Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dynamics of serum ferritin levels was studied in 87 adult patients with varying forms of acute leukemia at different stages of the disease development (the first attack, complete and non-complete remission, the first and second relapse, terminal stage). A direct correlation has been established between ferritin concentration and the disease course phase. It has been shown that ferritin is a universal criterion for the evaluation of leukemia process activity useful for all forms of acute leukemia: lymphoblastic, non-lymphoblastic and low-percent.
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PMID:[Dynamics of serum ferritin level at various points in the course of acute leukemia]. 177 84

Serum ferritin concentration was studied in 136 patients with different types of acute leukemia. Pretreatment serum ferritin concentrations in the immature myeloblastic leukemia (M1 and M2 of the FAB-classification of acute leukemias) was found to be highly increased compared to the more mature types of acute myeloblastic leukemias (M3 to M5) and the acute lymphoblastic leukemias (L1 to L3). Investigation of the intracellular ferritin concentration showed, that the serum ferritin levels paralleled the intracellular ferritin concentration within the leukemic blasts. Within the immature myeloic blasts (M1) the intracellular ferritin concentration was 14-fold increased compared to normal granulocytes. This correlated with the 17-fold increased serum ferritin levels in these patients. Intracellular ferritin concentrations within the leukemic blasts of more mature types of acute leukemia (M3 to M5) were found to be only slightly increased. These data support the concept, that an increased synthesis and release of ferritin by the leukemic blasts is responsible for the increased serum ferritin concentration. This concept is also supported by the observation, that a further increase of serum ferritin concentration was seen during a cytotoxic chemotherapy. It is noteworthy, that this increase was more pronounced in the immature leukemias obviously caused by a loss of intracellular ferritin from the damaged leukemic blasts. The serum ferritin levels followed closely the activity of the disease. Increased pretreatment serum ferritin concentrations normalized completely when patients achieved complete remission. In contrast, in patients with tumor relapse or tumor progression serum ferritin concentrations increased again. These data suggest that the serum ferritin in immature myeloblastic leukemia has the characteristics of a tumor associated marker.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ferritin in acute leukemia. Serum ferritin concentration as a nonspecific tumor marker for M1 and M2 myeloid leukemia]. 188 10

The patient is 11-year-old girl who was diagnosed as having hybrid acute leukemia (myeloid and lymphoid) from morphological (cytochemistry) findings, immunophenotype and genotype. During reinduction therapy after a second relapse, she presented hepatosplenomegaly and the remittent fever unresponsive to the intensified antibiotics. The diagnosis of reactive histiocytosis was made because of the remarkable elevation of serum ferritin value and proliferation of mature histiocytes in the bone marrow. Treatment with etoposide resulted in the disappearance of her fever and other symptoms. The subsequent refractoriness to platelet transfusion was also overcome by etoposide (p.o.) therapy. The results suggested that the treatment with etoposide might be effective for reactive histiocytosis and the related refractory state to platelet transfusion during therapy for leukemia.
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PMID:[Effectiveness of etoposide on reactive histiocytosis and refractory state to platelet transfusion during therapy of leukemia: case report]. 194 43

Serum ferritin level has been shown by many investigators to be a good indicator of bone marrow iron stores in normal subjects. Although this correlation may hold in some pathological situations, it is lost in others. In leukemia a dissociation has been observed between serum ferritin levels and bone marrow iron stores. Leukemic cells were demonstrated to contain high levels of ferritin and to secrete it in the serum, causing this dissociation. In this study we investigated the possibility of having an analogous situation in patients on chronic hemodialysis. The latter patients have normal or high ferritin levels irrespective of bone marrow iron stores. Our results show that blood neutrophils and lymphocytes do not contribute to the high serum ferritin levels in these patients. Ferritin level in blood monocytes, however, was found to correlate with the serum ferritin levels and bone marrow iron stores in dialysis patients. Hence we concluded that sources other than blood leukocytes must be contributing to the high serum ferritin level in these patients. On the other hand, to unravel the role played in these changes by the monocytic cell population requires dynamic studies.
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PMID:Blood leukocyte contribution to serum ferritin levels in patients on chronic hemodialysis. 202 Mar 40

