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PubMed1991

[Encephalopathy in leukemia treatment in children].

Side effects on the central nervous system by antileukemic treatment have been well known for a long time. We report on 2 patients suffering from a severe encephalopathy during antileukemic therapy. Furthermore the results of cerebral computer tomography in 50 children with acute leukemia have been analysed. In 21 patients morphological findings were evident. Four patients had CCT-changes already before the beginning of their treatment. Initially in 2 patients leukemic cerebral infiltrations were detected. The importance of the computer tomography for the detection of cerebral affections by disease and treatment is demonstrated.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1991

[A case of adult T-cell leukemia with a defective HTLV-I proviral DNA, in which the single T-cell clone appeared to have progressed from chronic phase to crisis].

A 39-year-old woman was first admitted to our hospital with increased white cell count on May, 1983. Physical examination showed only mild splenomegaly. Hematological examination revealed leukocytosis (14,600/microliters) with ATL cells (59%). Serum anti-HTLV-I antibody was positive. Examination of HTLV-I provirus in the abnormal T cells revealed the defective type. She was diagnosed as chronic type of ATL based on the clinical features. Cytogenetic study of the ATL cells revealed 47, xx, +4. For 12 months, she was followed without any therapy. WBC reduced to almost normal range and ATL cells decreased to 3 to 6% for 8 months. On May, 1985, she was readmitted to our hospital because of leukocytosis (32,200/microliters), and increased ATL cells (57%). She was diagnosed as crisis of ATL. Investigation of the proviral DNA and chromosome showed the same results as those of the chronic phase, indicating that ATL cells in both the chronic phase and the crisis phase originated from the same clone. She died after 3 months from massive diarrhea. Postmortem examination showed the extensive infiltration of leukemic cell in the small intestine.

Adult↗
PubMed1991

[An autopsy case of acute mixed lineage leukemia with monosomy 7 in a child].

A five-year-old boy initially diagnosed common ALL was developed to acute myelomonocytic leukemia. At onset, the bone marrow was hypercellular and 77% of the cells were blasts, mainly lymphoblast-like cells and cytogenetic study demonstrated 45, XY, -7 in all blasts. Cytochemically most of those blasts were negative for peroxidase, sudan black B, alpha-NB esterase staining. The immunological phenotype was J5 (CD10)+, I2 (HLA-DR)+, SmIg-, CyIgmu-, Leu1 (CD5)-, OKT11 (CD2)-, MY7 (CD13)-, suggesting common ALL. Eight months later, the bone marrow cells were occupied with large sized blasts which were almost positive for peroxidase stain and the cells showed coexpression of Mo1 (CD11b)+, MY4 (CD14)+, MY7+, MY9 (CD33)+, MCS2 (CD13)+, I2+, J5-, B4 (CD19)-, Mo2 (CDw14)-, at relapse. He died 2 years and 6 months after his initial diagnosis. An autopsy was performed which revealed generalized infiltration of leukemic cells and aspergillosis of the lung. In general, monosomy 7 is associated with myelodysplastic syndrome in childhood, and is terminated to acute myeloblastic leukemia. In this case, bone marrow blasts demonstrated monosomy 7 cytogenetically, and this case was considered as an acute mixed lineage leukemia of bilineal type. And this case proved that a monosomy 7 can also be terminated to acute mixed lineage leukemia with both lymphoid and myeloid phenotypes.

Child, Preschool↗
PubMed1990

Induction of leukemia in chicken by bovine leukemia virus due to insertional mutagenesis.

Bovine leukemia virus (BLV) was inoculated into one-day-old chickens. In a small part of inoculated chickens leukemia developed during observation period of one year. Out of 88 birds inoculated, only 4 developed histopathologically verified leukemia. The induced leukemia was characterized by enlarged liver and spleen. The organs were infiltrated with leukemic cells. The DNAs of body organs of inoculated chickens were analysed by Southern blot hybridization for the presence of BLV specific sequences. Out of 9 suspicious chickens tested in 6 birds the BLV was found to be integrated into host DNA either as a complete viral genome or as a part corresponding to its 3'-end. The leukemic cells were monoclonal as regard to the integration site of the BLV provirus. Neither the expression of BLV provirus in chicken leukemic cells nor the antibody response to BLV antigens in inoculated birds was detected. The rearrangements and amplification of erb-B and myb loci of protooncogenes in leukemic cells was detected. There were no changes in loci of following protooncogenes: myc, sis, fes, fps, erb A, src and yes. All obtained data taken together suggest that the BLV induced leukemia in chickens is caused by insertional mutagenesis.

