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Results for “BONE MARROW DISEASES”

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PubMed1994

Molecular evidence for minimal residual bone marrow disease in children with 'isolated' extra-medullary relapse of T-cell acute lymphoblastic leukemia.

Central nervous system (CNS) relapse confers a poor prognosis in children with acute lymphoblastic leukemia (ALL). It is uncertain whether morphologically undetectable leukemia is present in the bone marrow at the time of CNS relapse, or whether the CNS acts as a 'sanctuary' site to allow reseeding of the marrow at a later time. We examined DNA from bone marrow samples from six patients with T-cell ALL with isolated CNS relapse using sensitive polymerase chain reaction (PCR) assays to detect minimal residual disease. One of these PCR assays was based on amplification of leukemia-specific TCR-delta gene rearrangements, while the other assay relied upon detection of the c-tal deletion. In four patients, where bone marrow samples were taken at the time of CNS relapse, residual disease was detectable in every sample at a level below morphological detection. In addition, three patients had residual disease detected in their subsequent bone marrow when CNS disease was not evident. Our findings, although preliminary, suggest that relapse of leukemia in the CNS reflects resurgence of the disease in the bone marrow that is first detected clinically in the CNS. The concomitant molecular detection of bone marrow leukemia at time of 'isolated' CNS relapse in children with T-cell ALL explains subsequent bone marrow relapse in some of these children, and argues for intensive systemic therapy of these patients.

Adolescent↗
PubMed1991

Magnetic resonance imaging of disseminated bone marrow disease in patients treated for malignancy.

Magnetic resonance imaging (MRI) is a sensitive method for the diagnosis of bone marrow abnormalities, but its usefulness in detecting active disseminated cancer in this tissue in treated patients has not been determined. We therefore examined 14 children who had been treated for disseminated bone marrow involvement by neuroblastoma (n = 6), lymphoma (n = 3), Ewing's sarcoma (n = 3), osteosarcoma (n = 1), and leukemia (n = 1). MRI studies were performed at 21 marrow sites to evaluate residual or recurrent tumor and were correlated with histologic material from the same site. T1- and T2-weighted sequences were employed in 21 and 14 studies, respectively; short tau inversion recovery (STIR) in 18; and static gadolinium diethylene triamine pentaacetic acid (Gd-DPTA)-enhanced. T1-weighted sequences in 13. All MRI studies showed an altered bone marrow signal. Technetium 99m methylene diphosphonate (99mTc-MDP) bone scintigraphy was also performed (19 studies). On histologic examination, 7 marrow specimens contained tumor, and 14 did not. Of the 7 tumor-positive lesions, all T1-weighted, 4 of 6 T2-weighted, and all 6 STIR sequences showed abnormal signal; all 5 Gd-DTPA-enhanced. T1-weighted sequences showed enhancement of the lesion. However, abnormal signals were also observed on all T1-weighted, 6 of 8 T2-weighted, 11 of 12 STIR, and 5 of 8 Gd-DTPA-enhanced, T1-weighted images of the tumor-negative sites. In this clinical setting, MRI did not consistently differentiate changes associated with treatment from malignant disease.

Biopsy↗
PubMed2005

The faces of mast cell disease: bone marrow infiltrates in 3 patients with systemic mastocytosis.

The clinical spectrum of mast cell disease ranges from relatively innocuous and histologically subtle urticarial skin lesions to an aggressive and fatal leukemic form of mast cell proliferation. Not surprisingly, mast cell infiltrates may show significant microscopic heterogeneity, particularly in the bone marrow, the most common site of involvement in systemic mastocytosis (SM). Herein, 3 cases are presented to illustrate the clinical and morphologic heterogeneity of mast cell disease: the first patient, with long standing urticaria pigmentosa, developed anemia and thrombocytopenia; the second patient presented with a pathologic fracture; and the third patient was suspected to have refractory anemia. Upon bone marrow examination, all 3 patients showed mast cell infiltration with distinct morphologic features and all met the WHO criteria for aggressive systemic mastocytosis. Histochemical methods continue to play a role in the identification of mast cells, with some limitations depending on the degree of differentiation of the mast cells and tissue processing methods. Immunohistochemistry has contributed to the identification of mast cells. Coexpression of CD117 and CD25, as well as expression of the more specific immunohistochemical marker tryptase, is seen in systemic SM. The latter may also be employed as a serum marker in the diagnosis and follow-up of patients with SM. The mast cells, in the majority adults with SM, have somatic point mutations of KIT.

