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PubMed1992

Chemoprevention of rat liver carcinogenesis by S-adenosyl-L-methionine: a long-term study.

Previous work has shown a consistent fall in S-adenosyl-L-methionine (SAM) in the liver of diethylnitrosamine-initiated rats, during the development of preneoplastic lesions, in persistent nodules (PNs), and hepatocellular carcinomas. The injection of SAM into rats causes the reconstitution of the SAM pool, coupled with growth restraint, remodeling, and apoptosis of preneoplastic cells, and inhibits the development of PNs and hepatocellular carcinomas. To evaluate if SAM treatment causes a long-term prevention of preneoplastic and neoplastic liver lesions or merely causes a delay in their development, we evaluated the effect of a relatively short SAM treatment on the development of preneoplastic and neoplastic lesions in a long-term study. Male Wistar rats were subjected to initiation with diethylnitrosamine, followed by selection and then by the administration of phenobarbital for 16 weeks. After selection, the rats were given i.m. injections of a purified SAM preparation (384 mumol/kg/day) for 24 weeks. In SAM-treated rats, a decrease in the incidence of PNs was found 6, 14, and 24-28 months after initiation. At the end of SAM treatment the number of PNs per rat liver, nodule diameter, and labeling and mitotic indices of nodular cells decreased considerably in control rats. Nodule diameter started to increase rapidly again only 8 months after arresting SAM treatment, when complete recovery of DNA synthesis in nodular cells occurred. The majority of nodules present in the liver 6-28 months after initiation belonged to the clear and acidophilic cell types, with lower percentages of mixed cell and basophilic cell types. A decrease in basophilic nodules occurred in SAM-treated rats. Fourteen and 24-28 months after initiation hepatocellular carcinoma incidence was 11 of 12 and 10 of 10 in control rats, respectively, and only 1 of 12 and 3 of 11 in SAM-treated rats. At the 24th-28th month all control rats had tumors identified as 2 poorly differentiated carcinomas, 6 trabecular carcinomas, or 3 adenocarcinomas, while only 2 relatively small trabecular carcinomas and 1 small glandular tumor developed in SAM-treated rats. In 3 of 11 SAM-treated rats, but in none of the control rats, leukemic infiltration of liver occurred 24-28 months after initiation. Leukemic infiltration of the spleen occurred in 5 and 3 control and SAM-treated rats, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1999

Suppression of growth and dissemination in human pre-B leukemia cells by tumor necrosis factor-alpha in scid mice.

Tumor necrosis factor (TNF) has been shown to inhibit the growth of ALL cells. Since the systemic administration of TNF for malignancy results in poor response and severe toxicity, future efforts should concentrate on local treatment. Here we examined the suppressive effect of TNF alpha on leukemic cells engrafted in scid mice. NALM6 cells derived from pre-B ALL were injected in scid mice subcutaneously with or without Matrigel. In mice with Matrigel, subcutaneous tumors rapidly increased with time, whereas none of the mice without Matrigel showed any obvious signs of disease or apparent tumors. High levels of leukemic infiltration were observed in peripheral organs in mice with Matrigel by flow cytometry and PCR for human beta-actin mRNA expression, while mice without Matrigel showed low or undetectable infiltration in these organs. Human TNF alpha was also coinjected subcutaneously with NALM6 cells and Matrigel into scid mice. Mice with 10 ng of TNF alpha showed small subcutaneous tumors at 8 weeks, which slowly increased. They were found to have a small number of leukemic cells in peripheral organs by flow cytometry. By PCR, all organs with the exception of lung and brain showed low or undetectable expression of beta-actin. However, a large dose of TNF alpha (100 ng) had no suppressive effect on tumor growth and leukemic infiltration in mouse organs. Similar results were obtained in colony formation of leukemic cells in vitro. To examine the mechanism of the suppressive effect of TNF alpha, the expression of TNF receptors in tumor cells was analyzed by flow cytometry. Parental NALM6 expressed both TNF alpha receptors I (TNFR60) and II (TNFR80), but these expressions were suppressed in tumor cells from mice with Matrigel. Only TNFR80 expression was induced in tumor cells of mice with 10 ng of TNF alpha. The induction of Fas expression was also detected, whereas neither DNA fragmentation nor apoptotic change in histology was observed in tumor cells of mice with TNF alpha. These results suggest that the suppressive effect of TNF alpha on the growth of leukemic cells in scid mice is mediated through the activation of TNFR80 without apoptotic signal.

Animals↗
PubMed1992

Relapse of acute leukemia presenting as acute cholecystitis following bone marrow transplantation.

Though included in the differential diagnosis of jaundice and abdominal pain, acute acalculous cholecystitis is an uncommon hepatobiliary complication of bone marrow transplantation. Leukemic infiltration of the gallbladder presenting as acute cholecystitis is rare. We describe two cases of acute cholecystitis following marrow transplantation that represented an unexpected relapse with leukemic infiltration of the gallbladder wall.

Acute Disease↗
PubMed1989

Temporal bone pathology of a patient without hearing and caloric reaction, and with counter-rolling after chronic myelocytic leukemia.