Animals↗
PubMed1990

[Acute lymphocytic leukemia with thrombophlebitis of lower limbs and translocation (4;11)].

On November 22, 1985, a 54-year-old male was admitted to the cardiovascular department of our hospital suffering from thrombophlebitis, with redness, swelling and pain around the right ankle and left knee. He was transferred to our department on Nov. 26, because of hyperleukocytosis. Peripheral blood examination revealed hyperleukocytosis with 93.0% blastic cells and thrombocytopenia. The bone marrow aspirate was hypercellular and almost all cells were consistent with peroxidase negative blastic cells. The blastic cells were Leu M1 positive and Leu M2, M3 and lymphocytic markers were negative. The patient was diagnosed to have acute lymphocytic leukemia with Leu M1 positive blast cells. BH-AC/DMP therapy was began on the 1st hospital day but he died of cerebral haemorrhage on the 4th hospital day. An autopsy revealed systemic infiltration of leukemic cells including thrombophlebitis of the legs. Chromosome analysis of the bone marrow cells showed t(4;11)(q21;q23).

Antigens, Differentiation, Myelomonocytic↗
PubMed1989

[Relapse of gingival tumor during hematological remission in acute promyelocytic leukemia].

A 56-year-old man was admitted to the hospital in April, 1986, with the chief complaint of fatigue. The diagnosis of acute promyelocytic leukemia (APL) was made based on the proliferation of atypical promyelocytes in the bone marrow. No gingival swelling was found on admission. A complete remission was achieved by the BHAC-DMP therapy and maintained by the consolidation therapy and the intensification therapy. In July, 1987, he noticed a solitary gingival tumor around the left lower second molar. The biopsy showed the massive infiltration of leukemic cells, despite the hematological remission. Combination chemotherapy was not effective but the tumor disappeared by irradiation. A hematological relapse occurred in November, 1987, but the second complete remission was achieved by the AB-triple V therapy. He died because of the second hematological relapse in July, 1988. Along with the wide use of intensive chemotherapy for acute leukemia, tumor forming leukemia during the hematological remission, as seen in this case, would be increasing. Thus, we should not overlook any newly formed tumor in the treatment of leukemia.

Aclarubicin↗
PubMed1988

[Granulocytopoiesis in acute lymphoblastic leukemia in children].

The number, proliferative potential and differentiation potentialities of bone marrow granulocytic-macrophagal precursors were investigated in 130 ALL patients (77 children in the acute period of disease, 53 children in remission) and in the bone marrow of 65 controls without hematologic pathology. A decrease in the number of clonogenic precursors was observed in all stages of acute lymphoblastic leukemia, the decrease being particularly marked in the acute period of disease characterized by substantial bone marrow infiltration by leukemic cells. A decrease in the number of precursors and their proliferative potential was shown to be associated with the influence of leukemic blasts. In remission the numerical reduction of the precursor pool was determined by a cytostatic therapeutic effect. The ability to differentiation of granulocytic and macrophagal clonogenic precursors in ALL children was unchanged.

Adolescent↗
PubMed1988

Acute eosinophilic leukemia with a (10;11) chromosomal translocation.

We report a patient with acute eosinophilic leukemia and a translocation (10;11)(p14;q21). Clinically, the disease was characterized by extreme hypereosinophilia with most eosinophils being immature, pronounced marrow infiltration with abnormal eosinophil precursors, skin and lymphoid infiltration with leukemic eosinophils, and only a brief remission from chemotherapy. This is the second report of a patient with this cytogenetic/clinicopathological association. In our patient, t(10;11)(p14;q21) was the sole karyotypic abnormality seen in the bone marrow, both at diagnosis and relapse. Thus, acute eosinophilic leukemia with t(10;11)(p14;q21) appears to be a rare, new clinical/cytogenetic association. Because both patients with this translocation responded only briefly to chemotherapy, this chromosomal abnormality may confer a poor prognosis.

Adult↗
PubMed1987

Pulmonary aspergillosis in a horse with myelomonocytic leukemia.

