Multiple chromosomal aberrations have been reported in head and neck squamous cell carcinoma (HNSCC). But less information is available on specific patterns of chromosomal amplifications which distinguish different areas of head and neck tumors. To elucidate genetic mechanisms causing the aggressive growth and high proliferation of hypopharyngeal squamous cell carcinoma (SCC), we performed reverse chromosome painting (RCP) on a total of eight hypopharyngeal SCC including invasive carcinoma and preinvasive tissue. Five hypopharyngeal invasive carcinomas showed amplifications on chromosome 3q. Furthermore, we detected gains on chromosomes 11q and 6p. Compared to the histologically classified preinvasive tissues, we found amplified alterations on chromosome 6p, 11q and 12q, but none of them showed gains on chromosome 3q. This observed heterogeneity in hypopharyngeal SCC might reflect a specific role of chromosome 3q as a late event in the highly invasive capacity of these SCC.

Carcinoma, Squamous Cell↗

PubMedDate not supplied

[Cardiovascular polymorbidity as a function of psycho-organic status. A series of 904 pathological and neuropathological comparisons].

In the past decades, the recognition of polymorbidity as an important characteristic of geriatric medicine lead to important improvements in the multidisciplinary approach of the elderly. Coexistence of somatic and psychiatric diseases with various forms of etiopathogenic relations has been described early in this century. Dementia may be caused, aggravated, revealed or randomly accompanied by somatic diseases and inversely. However, very few attempts have been made in order to analyze the significance of these associations. This study is meant to give a better epidemiological knowledge of the relation between cardiovascular diseases and cerebral aging. This could lead to a better diagnostic approach and to a more complete physiopathological conception of dementia. 904 autopsy reports (patients who died between 1972 and 1986 in the Hôpital de Gériatrie of Genova) have been reviewed and classified in three groups according to neuropathological findings: 335 subjects with vascular encephalopathy of various types, 382 patients with degenerative diseases of Alzheimer type and 187 patients with normal brain. The subjects of these three groups had not all been considered demented. For each patient, age, sex, cause of death and 14 cardiovascular items have been appointed. The patients of the Alzheimer group died older and were more often women than those of the two other groups. The subjects of the vascular group died older than those of the normal group and were more often men than those of the two other groups. Stoke was considered to be the cause of death in 3% of the vascular patients whereas, by definition, it was absent from the two other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMedDate not supplied

Asymmetrical cerebral atrophy in Alzheimer's disease.

In most Alzheimer patients brain atrophy seems to be symmetrical. Recent neuropsychological and brain imaging investigations suggest, however, that in some patients one hemisphere is more severely affected from the onset of symptoms. We have observed four Alzheimer patients with grossly asymmetrical cerebral atrophy at autopsy, in whom the topography of the most severe atrophy was consistent with the earliest clinical signs of focal brain damage. In the three patients who at onset had relevant language disorders, atrophy of the brain was more severe in the association areas surrounding the left sylvian fissure. In the fourth patient, who first complained of visuospatial troubles, the right, nondominant hemisphere was more affected. These clinical and pathological findings suggest that association areas of one hemisphere were involved quite early in the evolution of the disease, conceivably at the same time as the hippocampus and related limbic structures. In these patients, a morphometric analysis of cortical changes in homologous areas of the cortex (area 22) was carried out in order to investigate the effect of the evolution of the disease upon cortical changes. This analysis showed that the numerical densities of nerve cells and tangle-bearing neurons were lower on the more atrophied side and suggested that the severity of cortical atrophy might have affected the size, but not the density, of senile plaques.

Aged↗

PubMedDate not supplied

[Huntington chorea. Anatomoclinical and genetic study of 17 cases].

Seventeen cases of Huntington's chorea have been studied on a clinical and anatomopathological basis. Fourteen genealogical trees have been established. Clinically, involuntary movements of choreic type and an impairment of higher brain functions are constant symptoms. Gait disorders, dysarthria and a tendinous hyperreflexia are usual (present in 95, 95 and 80% of cases). Anorexia, muscular hypotony and dysphagia are also frequent (present in 75, 60 and 50% of cases). The neuropathological examination shows macroscopically a neostriatal atrophy in 90% of cases and a cerebral cortical atrophy in 75%. Microscopically, a neuronal loss--mainly in small cells (Golgi II)--is evident in the neostriatum of all the cases. The pallidum is also affected, but to a lesser degree. A cortical cell loss is present in 90% of the cases, mainly in layers III, IV, V and sometimes also in layer VI of frontal and parietal lobes. In 75% of the cases, a cortical gliosis is noticed, mostly at the level of the frontal pole.

Adult↗