Using Prolifigen TK kit "Daiichi", the serum TK level were determined in patients with adult T-cell leukemia (ATL) and its related disorders. The mean level of serum TK at diagnosis was 279.9 U/l in acute type ATL, 27.8 U/l in chronic type ATL, 59.0 U/l in lymphoma type ATL, 3.1 U/l in pre-ATL and 2.4 U/l in HTLV-I carriers. In these patients, six other kinds of tumor markers such as lactic dehydrogenase, beta 2-microglobulin, immunosuppressive acidic protein, ferritin, tissue polypeptide antigen and carcinoembryonic antigen were also examined. Among the seven tumor markers, TK level showed the most significant difference among clinical subtypes of ATL. This indicates that the TK level is one of the promising parameters indicative of aggressiveness of ATL cells.
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PMID:[Serum deoxythymidine kinase in adult T-cell leukemia and its related disorders]. 228 66

In four patients with trisomy 21 (three constitutional, one acquired) with a morphological undifferentiated leukemia, diagnosis of erythroid leukemia was established by both immunophenotyping and ultrastructural studies. Indeed, a majority of blasts from three patients expressed several erythroid markers such as carbonic anhydrase 1, spectrin beta chain, and glycophorin A. In addition, band 3 and hemoglobin were immunologically detected in a fraction of the blast cells from two cases. At ultrastructural level, a majority or all blast cells exhibited erythroid differentiation features such as theta granules and ferritin molecules. However, platelet glycoproteins GP Ib, GP IIb, and GP IIIa were also immunologically detected in a fraction (from 14-82%) of the blasts. Since the ultrastructural study indicated that some promegakaryoblasts were also present in three patients, double labeling between erythroid markers (glycophorin A or carbonic anhydrase I) and platelet glycoprotein (Ib or IIIa) was performed and showed a clear overlap between the two kinds of markers. A similar approach was performed at ultrastructural level and indicated that blast cells with ultrastructural erythroid features of differentiation may have three distinct phenotypes, i.e., presence of glycophorin A without platelet glycoproteins or, conversely, the presence of platelet glycoproteins without glycophorin A and coexpression of glycophorin A and platelet glycoproteins. Expression of glycophorin A correlated directly with the differentiation level of the erythroid blasts, whereas platelet glycoproteins were essentially expressed in the more primitive leukemic erythroid cells. The GP Ib synthesized by these blasts was subsequently studied. The GP Ib alpha mRNA analyzed by Northern blot from these erythroid cells was identical in size with that from megakaryocytic cells as was the molecular weight of the GP Ib molecule from both after immunoprecipitation by a monoclonal antibody. Therefore, "in vivo" erythroid leukemic cells may express the main platelet glycoproteins including GP Ib.
Leukemia 1989 Sep
PMID:Expression of platelet glycoproteins by erythroid blasts in four cases of trisomy 21. 252 26

Ultrastructural and ultracytochemical studies were performed on blast cells from 12 Down's syndrome neonates with transient myeloproliferative disorder (TMD) and 13 Down's syndrome patients with megakaryoblastic leukaemia (MKL), in order to clarify the cytological characteristics of these cells. Average platelet peroxidase-positivity in blast cells of TMD patients was similar to that found in cases of MKL. Blast cells from subjects with TMD contained a number of different granules, namely, alpha granules, those that were myeloperoxidase (MPO)-positive, electron-lucent or basophil-like, and those containing membrane components or ferritin particles. On the other hand, granules found in the blast cells of MKL patients with Down's syndrome included the electron-lucent variety, those with membrane components and a few that were basophil-like, but not alpha and MPO-positive granules nor those containing ferritin particles. A demarcation membrane system was observed in blasts from the TMD group, but not in the MKL group. These findings suggest that blast cells in TMD patients differentiate to megakaryocytes, neutrophils, basphils and erythroblasts, while those in cases of MKL show limited differentiation to immature megakaryocytes, erythroblasts and, sometime, basophils. Such results correspond well with those of culture studies, in which TMD blasts were found to be precursors of various types of blood cells.
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PMID:Ultrastructural and ultracytochemical differences between transient myeloproliferative disorder and megakaryoblastic leukaemia in Down's syndrome. 253 35

