginning as cells acquire numerical and structural chromosomal aberrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Frequent rearrangement of chromosomal bands 1p22 and 11q13 in squamous cell carcinomas of the head and neck.

We report the finding of clonal structural chromosome abnormalities in short-term cultures from 15 squamous cell carcinomas of the head and neck region. When the distribution of chromosomal breakpoints in these 15 tumors and in the 16 head and neck carcinomas previously described are assessed, a marked clustering is seen at bands 1p22 and 11q13, which are rearranged in eight and nine tumors, respectively. No other band was involved in aberrations in more than five tumors. Cytogenetic evidence of gene amplification was seen in four tumors, three times in the form of homogeneously staining regions (twice located in 11q13), and in one tumor as double minutes. Among the candidate genes for such amplification are BCLI, INT2, and HSTI, all of which map to 11q13, and NRAS, which maps to 1p22. All these oncogenes have previously been shown to be amplified in subsets of head and neck carcinomas. We conclude that bands 1p22 and 11q13 are nonrandomly involved in chromosomal rearrangements in head and neck carcinomas and suggest that activation of oncogenes located in these bands may proceed via cytogenetic mechanisms.

Aged↗

Increased incidence of Kaposi sarcoma in Sweden before the AIDS epidemic.

Clinical factors of possible importance for the greater than two-fold rise in the incidence of Kaposi sarcoma of the elderly in Sweden before the AIDS epidemic were reviewed in 63 regional patients. 5 patients had lymphoproliferative disease before or at the time of Kaposi sarcoma, and 4 patients had been receiving steroids (including 1 with lymphoma) at diagnosis. 2 of these 9 patients plus 2 additional patients had received blood transfusions 1-9 years before diagnosis. None of 17 patients tested was positive for HIV-1, and none had signs of an unexplained progressive immune defect. Of the evaluable cases, 27% had diabetes mellitus and 7% had had previous myocardial infarction. However, only the frequency of congestive heart failure (47%) was significantly greater than that of an ambulatory control group (P = 0.001) in the age group 75-84 years. Exposure to cytomegalovirus (CMV) was not more common in 15 Kaposi sarcoma patients than in an age and sex matched control group. No single factor could account for increased Kaposi sarcoma among the elderly. If the classical form has an infectious aetiology, the tumour could arise after effective transmission of the agent (as by a transfusion), especially combined with some degree of immune deficiency or perhaps congestive failure late in life.

Adult↗

In situ hybridisation in herpetic lesions using a biotinylated DNA probe.

In situ hybridisation was performed with a biotinylated DNA probe for herpes simplex virus (HSV) using high temperature denaturation on formalin fixed, paraffin wax sections of lung, brain, ganglion and keratinising and non-keratinising squamous epithelia. Eosinophilic viral nuclear inclusions or characteristically moulded multiple nuclei with altered chromatin, which were present in two cases of HSV encephalitis and one case of viral pneumonitis, all showed complete hybridisation visualised by an alkaline phosphatase/nitroblue tetrazolium detector system. HSV encephalitis and trigeminal ganglionitis, which were confirmed serologically or clinicopathologically but lacked nuclear changes, also gave positive dense nuclear signal in neurons, glias and satellite cells. No staining was present in the ganglion cells in trigeminal zoster, the glia in progressive multifocal leucoencephalopathy, or in a variety of cells in a lung coinfected with cytomegalovirus. In 10 herpetic blisters of squamous epithelia, infected cells hybridised strongly, while morphologically similar herpes zoster lesions remained negative. In neural tissues non-hybridisation staining was most obtrusive in corpora amylacea and seemed to reflect nonspecific probe adherence. In squamous epithelium, major non-hybridisation staining was caused by probe and antibody possibly adhering to intracellular keratin. The HSV probe permits specific detection of virus in the absence of characteristic nuclear changes and allows varicella zoster virus to be differentiated from HSV, provided that the aforementioned problems with non-hybridisation staining are borne in mind.

Biotin↗

Epidemiology of Kaposi's sarcoma in Sweden prior to the acquired immunodeficiency syndrome.

We studied retrospectively 529 cases of Kaposi's sarcoma (KS) reported to the Swedish Cancer Registry between 1958 and 1982 to determine incidence rates, survival and rate ratios, together with the frequency and types of associated malignancies. The age-standardized (Swedish population 1970) incidence rate generally increased over the time period, with a mean of 0.27 cases per 100,000 population per year (males 0.40, females 0.14). The incidence rate ratio (based on 5-year intervals and relative to the earliest period) reached 2.06 for males and 3.76 for females in the 1968-1972 interval, while the actual peak occurred between 1971 and 1974 for both sexes. Poisson regression modelling suggested a transient shift in the age-specific male incidence rate pattern with a relative increase of the disease in younger age groups (p = 0.05) up to 1968-1972. The age-adjusted male:female ratio did not change significantly from 2.9 during the period of study. In relation to the general population, 18% fewer men and 24% fewer women were alive 10 years after the diagnosis had been made. Ninety-nine (19%) cases had other primaries, of which 17 were neoplasms of lymphocytic origin. Lymphoproliferative malignancy was 2.5 times (95% CI 1.38, 4.37) more common than expected in patients with KS (in particular in females) but a definite increase in other malignancies was not apparent. It is questionable whether immune dysfunction due to other malignant disease or drug therapy can account for the epidemiologic changes in KS, which began almost 2 decades prior to the AIDS epidemic in Sweden.

