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Biomedical subjects

F Guilhot

Publications and source records attributed to F Guilhot.

At least 127 records · Page 7Linked to original sources
PubMed1988

[Therapeutic leukapheresis in a leukostasis syndrome complicating chronic lymphoid leukemia].

A 50 year old man with chronic lymphocytic leukemia (CLL) and extreme hyperleukocytosis (600 x 10(9)/liter) presented with a respiratory distress syndrome, congestive heart failure with cardiomegaly, endotoxic shock and anuria. Examination revealed nodes in all areas and hepatosplenomegaly; laboratory studies showed hypoxemia and a chest X-ray diffuse bilateral alveolar infiltrates. He was treated twice by leukapheresis using a cell separator. This procedure removed 10.1 x 10(10) white blood cells with marked clinical improvement and resolution of air-space diseases over the subsequent 48 hours. Despite this unusual indication for leukapheresis in CLL, this procedure may be of value in treating the leukemic phase of CLL with pulmonary leukostasis.

Humans↗
PubMed1988

[Acute leukemia with translocation (8;16)].

Three cases of M5 acute leukemia, 1 with a t(8;16)(p11;p13), 2 with variant translocations, both with a breakpoint at band 8p11, t(6;8)(q27;p11) and t(8;19)(p11;q13) are reported and 12 other published cases reviewed. This is a rare new entity, of variable but rather poor prognosis, seen from birth to 75 years of age, with several cases in infants. Leukemic cells, which often show conspicuous phagocytic activity on bone marrow smears, bear both monocytic and granulocytic markers in at least some cases. The best therapeutic regimen is not well-defined. The molecular basis of the disorder remains to be elucidated.

Adult↗
PubMed1988

Malignant histiocytosis: a specific t(2;5)(p23;q35) translocation? Review of the literature.

In this paper, the investigators report a well documented case of malignant histiocytosis (MH) with a t(2;5)(p23;q35) translocation. A breakpoint in 5q35 appears to be specific, either for the disease or for a subclass of the disease. Additional cases of MH with cytogenetics are needed. This will help to determine if one class of MH or several subclasses can be defined by cytogenetic anomaly(ies).

Adolescent↗
PubMed1987

[Rearrangement of the short arm of chromosome 12 in chronic myelomonocytic leukemias].

A rearrangement of the short arm of chromosome #12 with a breakpoint at band 12 was found in 4 out of 15 patients with CMML: two deletions, one simple translocation (9;12)(p21;p12) and one complex t(11;12;13)(p11;p12;q21). Their haematological and clinical characteristics were investigated together with those of 5 other similar published cases. Although this alteration is not very frequent in this myelodysplastic syndrome, and is also found in various other malignant blood disorders, it is clearly a non-random phenomenon, the consequences of which are discussed.

Chromosome Aberrations↗
PubMed1985

Agar human T cell colony growth promoted by a B + null cell-derived lymphokine distinct from IL 2.

Human T cell agar colonies can be grown under PHA stimulation from either mature T cells or their E rosette-negative (E-), OKT3- peripheral blood and bone marrow precursors. Colonies comprise a majority of mature E+, OKT3+ cells and a minor (5 to 10%) population of immature E-, T3-, T8-, T4-, DR+, T10+, RFB1+ cells, which upon replating in subculture, can generate secondary colonies of OKT3+, E+, OKT4+, OKT8+ cells. Secondary colony formation can serve as a test for growth requirement of colony precursors, because it depends on the presence of both PHA and a colony-promoting activity (CPA) recovered in PHA-stimulated B + null or T + adherent cell supernatants. CPA production by B + null cells was not affected by their treatment with OKT3 or D66 (T11-like) monoclonal antibodies (MAB) + complement but was abolished by an anti-HLA-DR MAB + complement. However, B cells sorted by panning with the same anti-HLA-DR MAB did not release CPA, demonstrating the requirement of both B cells and null cells for CPA production. Neither IL 2 nor IL 1 could account for B + null cell-derived CPA.

B-Lymphocytes↗
PubMed1984

Self-renewal and maturation of immature T-cell progenitors within PHA-induced agar T-cell colonies.