Aged↗
PubMed1997

Graft-vs.-host disease.

Bone marrow transplantation (BMT) is the treatment of choice for many leukemias, lymphomas, bone marrow failure syndromes, and immunodeficiency disorders, and is the primary and salvage therapy for many solid malignancies. With the establishment of national and international marrow banks, unrelated allogeneic BMT is being performed with increasing frequency. Graft-vs.-host disease (GVHD) remains a major complication of allogeneic BMT, occurring in 25% to 70% of patients despite GVHD prophylaxis, with the skin, gastro-intestinal tract, and liver as primary target organs. Oral findings are seen in both acute and chronic GVHD. In acute GVHD, the oral lesions are often painful, erythematous, ulcerative, and desquamative. In chronic GVHD, they are lichenoid with associated erythema and ulcerations; additionally, they may be associated with a sicca syndrome characterized by xerostomia and progressive salivary gland atrophy. General principles of BMT are discussed, as are systemic and local therapeutic options for oral GVHD.

Acute Disease↗
PubMed2005

Targeting an MMP-9-activated prodrug to multiple myeloma-diseased bone marrow: a proof of principle in the 5T33MM mouse model.

Multiple myeloma (MM) is an incurable B-cell cancer characterised by the monoclonal proliferation of tumour cells in the bone marrow (BM). It has been described that matrix metalloproteinases (MMPs) and especially MMP-9 is secreted by MM cells. In this study, we investigated the possibility to exploit MMP-9 activity to activate prodrugs and to target MM cells as a new tumour-specific therapy. Cleavage of the prodrug EV1-FITC by MMP-9 resulted in release of fluorescence which can be used as a measure of prodrug activation. The 5T33MM mouse model was used in this proof-of-principle study. The prodrug was activated in a higher amount by addition to MMP-9-producing 5T33MMvv cells, homogenates from tumour-bearing organs (BM, spleen) and isolated 5T33MM-diseased BM and spleen cells compared to non-MMP-9-producing 5T33MMvt cells and homogenates/cells from non-tumour-bearing organs/mice, as measured by fluorescence release. This fluorescence release could be inhibited by the MMP-2/MMP-9-specific inhibitor, CTT. Activation of the prodrug in the 5T33MM spleen and BM homogenates was confirmed by chromatography. EV1-fluorescein isothiocyanate injection into 5T33MM-diseased animals resulted in a higher fluorescence release by the isolated BM and spleen cells compared to injection into healthy animals. In conclusion, MMP-9 activity can be used to activate prodrugs that target MM.

Animals↗
PubMed1990

Bone marrow transplantation for genetic diseases.

Bone marrow transplantation is the treatment of choice for a number of genetic diseases. Recently, bone marrow transplantation has been increasingly used for erythroid disorders, such as thalassemia and sickle cell anemia. A number of inherited metabolic disorders (i.e., storage diseases, leukodystrophies, and the like) may be corrected with a marrow transplant. Successful correction of genetic diseases with allogeneic bone marrow transplantation lays the groundwork for the use of specific gene therapy.

Bone Marrow Transplantation↗
PubMed1987

Bone marrow diseases of the spine: differentiation with T1 and T2 relaxation times in MR imaging.

Forty-two patients underwent magnetic resonance (MR) imaging for a variety of lesions in the vertebral body. A 0.15-T MR system was employed. Twenty-six patients were found to have malignant metastatic lesions (group 1); 16 had nonneoplastic lesions (group 2). The ability to differentiate between the two groups with MR imaging was evaluated. With the longer spin-echo repetition time, the image was variable in both groups. All malignant metastatic lesions appeared as low-intensity areas on T1-weighted images, but 50% of the nonneoplastic lesions also appeared this way. The mean T1 for group 1 was longer than that for group 2, but not significantly so. However, there were significant differences in the ratios of T1 to T2 and of the T1 ratio to the T2 ratio (T1 ratio = T1 for affected vertebrae/T1 for normal vertebrae, T2 ratio = T2 for affected vertebrae/T2 for normal vertebrae). These ratios were therefore useful in distinguishing malignant metastatic from nonneoplastic lesions.

Adolescent↗
PubMed1987

[Results of bone marrow scintigraphy in hematological diseases].