Acute myelomonocytic leukemia was diagnosed in a 2-year-old Standardbred mare that had hind limb edema and fever unresponsive to antibiotics. The mare had anemia, thrombocytopenia, and leukocytosis, with circulating myeloblasts and monocytoid cells. A bone marrow specimen was hypercellular, with myeloblasts and monocytoid cells. Peroxidase, chloroacetate esterase, and alpha naphthyl acetate esterase activities were detected in many bone marrow cells. Interstitial pulmonary densities were seen radiographically. The mare was euthanatized and necropsied. Infiltrates of leukemic cells were found microscopically in specimens of spleen, lymph nodes, liver, kidneys, gastrointestinal tract, and lungs. Granulomas containing fungal hyphae were seen microscopically in the lungs, and Aspergillus sp was isolated from the lesions.

Animals↗
PubMed1984

Adult T-cell leukemia/lymphoma in Jamaica and its relationship to human T-cell leukemia/lymphoma virus type I-associated lymphoproliferative disease.

We had shown previously that the prevalence of human T-cell leukemia/lymphoma virus type I (HTLV-I)-antibody positivity is high in Jamaican non-Hodgkin's lymphoma (NHL) patients and that virus-positive patients have the clinical features and poor prognosis of adult T-cell leukemia/lymphoma (ATL). Sixty-two % of 45 NHL patients diagnosed consecutively between 2/1/82 and 1/31/84 and studied prospectively were HTLV-I-antibody positive. Skin involvement (38%), hypercalcemia (44%), and leukemia (40%) were unusually prevalent and there was a strong association (p less than 0.05) with HTLV-I-antibody positivity. Fifty-two % of the patients had bone marrow infiltration, and 74% of these patients were HTLV-I-antibody positive (p = 0.06). Lymphadenopathy (96%), hepatomegaly (60%), and splenomegaly (25%) were detected with about the same frequency as in other series of NHL patients with advanced disease, and 61-88% of these patients were HTLV-I-antibody positive. Patients were classified into those with "typical ATL" (NHL associated with 2 of the 4 features i) hypercalcemia; ii) histologically proven skin infiltration; iii) leukemia; and iv) bone marrow infiltration, providing that the morphology of infiltrating or leukemic cells was characteristic of ATL; those "consistent with ATL" (NHL associated with 1 of these 4 features); and "non-ATL" (NHL without any of these 4 additional features). Thirty-two (71%) of the NHL patients were ATL patients, i.e., had features typical of or consistent with ATL, and 78% of these were HTLV-I-antibody positive. HTLV-I provirus was detected in tumour cells of all HTLV-I-antibody positive patients tested. Three (23%) of the non-ATL patients were HTLV-I-antibody positive. There was no correlation between histopathological features and the clinical classification or HTLV-I-antibody positivity. Median survival of ATL and non-ATL patients was 16 and 53 weeks. Although the disease was usually fulminant, 34% of the ATL patients had a subacute or chronic course. Skin involvement and leukemia were prominent in these patients. Hypercalcemia was the chief prognostic determinant. Median survival of hypercalcemic and normocalcemic ATL patients was 13 and 86 weeks (p less than 0.05). Hypercalcemia caused 10 deaths, infections 12, and death was due to tumour progression in 4 patients. Infections were usually due to pyogenic organisms and only 2 patients had systemic opportunistic infections. Six (27%) of 22 chronic lymphocytic leukemic (CLL) patients were HTLV-I-antibody positive.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1984

Increased prostate-type acid phosphatase activity in serum and typical bone lesions simulating the presence of prostatic carcinoma.

In a man with myelomonocytic leukemia, the association of increased prostatic acid phosphatase activity in serum and the presence of typical bone lesions on roentgenography suggested the existence of disseminated prostatic carcinoma. During the clinical observation period, however, prostatic involvement could not be proved. Moreover, bone pain and prostatic-type acid phosphatase activity in serum closely paralleled monocyte counts and the degree of hepatosplenomegaly and leukemic skin lesions. Finally, meticulous postmortem examination of the prostate showed no prostatic carcinoma. This clinical picture appears to be entirely explicable in terms of leukemic organ infiltration and the proliferation of monocytes, which are known to contain acid phosphatase isoenzymes like those in the prostate.

Acid Phosphatase↗
PubMed1984

[Leukemic meningiosis in children].

Leukemic cells infiltration ways of the CNS are described and the risk factors are valued. The rational for the prophylactic treatment, the therapy of the meningopathy and AIL- AIEOP protocols are exposed. Early and late effects which can derivate are considered.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1983

Cutaneous lesions in hairy-cell leukemia. Case report and review of the literature.