Diagnosis of megakaryoblastic and early erythroid leukemia requires the use of differentiation markers that in most cases permit their precise diagnosis. In some cases, their use can be misleading. Here we report and discuss some examples. A platelet peroxidase (PPO) activity is detected in most cases of early erythroid leukemias as well as in the CFU-E-like cells of normal marrow, thus providing evidence that PPO activity must be studied along with other (immunologic or ultrastructural) markers to permit a reliable diagnosis of megakaryoblastic leukemia. Ferritin molecules an erythroid marker, could be detected as a cluster at ultrastructural level in leukemic platelets and in micromegakaryocytes of one patient. However, in blasts of the erythroid lineage, ferritin molecules are also either dispersed in the cytoplasm or localized in theta granules. Immunologic markers have also their own limit. Indeed, in one patient, GB IIb and IIIa were detected on erythroid blasts, resulting in a phenotype very similar to HEL cells. Carbonic anhydrase (CA) I, an early erythroid marker, was detected in the platelets of four leukemic patients and was present along with an increased expression of CA II. This study emphasizes the fact that precise diagnosis of leukemia cannot be performed with a single marker of differentiation, but requires the simultaneous use of several lineage restricted markers.
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PMID:Limits of phenotypic markers for the diagnosis of megakaryoblastic leukemia. 264 84

Serum and CSF ferritin were estimated in 35 consecutive patients of acute leukaemia at the time of admission and on induction of remission. Serum ferritin levels were significantly raised in 94 per cent patients of acute leukaemia. The mean (+/- SD) serum ferritin (314.36 +/- 158.4 micrograms/1) was significantly higher when compared with control values (P less than 0.001). Remission induction resulted in significant fall in serum ferritin values to a mean of 149 (+/- 98.7) micrograms/l (P less than 0.05). Serum ferritin is thus of value in assessing the state of remission and is a sensitive indicator of the leukaemic cell mass and the state of activity of the disease. CSF ferritin levels in acute leukaemia were comparable to normal control values. CSF ferritin did not reflect CNS involvement in acute leukaemia and therefore its value as a tumour marker of CNS infiltration is doubtful.
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PMID:Serum & cerebrospinal fluid ferritin levels in children with acute leukaemia. 276 45

We have examined the efficacy of various drugs in 44 patients with MDS and found the different effectiveness which depends on the type of MDS. Namely, RA appears to respond to steroid hormone, androgen, and/or vitamin D3, regardless of single or combined use. In particular, it is obvious in androgen, and as our previous reports, high content of acidic ferritin in RBC with RA have changed to more basic ones by treatment with androgen. On the contrary, these drugs were not effective on RAEB, RAEB-T, and CMML. A long-term observation is needed to determine whether the prolonged or decreased occurrence of leukemia could be obtained in the effective cases with RA. Most of the cases who did not develop overt leukemia during this study died of bleeding or infections due to thrombocytopenia or leukocytopenia, thus indicating that supportive therapies are important in patients with MDS. Since it has recently been reported that recombinant G-CSF or GM-CSF is helpful to increase the number of leucocyte and to enhance their functional recovery in MDS, these factors may be powerful agents against infections when they are carefully used with regard to the activation of leukemic clones.
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PMID:[Therapy of the preleukemic state: effect of androgens on refractory anemia]. 283 1


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