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M Sanson

Publications and source records attributed to M Sanson.

63 records · Page 4Linked to original sources
PubMed1992

Allelic loss on chromosome 22 correlates with histopathological predictors of recurrence of meningiomas.

Meningiomas are common tumors of the nervous system. Although usually benign, they may exhibit variable degrees of aggressiveness. Their probability of recurrence after subtotal resection has been correlated with several histological parameters. Independently, a loss of chromosome 22, as evidenced either by cytogenetics or by somatic loss of alleles, has been observed in about half of the cases studied. In 34 meningiomas we have examined the relationship between loss of chromosome 22 alleles and 6 histological predictors of recurrence. Significant correlations were found for 3 of these, i.e. prominent nucleoli (p less than 0.002), microscope count of mitoses (p less than 0.05) and nuclear pleomorphism (p less than 0.02). Correlation with the other 3, i.e. sheeting of cells, vascularity and micronecrosis, did not reach significance. Total tumor score, defined by the sum of the individual scores for these 6 parameters, was strongly correlated to allelic loss (p less than 0.0001). Thus, the loss of chromosome 22 alleles, which possibly contribute to the inactivation of tumor-suppressor gene(s), might be a potent genetic marker of the aggressiveness of meningiomas.

Aneuploidy↗
PubMed1992

[Selective sensitivity of cysts to praziquantel and albendazole in a case of cerebral cysticercosis].

A case of neurocysticercosis in a Zaïrian patient with clinical and neuro-radiological follow-up is reported. Treatment with praziquantel resulted in the regression of only some of the cysts. Subsequent treatment with albendazole was effective, eliminating most of the remaining lesions. This case illustrates a selective sensitivity of cysts to praziquantel and albendazole in a single patient.

Adult↗
PubMed1991

Parental origin of chromosome 22 loss in sporadic and NF2 neuromas.

It has recently been proposed that the maternally derived chromosome might be preferentially lost in nonfamilial cases of embryonal or early onset malignant tumors. This observation pointed to a potential role of the parental imprinting of the genome during gametogenesis which would be at least partly maintained in the somatic cells. Neuromas are benign tumors that develop from Schwann cells. They occur either sporadically or in individuals that have a genetic predisposition due to neurofibromatosis type 2 (NF2) and usually are multiple. Regardless of the context of occurrence, in approximately 40% of the investigated cases a loss of a chromosome 22 has been documented either by karyotype analysis or by monitoring somatic loss of heterozygosity. We have now examined the parental origin of the chromosome 22 lost in 19 cases of neuromas of patients with unaffected parents among which 11 were non-NF2 patients (sporadic and unique neuroma) and 8 were NF2 patients (bilateral acoustic or multiple neuromas). In both sets of tumors, the lost chromosome 22 can be of either parental origin. A close to threefold preference for the loss of the maternally derived chromosome was observed and should be either confirmed or disproved by studying a larger number of patients.

Adult↗
PubMed1989

[Immunohistochemistry of epidermal growth factor receptors in human meningioma].

EGF receptors were assayed by immunohistochemistry using a monoclonal antibody against EGF-R in 32 surgical samples of meningioma. EGF-R were found in all samples (32/32). Only tumor cells were stained and staining was homogenous in tumor tissue. EGF-R was simultaneously assayed by 125I-EGF binding on membrane preparation and immunohistochemistry on frozen sections in 10 meningiomas. Results were qualitatively equivalent in 9 cases. Staining intensity was not correlated with the histological type, the proliferative status of the tumor or the age and hormonal status of the patients. The immunohistochemical data are in agreement with previous biochemical assays on tissue homogenates.

ErbB Receptors↗
PubMed1988

[Benign intracranial hypertension and minocycline].

A 19 year-old woman complained of headache and nausea occurring while she was taking minocycline for acne. Examination showed bilateral papilloedema and a bilateral VIth nerve palsy. Symptoms and signs rapidly resolved after the drug was stopped. Benign intracranial hypertension due to tetracyclines is well known in infants. It is rare in adults. Its pathophysiology remains unknown. The role of vitamin A is inconsistent. Others biological factors or personal susceptibility could be involved.

Acne Vulgaris↗
PubMed1988

[Benign cerebral angiopathies and phenylpropanolamine].

Heroin, cocaine, amphetamines, sympathomimetic drugs can cause cerebral angiopathy. We report 2 patients with cerebrovascular disorders after ingestion of a nasal vasoconstrictor containing phenylpropanolamine (P.P.A.). The first patient had two acute repetitive attacks of severe headache and vomiting, occurring after a daily treatment with 180 mg of P.P.A. during 6 weeks. The second patient had an intracerebral hemorrhage, occurring some hours after taking for the first time 120 mg of P.P.A. In both cases, cerebral angiography, performed in the next week, demonstrated segmental narrowing and dilatations of medium-size intracranial arteries. None of the usual causes of cerebral vasculitis were present. The outcome was favorable and follow-up angiograms showed the disappearance of the beading pattern. P.P.A. is widely used over the counter in diet pills and stimulants. Cerebral vascular complications have been rarely reported, always hemorrhagic and often associated with cerebral vasculitis. They are unrelated to duration or dosage of treatment. The mechanism is unclear but could result from several factors: chronic or paroxystic high blood pressure, immuno-allergic vasculitis, arterial spasm, direct "toxic" effect of the P.P.A. on the arterial wall may be increased by other drugs and caffeine.

Adult↗