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At least 613 records · Page 34Linked to original sources
PubMed1993

Chromosome abnormalities in bone marrow of Fanconi anemia patients.

We report the clonal chromosome abnormalities of five patients with Fanconi anemia (FA). In one with myelodysplastic syndrome (MDS), an abnormal clone was present in the bone marrow (BM): 47,XY,trp(1)(q32q44), + mar. Two had acute myeloblastic leukemia (AML), one with monosomy 7 and the other with 46,XY,add(1)(p34),del(7)(p13). In the two others without signs of MDS or AML, pseudodiploidy with 46,XX,-5, +8 and 46,XX, +5, -21 were present, respectively. The significance of these abnormalities is discussed.

Adult↗
PubMed1993

Translocation (8;13) and T-cell lymphoma. A case report.

A patient with a myeloproliferative disorder is described with an eosinophilia together with T-cell lymphoma. A unique translocation t(8;13)(p11.2;q12) was present in all bone marrow cells examined at presentation. No evidence of this translocation was found in a peripheral blood lymphocyte culture. Chromosome analysis after 9 months revealed this same translocation as well as an extra chromosome 21 in all cells; 4.5% of cells also had an additional chromosome 9. The morphologic diagnosis at this stage was chronic myelomonocytic leukemia. Immunophenotyping 3 months later was consistent with a stem-cell leukemia.

Bone Marrow↗
PubMed1993

Translocation (12;14)(q13;q32) in myelodysplastic syndrome.

We report a patient diagnosed with refractory anemia with excess blasts in transformation (RAEB-t) who underwent an evolution to a nonlymphocytic acute leukemia (ANLL-M5a). Initial cytogenetic study showed a diploid karyotype; however, when ANLL-M5a was diagnosed, the bone marrow (BM) cells showed a t(12;14)(q13;q32), which to our knowledge has not been described previously in a myelodysplastic syndrome (MDS).

Anemia, Refractory, with Excess of Blasts↗
PubMed1993

t(8;21) prior to acute leukemia.

A t(8;21)(q22;q22) without blood and bone marrow invasion by immature myeloid precursor cells occurred in a patient previously treated for polycythemia vera. The presence of a molecular rearrangement confirmed that the chromosomal abnormality was identical to that observed in acute leukemia with t(8;21). This case shows that the translocation, t(8;21), may occur in myelodysplasia and suggests that it can precede the appearance of overt leukemia.

Chromosomes, Human, Pair 21↗
PubMed1993

5q- anomaly preceding acute myeloblastic leukemia with 53 chromosomes without chromosome 5 abnormality.

Partial deletion of the long arm of chromosome 5 (5q-) was found in a patient with a myeloid disorder. After treatment, hematologic parameters became normal, but acute myeloblastic leukemia occurred after 58 months. At that time, cytogenetic studies showed the presence of an abnormal clone with 53 chromosomes and without 5q-. This exceptional case suggests that the 5q- abnormality may precede the occurrence of an acute leukemia in favoring the appearance of unrelated malignant clones.

Anemia↗
PubMed1983

Appearance of altered cell-surface fucosyl glycopeptides in concomitance with chromosomal alterations in the gross virus-infected pre-leukemic thymus of the rat.

The appearance of a class of fast-eluting cell-surface glycopeptides that are encountered almost exclusively in malignant and certain pre-malignant cells was monitored in the course of leukemogenesis in the thymus of rats injected at birth with Gross leukemia virus. The altered glycopeptides appeared as early as 15 days after virus injection, when the animals were still clinically healthy and no histological signs of the disease were present in the thymus. Their amount was further increased at 30 days, and reached a maximum in the fully developed lymphoma. The development of this early phenotypic marker of malignancy appeared to be concomitant with that of chromosomal anomalies in the thymus. Since these anomalies are non-random, the existence of a causal relationship between the glycopeptide change and the loss of specific chromosomes might be hypothesized.

AKR murine leukemia virus↗
PubMed1991

Reversal of multidrug resistance in HL-60 cells by verapamil and liposome-encapsulated doxorubicin.

The means of circumventing multidrug resistance was investigated in HL-60 and HL-60R (a drug resistance variant) cell lines. The HL-60R cell line was developed from the parent line by serial exposure to increasing concentrations of doxorubicin over a 4-month period. This drug resistant cell line expressed P-glycoprotein in its cell surface and is 80-fold more resistant than the parent cell line. Multidrug resistance, as evaluated by a cell cytotoxicity assay using doxorubicin, can be overcome by use of verapamil. Multidrug resistance can also be circumvented when doxorubicin is encapsulated in liposomes. The combination of verapamil and doxorubicin-encapsulated liposomes does enhance circumvention of multidrug resistance beyond the effect of each agent alone, implying a synergistic effect. The lipid composition of the liposomes does affect the rate of drug uptake but not the overall cytotoxic effect of doxorubicin. The synergistic reversal of multidrug resistance by doxorubicin-encapsulated liposomes and verapamil suggests a multifactorial basis for drug resistance in this cell line.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1985

Target cells and thymus microenvironment in the pathogenesis of thymic lymphomas in C57BL/Ka mice.

In C57BL/Ka mice, the induction of thymic lymphomas either by inoculation of radiation leukemia virus (RadLV) or by a split dose irradiation requires complex cellular events: Target cells are found among the population of thymic subcapsular blast cells, or, alternatively, of marrow or spleen prothymocytes; Progression of target cells to lymphoma growth requires a multi-step process, which occurs only within thymic microenvironment; Target cells are rapidly induced as "preleukemic" cells; After inoculation of RadLV, the initial events occur when target cells are in close association with cells of a specialized component of thymic epithelium, i.e., the so-called "nurse cells"; The leukemogenic agents induce damages to the thymic microenvironment itself; Lymphoma prevention by marrow grafting after irradiation results from mechanisms still unknown which inhibit the progression of "preleukemic" cells to neoplastic growth.