Acquired Immunodeficiency Syndrome↗

The cause of Kaposi's sarcoma: an avian retroviral analog.

Changes in the epidemiologic patterns of Kaposi's sarcoma prior to and during the epidemic of acquired immunodeficiency suggest that a virus transmitted similarly to the human immunodeficiency virus (HIV) may be responsible. We propose a natural avian model for Kaposi's sarcoma. Hemangiomatosis of fowls corresponds clinically and pathologically to the human disease, with characteristics including predilection for distal skin, multicentricity with organ involvement, bleeding and recurrence after excision. Pathologic stages are also similar and include initial dissection of collagen by benign endothelial cells, the formation of large blood-filled spaces, spindle cell growth, and progression to fibrosarcomalike tumors. Avian hemangiomatosis is induced by a retrovirus of the lymphoid leukosis group and has been associated with laboratory transmission of lymphomatosis. An etiopathologic parallel should be sought in man.

Acquired Immunodeficiency Syndrome↗

Lymphaticovenous differentiation in Kaposi's sarcoma. Cellular phenotypes by stage.

The histogenesis of Kaposi's sarcoma was investigated by immunohistochemical staining of 20 skin specimens that represented four main histologic stages. The early phase of Stage 1 contained lymphatic-like clefts lined by endothelial cells with thin, discontinuous basement membranes shown by anti-laminin, absent Factor VIII-related antigen reactivity (FVIIIRAg), and only rare staining with dilute Ulex europaeus agglutinin I (UEA-I). In the late phase of Stage 1, the clefts developed into anastomosing, blood-filled channels, and the basement membrane became complete. Endothelial marker reactivities were not definitive, but weak staining with UEA-I and variable staining for FVIIIRAg characterized the spindle cells of Stage 2. However, spindle cells in monomorphic nodules were individually enclosed by immunoreactive laminin. The sequence of events, particularly in light of previous angiographic findings of lymphaticovenous union, suggests a disturbance in lymphaticovenous differentiation in Kaposi's sarcoma. Sclerotic closure of channels unable to maintain competent blood flow may select against lymphendothelial traits in the developing spindle cell nodule.

Acquired Immunodeficiency Syndrome↗

Fulminant course of infectious mononucleosis with virus-associated hemophagocytic syndrome.

A fatal case of infectious mononucleosis due to serologically verified Epstein-Barr virus infection in a previously healthy 30-year-old man is presented. The clinical course was characterized by severe prostration, persistently high spiking fever, and continuous development of enlarged lymph nodes. Hematologic examination revealed peripheral leukopenia and thrombocytopenia, and in the bone marrow an increased number of benign histiocytes showed marked hemophagocytosis. At autopsy abnormal lymphoid infiltrates were present in several tissues. The pathogenesis of this infection-associated hemophagocytic syndrome is discussed in terms of the possibility of an impaired immune response to infectious agents.

Adult↗

Kaposi's sarcoma. Origin and significance of lymphaticovenous connections.

Review of histopathological material in nine autopsies and 35 skin biopsy specimens of Kaposi's sarcoma in male homosexuals suggested that aberrant lymphaticovenous connections occur in the earliest stage of the Kaposi lesion. Venular glomeruloid structures in the dermis and their analogous radial venolymphatic channels in medium-sized and larger veins signified coupling of the lymphatic and venous systems, a characteristic previously noted in angiographic studies and considered to be unique in Kaposi's sarcoma. Lymphatic channels penetrated veins selectively rather than arteries, particularly in deep fat, liver, gastrointestinal submucosa and the hilum of lymph nodes. The initiation of the Kaposi lesion thus may be an abnormal recapitulation of the coupling of venous and lymphatic systems which occurs during embryonic growth. A chronological staging scheme is used which proposes lymphaticovenous union as the initial morphological differentiating event. The precise origin of the characteristic spindle cells in the developing lesion remains unclear, although convergent differentiation of lymphatic and blood vascular endothelium may be considered. Alteration of the microcirculation, particularly that distal to the capillary bed, may explain several of the histopathological and haemodynamic features of Kaposi's sarcoma, including lesional thrombosis and infarction, tissue haemorrhage, vascular dilatation, cavernous pseudoangiomas and acute right-sided heart failure.

Adult↗

Malignant mixed mesodermal tumor of the ovary: a report of 22 cases.