Bone marrow scintigraphy was performed in 40 patients with haematological disorders (lymphomas, multiple myeloma, myeloid leukaemia, panmyelopathy and others). Routine skeletal scintigraphy was available for comparison in 18 patients. In agreement with the literature it became evident that marrow scintigraphy can show infiltrations of the bone marrow in haematological disorders earlier than skeletal scintigraphy. Hot lesions were caused by reactive proliferation of the bone marrow such as may occur with acute inflammatory joint diseases, osteomyelitis, fracture healing or other entities. Marrow imaging demonstrated reliably the actual distribution of the functioning bone marrow, a characteristic that is important for diagnosis and staging, especially in myeloproliferative diseases.

Bone Marrow↗
PubMed2005

Bone marrow abnormalities in HIV disease.

Bone marrow abnormalities are frequently observed in HIV infected individuals at all stages of the disease. The most common abnormal finding is dysplasia affecting one or more cell lines. Erythroid dysplasia is the most common type of dysplasia and is recognized in over 50% of HIV infected patients, abnormal granulocytic and megakaryocytic development is encountered in one-third of patients. Plasma cells are strikingly increased in bone marrow of HIV infected patients. It may represent a physiological response to antigenic stimulation by viruses, other infective agents or secondary to dysregulated B-cell proliferation due to HIV. Herein we present a review discussing the various bone marrow abnormalities associated with the HIV disease.

AIDS-Related Complex↗
PubMed1998

Bone marrow transplantation for autoimmune diseases.

Bone marrow transplantation (BMT) is now becoming a powerful strategy for the treatment of patients with autoimmune diseases. Using various animal models for autoimmune diseases, we have previously found that allogeneic BMT (not autologous BMT) can be used to treat autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), immune thrombocytic purpura, insulin-dependent diabetes mellitus (IDDM), chronic glomerulonephritis, and certain types of non-insulin-dependent diabetes mellitus. In contrast, we have found that the transplantation of T-cell-depleted bone marrow cells or partially purified hemopoietic stem cells (HSCs) from autoimmune-prone mice to normal mice leads to the induction of autoimmune diseases in the recipients. These findings have recently been confirmed even in humans; autoimmune diseases such as RA, SLE, multiple sclerosis, and Crohn's disease were resolved after allogeneic BMT. However, there have recently been reports on the rapid recurrence or persistence of autoimmune diseases after autologous BMT. Conversely, the adoptive transfer of autoimmune diseases such as myasthenia gravis, IDDM and Graves' disease by allogeneic BMT from donors to recipients has been reported. Based on these findings, we have proposed that autoimmune disease is 'a stem cell disorder'. To clarify the differences between normal and abnormal HSCs, we have established a new method for purifying HSCs. Using this method, we purified HSCs from normal and autoimmune-prone mice and compared the former with the latter. We have found that a major histocompatibility complex (MHC) restriction exists between normal HSCs and stromal cells, whereas there is no MHC restriction between abnormal HSCs and stromal cells either in vivo or in vitro; abnormal HSCs proliferate even in allogeneic environments. Abnormal HSCs thus appear to be more resilient than normal HSCs. In humans, BMT across MHC barriers has had a low success rate as a consequence of (1) graft-versus-host disease (GVHD), (2) graft rejection and (3) incomplete recovery of T cell functions. However, we have found that such problems can be overcome in mice. GVHD can be prevented if T-cell-depleted bone marrow cells are used. Graft rejection can be prevented by bone grafts to recruit donor stromal cells, since, as we have found, an MHC restriction exists between HSCs and stromal cells. In addition, we have found that stromal cells migrate from the bone marrow to the thymus, where they become engaged in positive selection. Therefore, the bone grafting to recruit donor stromal cells leads to a complete recovery of T cell functions, since T cells, which are positively selected by donor stromal cells in the thymus, can cooperate with donor B cells and antigen-presenting cells. In humans, it is well known that the success rate of BMT in patients more than 45 years old is low. Recently, we have found that the low success rate is due to the aging of the thymus, and that BMT plus embryonal thymus grafts can be used to treat late-onset autoimmune diseases in MRL/+ mice. Based on these findings, we would like to suggest that the transplantation of the embryonal thymus in conjunction with BMT will become a valuable strategy for treating older patients with various intractable diseases, including autoimmune diseases. We believe that similar conditions (to permit successful allogeneic BMT) to those in mice will be realized in humans in the near future.

Animals↗