Animals↗
PubMed1995

Fanconi anaemia research: current status and prospects.

Fanconi anaemia (FA) is an autosomal recessive disease featuring diverse clinical symptoms in addition to chromosomal instability and hypersensitivity to crosslinking agents. The much increased risk of FA patients developing leukaemia and squamous cell carcinomas makes FA an important model disease for cancer predisposition. Studies documenting the characteristics of FA cells and their response to environmental toxins have failed thus far to disclose the basic cellular process that is primarily disturbed in FA cells. Complementation analysis suggests that mutations in at least four different genes can cause FA (complementation groups FA-A to FA-D). The cDNA for FA-C has been cloned and found to encode a novel protein that localises to the cytoplasmic compartment of cells. Even though the protein's function is still unknown at present, research has now reached the point from where rapid progress to a detailed understanding of this syndrome may be foreseen.

Child↗
PubMed2006

Cbf beta-SMMHC induces distinct abnormal myeloid progenitors able to develop acute myeloid leukemia.

The acute myeloid leukemia (AML)-associated CBF beta-SMMHC fusion protein impairs hematopoietic differentiation and predisposes to leukemic transformation. The mechanism of leukemia progression, however, is poorly understood. In this study, we report a conditional Cbfb-MYH11 knockin mouse model that develops AML with a median latency of 5 months. Cbf beta-SMMHC expression reduced the multilineage repopulation capacity of hematopoietic stem cells (HSCs) while maintaining their numbers under competitive conditions. The fusion protein induced abnormal myeloid progenitors (AMPs) with limited proliferative potential but leukemic predisposition similar to that of HSCs in transplanted mice. In addition, Cbf beta-SMMHC blocked megakaryocytic maturation at the CFU-Meg to megakaryocyte transition. These data show that a leukemia oncoprotein can inhibit differentiation and proliferation while not affecting the maintenance of long-term HSCs.

Acute Disease↗
PubMed2004

In utero origins of childhood leukaemia.

Chimaeric fusion genes derived by chromosome translocation are common molecular abnormalities in paediatric leukaemia and provide unique markers for the malignant clone. They have been especially informative in studies with twins concordant for leukaemia and in retrospective scrutiny of archived neonatal blood spots. These data have indicated that, in paediatric leukaemia, the majority of chromosome translocations arise in utero during foetal haemopoiesis. Chromosomal translocations and preleukaemic clones arise at a substantially higher frequency ( approximately 100x) before birth than the cumulative incidence or risk of disease, reflecting the requirement for complementary and secondary genetic events that occur postnatally. A consequence of the latter is a very variable and occasionally protracted postnatal latency of disease (1-15 years). These natural histories provide an important framework for consideration of key aetiological events in paediatric leukaemia.

Child↗
PubMed2004

Bone marrow stroma in childhood myelodysplastic syndrome: composition, ability to sustain hematopoiesis in vitro, and altered gene expression.

We studied bone marrow stromal cell cultures from patients with childhood myelodysplastic syndromes (MDS, refractory anemia with excess of blasts, RAEB) and from matched normal donors. Stromal cell monolayers were characterized as myofibroblasts by the expression of smooth muscle alpha-actin, collagen IV, laminin and fibronectin. When normal cord blood cells were plated onto myelodysplastic stromas, a pathologic cell differentiation was observed, indicating altered myelosupportive properties. cDNA array analysis showed that patient stromas expressed increased levels of thrombospondin-1, collagen-I alpha2-chain, osteoblast-specific factor-2 and osteonectin, indicating the presence of increased osteoblast content, as confirmed by enhanced alkaline phosphatase synthesis. Alterations in the myelodysplastic stroma environment might contribute to abnormal hematopoiesis in this pathology.

Actins↗
PubMed2005

Transcription factor expression in B-cell precursor-leukemia cell lines: preferential expression of T-bet.

A number of transcription factors (TFs) have been reported that play crucial roles in hematopoiesis. However, only little is known about how these factors are involved in the mechanisms of hematopoietic development and lineage commitment. To investigate the roles of TFs in human B-cell precursors (BCPs), the present study analyzed the expression of the following 16 hematopoietic TFs: AML1, C/EBPalpha, C/EBPbeta, C/EBPgamma, C/EBPepsilon, E2A, Ets-1, GATA-1, GATA-2, GATA-3, Ikaros, IRF-1, Pax5, PU.1, T-bet and TCF-1 in 30 human BCP-leukemia cell lines. All BCP-leukemia cell lines were found to be positive for the expression of AML1, C/EBPgamma, E2A, Ets-1, IRF-1, Pax5 and PU.1 at the mRNA level. The mRNA expression of C/EBPalpha, C/EBPbeta, C/EBPepsilon, GATA-2, Ikaros, T-bet and TCF-1 was detected in 2 to 29 of the cell lines. Eight BCP-cell lines showed positivity for the dominant negative Ikaros isoform Ik6, while others were positive for expression of Ik1, 2, 3 and 4. GATA-1 and GATA-3 were universally negative. The expression of C/EBPalpha, PU.1 and T-bet was positive at the protein level in five, 29 and four out of 30 BCP-cell lines, respectively. Cell lines were stimulated with interleukin (IL)-7 and/or interferon (IFN)-gamma to investigate the regulation of TF expression. T-bet was clearly induced in the two cell lines NALM-19 and NALM-29 after stimulation. C/EBPbeta and IRF-1 were up-regulated in both cell lines and TCF-1 was down-regulated in NALM-19. No significant changes were observed for the other 12 TFs. The present report could provide useful information in the study of the role of TFs on normal and malignant human BCPs.

Base Sequence↗