Clinicopathologic data are presented for 22 cases of malignant mixed mesodermal tumors of the ovary of both homologous and heterologous types. The results substantiate previous reports of low parity in the almost exclusively postmenopausal women with this tumor. Symptoms were the same as for ovarian malignancy in general. More than half the patients presented with stage III or IV disease, according to the International Federation of Gynecology and Obstetrics (FIGO) classification. Only four (19%) of 21 patients were alive at 18 months and had survived from three to more than 13 years. Their survival was associated strictly with stage I or II disease and with the purely homologous stromal pattern. Two tumors were contiguous with remnants of ovarian endometriosis. Differentiated malignant epithelium was most often of the serous/endometrioid type, frequently with squamous zones, and was of the mucinous type in only one case. Whereas spindle cell stroma was present in many tumors of both stromal types, atypical cartilage was the predominant heterologous element.

Adult↗

Abnormal B-cell proliferation associated with combined immunodeficiency, cytomegalovirus, and cultured thymus grafts.

A male infant in whom multiple recurrent multiorgan infections developed during the first six months of life was found to have combined immunodeficiency. Progressive pulmonary disease developed at age two years; cytomegalovirus (CMV) was isolated from the respiratory tract and urine. Three separate intramuscular grafts of cultured thymus fragments did not produce change in the course of the illness. Soon after age three years, IgG lambda appeared in the serum as an M-component. The patient died at age three and one-half years, with respiratory insufficiency due to pulmonary fibrosis. At autopsy, a malignant plasma cell infiltrate was limited to the retroperitoneum. The infiltrate replaced lymph node structures and surrounded nerve fascicles, which appeared necrotic, and contained CMV inclusions in ganglion cell nuclei. The plasma cells showed strong monoclonal staining for IgG lambda. Also noted was positive staining for J-chain, which has been reported previously in malignant plasma cells producing IgG. CMV could be responsible for abnormal B-cell proliferation in patients with defective immunoregulation who receive immunotherapy, as in lymphoid abnormalities associated with Epstein-Barr virus.

B-Lymphocytes↗

Ovarian malignant mixed mesodermal tumor: the occurrence of hyaline droplets containing alpha 1-antitrypsin.

Twenty-one of 22 cases of malignant mixed mesodermal tumor (including carcinosarcoma) of the ovary were found to contain periodic acid-Schiff(PAS)-positive, diastase-resistant hyaline droplets ranging in diameter from less than 1 micrometer to approximately 50 micrometers. Droplets were located both inside and outside undifferentiated mesenchymal cells, predominantly within myxomatous areas. In 13 cases, droplets also occurred in epithelial structures, including areas mimicking ovarian carcinoma. Immunoperoxidase staining for alpha-fetoprotein was consistently negative, but droplets and cell cytoplasm reacted strongly with anti-alpha 1-antitrypsin. Analysis of the structure of droplet antitrypsin may be necessary to determine the origin of the droplets themselves and the possible usefulness of serum alpha 1- antitrypsin as a tumor marker in ovarian carcinoma and malignant mixed mesodermal tumor.

Adult↗

Alpha-1-antitrypsin in a malignant mixed mesodermal tumor of the ovary.

A malignant mixed mesodermal tumor of the ovary was found to contain multitudinous clusters of eosinophilic hyaline globules in both its epithelial and mesenchymal components. These periodic acid-Schiff-positive, diastase-resistant globules revealed typical positive ring-like staining for alpha-1-antitrypsin (AAT) using an indirect immunoperoxidase technique. Similar findings have previously been reported in certain germ cell and liver tumors and hepatocytes of patients bearing the Z-allele for AAT. The globules also stained with antisera against kappa and lambda immunoglobulin light chains, indicating the presence of surface immunoglobulin. In the electron microscope, the inclusions appeared granular and may have been derived from flocculent material in the dilated rough endoplasmic reticulum. These observations suggest a structural change in the tumor AAT analogous to that proposed for hereditary AAT deficiency. As a histogenetic marker, the presence of AAT in both epithelial and stromal cells suggests their origin from a common precursor cell.U

Female↗

Senile plaques and tangles in dialysis dementia.

The brains of 7 patients treated with hemodialysis were studied. Four of these patients had the dialysis encephalopathy syndrome (DES). Senile plaques and or neurofibrillary tangles were found in 5 of the 7 cases, 3 with and 2 without DES. One case of each group had plaques to an extent compatible with that in Alzheimer's disease, though of a different distribution. Neurofibrillary tangles were generally sparse. Plaques and tangles, both containing paired helical filaments, are the principal changes in Alzheimer's disease. Aluminum has been implicated as a possible etiologic agent behind the paired helical filaments in Alzheimer's disease, where raised cerebral aluminum contents have been demonstrated. Aluminum is known to be increased in the central nervous system also in DES, most likely as a consequence of procedures in connection with the hemodialysis. The finding of neurofibrillary tangles and senile plaques in hemodialyzed patients, some of which have developed DES, may therefore support the theories concerning aluminum as an etiological agent for cerebral changes in Alzheimer's disease.

Brain↗