T-cell colonies derived from peripheral blood mononuclear cells plated in agar with phytohemagglutinin (PHA) contain about 5-7% E-, OKT3-, OKT6-, TdT-, SIg- cells phenotypically similar to bone marrow precursors since they are also RFB1+, OKT10+, HLA-DR+, and PNA+. These cells can generate secondary E+, OKT3+ T-cell colonies when replated in the presence of both PHA and a colony-promoting activity distinct from the T-cell growth factor, Interleukin 2. These observations suggest that E-, OKT3- cells detected in primary PHA-induced T-cell colonies belong to a pool of prethymic cells which are able to mature into T-lymphocytes of T4 and T8 type in the absence of the thymic microenvironment.

Clone Cells↗
PubMedDate not supplied

Acral erythema in children receiving high-dose methotrexate.

Scant information is available concerning the occurrence and evolution of chemotherapy-induced acral erythema in children receiving intravenous high-dose methotrexate (MTX). Among 50 children with acute lymphoblastic leukemia or lymphoblastic lymphoma receiving a total of 203 courses of high-dose MTX (3-8 g/m2), 3 cases of acral erythema were observed. Painful erythema of finger and toe pads was noted in three children 3 days to 2 weeks after MTX infusion. The lesions resolved completely after blister formation and desquamation. These patients subsequently received high-dose MTX therapy without cutaneous problems. The present work points out that the chemotherapeutic schedule need not be modified in selected patients who develop acral erythema following high-dose MTX infusion.

Adolescent↗
PubMedDate not supplied

Recurrence of childhood acute lymphoblastic leukemia presenting as a tumor of the middle ear: a case report.

PURPOSE: Extramedullary relapse of childhood acute lymphoblastic leukemia most commonly occurs in the central nervous system or in the testes. Otologic involvement is very rare and has only been reported as an autopsy finding. PATIENT AND METHODS: We describe the case of a 5-year-old girl with CD10 positive acute lymphoblastic leukemia (ALL) who developed an isolated otologic relapse 18 months after the initial diagnosis of ALL. RESULTS: This otologic relapse presented as an atypical otitis media related to a mass of the middle ear. The leukemic infiltration of the middle ear was demonstrated by histologic examination. A cytogenetic change characterized by the occurrence of t(1;19)(q23;p13) was observed in the leukemic cells from the middle ear, and the t(1;19) molecular fusion transcript E2A-PBX1 was detected in the bone marrow by polymerase chain reaction. CONCLUSION: The ear is an exceedingly rare site of relapse in children with acute lymphoblastic leukemia. Molecular analysis demonstrates that such an extramedullary relapse can represent an early manifestation of systemic relapse.

Child, Preschool↗
PubMedDate not supplied

Persistence of transcriptionally silent BCR-ABL rearrangements in chronic myeloid leukemia patients in sustained complete cytogenetic remission.

Persistence of BCR-ABL rearrangements was demonstrated by D-FISH technique in chronic myeloid leukemia (CML) patients in complete cytogenetic response (CCR) after allogeneic bone marrow transplantation (BMT) or interferon-alpha therapy (IFN-alpha). Samples from bone marrow aspirate or peripheral blood or both were analyzed by conventional cytogenetics, Southern blot, fluorescent interphase in situ hybridization (FISH), and quantitative reverse transcription polymerase chain reaction (Q-RT-PCR). In all patients, FISH detected 1% to 12% nuclei with a BCR-ABL fusion gene, whereas Q-RT-PCR were negative or weakly positive. Based on these results, we hypothesize that the BCR-ABL genomic rearrangement remains unexpressed in a small percentage of cells whatever the treatment (IFN-alpha or BMT), and this in spite of the negativity of the RT-PCR-based classical molecular remission criterion. These data corroborate those obtained by other investigators and point to the need for follow-up of CML patients in CCR over an extensive period, at the DNA level to evaluate the residual disease and at the RNA level (Q-RT-PCR) to estimate the risk of relapse and guide the therapeutic decision. Experimental models suggesting the persistence of positive BCR-ABL cells are discussed and tentative explanations of tumor "dormancy" are proposed.

Chromosomes, Human, Pair 22↗