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At least 37 records · Page 2Linked to original sources

Monocytic leukemia in a horse.

On clinical examination, a six-year-old Hassian gray gelding with a history of impaired performance, slight cough, colic, and edema of the ventral abdomen, prepuce and the legs had reduced skin turgor, pale mucous membranes, forced costoabdominal breathing, reduced venous return, enlarged lymph nodes, and splenomegaly. Hematologic findings revealed anemia, leukocytosis and a high percentage of monocytoid leukemic cells. Generalized lymphadenopathy, splenomegaly, ascites, hydrothorax, and a diffusely thickened gut wall were found at necropsy. Massive infiltration with monocytoid leukemic cells was detected in lymph nodes, spleen, bone marrow, liver, gut wall, kidneys, and choroid plexus. Incubation of living cells obtained from a leukocyte concentrate with latex particles revealed phagocytosis in the leukemic cells on light and electron microscopy. The leukemic cells also had a marked alpha-naphthyl-acetate and naphthol-AS-acetate esterase activity, but were only weakly positive to naphthol-AS-D-chloroacetate esterase. A very weak alkaline phosphatase activity only was demonstrated in a few leukemic cells. On scanning electron microscopy, the leukemic cells had prominent ruffles and ridge-like profiles. These features of the leukemic cells excluded lymphocytic and granulocytic leukemia, and monocytic leukemia was diagnosed.

Alkaline Phosphatase↗

[Chronic lymphoid leukemia followed by acute monocytic leukemia].

A 62 year old patient with CLL treated by alkylating drugs for more than three years, underwent acute leukaemia (AL). The clinical particularities of the onset and course of this AL, the cytological, cytoenzymological and ultrastructural characteristics of the blasts are discussed in order to find a relation between the two hemopathies. A possible drug-induced etiology of this AL is proposed.

Antineoplastic Agents↗

Acute monocytic leukemia presenting as acute respiratory failure.

Acute respiratory failure revealing acute monocytic leukemia is rare. We report 20 patients admitted to the intensive care unit (ICU) with three remarkable features: (1) rapidly progressive respiratory distress revealing acute leukemia, (2) monocytic leukemia, and (3) respiratory status deterioration after chemotherapy initiation. The median age was 50 years (17-72 years), and respiratory symptoms started 2 days (0-15 days) before ICU admission. The median leukocyte count was 98,250/mm3 (800-529,000), with circulating monocytic cells in all of the patients but one. Bone marrow examination was diagnostic of monocytic leukemia in all patients. At presentation, respiratory rate was 33 (18-50) per minute, and PaO2 on room air was 44.5 mm Hg (30-60). Chest radiographs revealed unilateral alveolar infiltrates (n = 1), bilateral alveolar infiltrates with (n = 3) or without (n = 11) pleural effusion, or diffuse interstitial infiltrates (n = 5). Alveolar hemorrhage was the main bronchoalveolar lavage finding, with monocytic cells retrieved from four patients. Respiratory function deteriorated after cancer chemotherapy initiation in all patients. Of the 15 patients who required mechanical ventilation, 10 died. Leukemic pulmonary infiltration as the first manifestation of acute monocytic leukemia should be recognized, and intensive management should be provided in anticipation of the respiratory function deterioration seen consistently after chemotherapy initiation.

Acute Disease↗

Generation of altered transcripts by retroviral insertion within the c-myb gene in two murine monocytic leukemias.

Two murine monocytic leukemia cell lines, WEHI-265 and WEHI-274, were found to carry a rearranged c-myb gene. The rearrangements are due to insertion of a deleted Moloney murine leukemia virus (Mo-MLV) provirus in the 5' region of the c-myb gene and thus are similar to rearrangements in the ABPL tumors (G. L. C. Shen-Ong, M. Potter, J. F. Mushinski, S. Lavu, and E. P. Reddy, Science 226:1077-1080, 1984). In each cell line, the retroviral insertion has induced high levels of two aberrant RNA species, which, as in the ABPL tumors (G. L. C. Shen-Ong, H. C. Morse, M. Potter, and J. F. Mushinski, Mol. Cell. Biol. 6:380-392, 1986), contain both viral (Mo-MLV) and cellular (myb) sequences. Both species lack the sequences encoding the amino terminus of the c-myb protein and thus could encode a protein which, like the v-myb gene products (and the predicted ABPL myb proteins), is truncated at the amino terminus. We have found that the larger (5.3 kilobase [kb]) and more abundant of the tumor-specific myb RNAs was predominantly nuclear, while the smaller species (3.9 kb) was cytoplasmic. Furthermore, our data imply that the 3.9-kb RNA was derived from the 5.3-kb RNA by an additional splice which utilized a cryptic splice acceptor site within the viral gag sequences. On the basis of subcellular distribution and predicted translational potential, we conclude that the 3.9-kb RNA is probably the mRNA which encodes a truncated myb protein. We also show that, due to different insertion points in W265 and W274, the W274 myb RNAs contained sequences from a c-myb exon upstream of the exons represented in the W265 (and ABPL) RNAs. The significance of our findings with regard to transformation by myb in these tumors is discussed.

Base Sequence↗

Early deaths due to hemorrhage and leukostasis in childhood acute myelogenous leukemia. Associations with hyperleukocytosis and acute monocytic leukemia.

There were 294 children with acute myelogenous leukemia (AML) entered into the German AML Berlin, Frankfurt, and Münster hospitals (BFM) 78 and 83 studies. Thirty (10%) died as a result of hemorrhage and/or leukostasis prior to or in the first 12 days of therapy. The risk of early death due to hemorrhage and/or leukostasis is significantly greater when certain features are initially present: acute monocytic leukemia (French-American-British [FAB] M5), hyperleukocytosis (greater than or equal to 100,000/microliter), and extramedullary organ involvement (P less than 0.001). The risk increases sharply when these factors exist in combination: 72% mortality with FAB M5 and hyperleukocytosis, and 43% with FAB M5 and extramedullary organ involvement. In 11 patients leukostasis alone or in combination with hemorrhage was probably the cause of death during the first 3 days after diagnosis. All 11 children presented with hyperleukocytosis and were classified as monocytic subtype FAB M4 or M5. After induction, a close temporal association between rapid blast reduction and occurrence of fatal hemorrhage was established in five patients. Thrombocytopenic hemorrhages were controllable and, therefore, responsible for death only in exceptional cases. It is difficult to avoid these early fatal complications with current therapeutic measures. Early exchange transfusion together with special supportive care may be useful.

Adolescent↗

Is t(10;11)(p11.2;q23) involving MLL and ABI-1 genes associated with congenital acute monocytic leukemia?

Congenital, or perinatal, leukemias are rarely observed, but retrospective molecular studies seem to suggest a more frequent onset in prenatal life. Myelocytic types are common, and chromosome band 11q23 rearrangements at the MLL locus are characteristic genetic markers. The fusion of the MLL gene with one of its partners, ABI-1, has recently been described in two infant leukemia patients with monocytic involvement and good clinical outcome. We report a case of congenital monocytic leukemia with the same gene involvement and good response to chemotherapy. The blast metaphases were probed by fluorescence in situ hybridization, and t(10;11)(p11.2;q23) involving MLL and ABI-1 genes was demonstrated with the same breakpoint in ABI-1. The congenital presentation of this case suggests a possible relationship of this genetic event with in utero leukemogenesis.

Adaptor Proteins, Signal Transducing↗