A patient is described in whom cutaneous lesions were the initial manifestation of hairy-cell leukemia. Touch preparations made immediately on removal of a 3-mm punch biopsy specimen of the cutaneous lesions revealed acid-phosphatase positive, tartrate-resistant staining in the leukemic cells, and helped to establish the diagnosis. Specific eruptions occur in approximately 7% of patients with hairy-cell leukemia, appearing grossly as disseminated, erythematous maculopapules, with a perivascular mononuclear leukemic cell infiltrate seen microscopically. A review of the English literature indicates that cutaneous manifestations are not generally recognized as a diagnostic source in individuals with hairy-cell leukemia, and biopsy is seldom undertaken.

Acid Phosphatase↗
PubMed1980

Dural venous sinus thrombosis in acute lymphoblastic leukemia.

Three children with acute lymphoblastic leukemia developed sagittal sinus thrombosis. One patient was in peripheral remission. One patient survived. In neither patient who died were the walls of the dural sinuses infiltrated with leukemic cells. Attention is drawn to this potentially treatable cause of central nervous system symptoms in childhood leukemia. Angiography is the diagnostic test of choice and can also demonstrate intracerebral hematoma and subdural hematoma, if present. Sinus thrombosis can occur either during exacerbation or remission of the basic leukemic process. The possibility that chemotherapeutic techniques predispose toward this complication is raised.

Adolescent↗
PubMed1982

[Two cases of central nervous system leukemia which responded excellently to intra-arterial injection of ACNU].

Local chemotherapy by intra-arterial administration of ACNU was performed in 2 cases with CNS leukemia, which responded well to this therapy. The first patient was a 42-year-old male who was diagnosed as having chronic myelogenous leukemia with local infiltration of leukemic cells to the optic nerves. By intra-arterial infusion of ACNU (60mg), symptoms and results of ophthalomological examinations were improved remarkably. The second case was a 16-year-old male diagnosed as having acute lymphoblastic leukemia, and complicating with meningeal involvement during the course of chemotherapy. Complete remission was achieved by intra-thecal administration ACNU. Intra-arterial infusion of ACNU would be an effective local chemotherapy of CNS leukemia and its effectiveness could be achieved by less dose of ACNU compared to that of intravenous infusion. Therefore, side effects, e.g., delayed myelosuppression caused by ACNU could be decreased by this method.

Adolescent↗
PubMed1980

Ultrastructral changes induced by 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)-1-nitrosourea in L1210 lymphocytic leukemia cells in mice.

Ultrastructural changes in L1210 leukemic cells infiltrated in the sinusoid of mouse liver after treatment with a single dose of a newly developed antitumor agent, 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)-1-nitrosourea hydrochloride, were observed by electron microscopy. In the earliest stage after injection of 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)-1-nitrosourea hydrochloride in tumor-bearing mice, marked changes were observed in both nucleolar and cytoplasmic ultrastructures. At 48 hr after administration, numerous Golgi complexes were observed in the cytoplasm, and lysosome-like granules also increased. The most striking change after treatment with 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)-1-nitrosourea hydrochloride, however, occurred in the nucleolus. The chromatin was condensed, tending to collect near the nuclear membrane. Segregation of the nucleolar constituents was observed in the nucleus. Many necrobiotic cells were also observed within the liver sinusoid at this stage.

Animals↗
PubMed1995

Biotherapy for xenografted human central nervous system leukemia in mice with severe combined immunodeficiency using B43 (anti-CD19)-pokeweed antiviral protein immunotoxin.

The study of central nervous system (CNS) leukemia has been hampered by the lack of a suitable animal model. We report that severe combined immunodeficiency (SCID) mice invariably develop rapidly progressive fatal CNS leukemia within 3 weeks after intravenous injection of NALM-6 pre-B acute lymphoblastic leukemia (ALL) cells. Colonization of the dura mater and subarachnoid space, usually of the distal spinal cord with occasional extension into the Virchow-Robin spaces of blood vessels subjacent to the meninges, followed involvement of bone marrow in the skull, vertebrae, and, occasionally, the appendicular skeleton. Occult CNS leukemia was detectable by polymerase chain reaction amplification of human DNA as early as 8 days postinoculation of leukemia cells. We used this in vivo model of human CNS leukemia to examine the therapeutic efficacy and toxicity of intrathecally administered B43 (anti-CD19)-pokeweed antiviral protein (PAP), an anti-B-lineage ALL immunotoxin directed against the pan-B-cell antigen CD19/Bp95. Intrathecal therapy with B43 (anti-CD19)-PAP immunotoxin at nontoxic dose levels significantly improved survival of SCID mice and was superior to intrathecal methotrexate therapy.

Animals↗