The temporal bone pathology of a 36-year-old man who suffered from chronic myelocytic leukemia and sudden hearing loss of both ears, was studied from the viewpoint of neurotology. Neurotological examination showed bilaterally profound hearing loss and no caloric reaction but good counter-rolling reaction to the right and the left head tilt and no other abnormal neurological findings. He died of intracranial hemorrhage. A study of histopathology of the temporal bones revealed extensive destruction of the organ of Corti, dilatation of Reissner's membrane, leukemic infiltration in the cochlea but good preservation of sensory hair cells in the vestibular endorgans. Leukemic cell infiltration in perilymphatic and endolymphatic spaces, and leukemic hemorrhage in the perilymphatic spaces were observed. And also in the left internal auditory canal, obvious leukemic infiltration and marked hemorrhage were observed, but in the right internal auditory canal, no abnormal change was found. We discuss the correlation between neurotological findings and histopathological findings.

Adult↗
PubMed1994

Investigation of karyotypic, morphologic and clinical features in patients with acute myeloid leukemia blast cells expressing the neural cell adhesion molecule (CD56).

The mechanisms of extramedullary leukemic infiltration are not well characterized. The cell-surface glycoprotein CD56, which is identical to the neural cell adhesion molecule, may be involved. Using the Leu-19 antibody and flow cytometric methods, the leukemic blasts of 22% (70 of 314) of patients were CD56 positive. This was most common in acute monocytic leukemia (15 of 18, 83%) and in patients with the cytogenetic abnormalities t(8;21) (seven of 13, 54%) and trisomy 8 (nine of 22, 41%). CD56 expression was not associated with extramedullary leukemic infiltration, but was correlated with positivity for CD11b (p < 0.001), CD14 (p < 0.001) and CD19 (p = 0.018). Although associated with morphologic and cytogenetic features, CD56 expression alone cannot account for most instances of tissue infiltration in acute myeloid leukemia (AML).

Adolescent↗
PubMed1979

Chronic myelogenous leukemia with reticulum-cell-sarcoma-like cell proliferation--significance of eosinophilic granules in sarcomatous cells.

A case of chronic myelogenous leukemia (CML) associated with proliferation of atypical cells resembling those of reticulum cell sarcoma (RCS-like cells) is presented. A number of immature eosinophils were present mingled with ordinary leukemic cells, which infiltrated in the bone marrow, lymph nodes, spleen, liver, lungs and testes. RCS-like cells either formed solitary nodular foci or randomly mingled with infiltrating leukemic cells. Charcot-Leyden crystals were seen in some areas where RCS-like cells proliferated. As a peculiar feature the presence of eosinophilic granules in some of the RCS-like cells was noted. They were proved to be immature form of specific granules of eosinophils by their staining properties and ultrastructural aspects. Based on these findings the myelogenous origin of RCS-like cells is suggested. The patient died of cerebral complication of aspergillosis.

Adult↗
PubMed2003

Rapid tumor formation of human T-cell leukemia virus type 1-infected cell lines in novel NOD-SCID/gammac(null) mice: suppression by an inhibitor against NF-kappaB.

We established a novel experimental model for human T-cell leukemia virus type 1 (HTLV-1)-induced tumor using NOD-SCID/gammac(null) (NOG) mice. This model is very useful for investigating the mechanism of tumorigenesis and malignant cell growth of adult T-cell leukemia (ATL)/lymphoma, which still remains unclear. Nine HTLV-1-infected cell lines were inoculated subcutaneously in the postauricular region of NOG mice. As early as 2 to 3 weeks after inoculation, seven cell lines produced a visible tumor while two transformed cell lines failed to do so. Five of seven lines produced a progressively growing large tumor with leukemic infiltration of the cells in various organs that eventually killed the animals. Leukemic cell lines formed soft tumors, whereas some transformed cell lines developed into hemorrhagic hard tumors in NOG mice. One of the leukemic cell lines, ED-40515(-), was unable to produce visible tumors in NOD-SCID mice with a common gamma-chain after 2 weeks. In vivo NF-kappaB DNA binding activity of the ED-40515(-) cell line was higher and the NF-kappaB components were changed compared to cells in vitro. Bay 11-7082, a specific and effective NF-kappaB inhibitor, prevented tumor growth at the sites of the primary region and leukemic infiltration in various organs of NOG mice. This in vivo model of ATL could provide a novel system for use in clarifying the mechanism of growth of HTLV-1-infected cells as well as for the development of new drugs against ATL.

Animals↗
PubMed1991

[Isolated gingival relapse during hematological remission in a patient with erythroleukemia].

A 54-year-old man was admitted to Kitano Hospital because of nuchal pain in November, 1984. The bone marrow was hypercellular with 18% of myeloblasts and 45% of erythroblasts many of which were megaloblastoid and positive for PAS-staining. BH-AC . DMP therapy induced a complete remission which was maintained for more than 3 years until April, 1988, when gingival swelling occurred. A biopsy of the gingiva revealed a diffuse infiltration of myeloblasts together with a few erythroblasts. Local irradiation resulted in he disappearance of the swelling. However, the microscopic infiltration of the leukemic cells in the gingiva still remained in December, 1988 when there was no apparent gingival swelling and the patient was in a second hematological remission. Bone marrow relapse occurred in September, 1988 and twice thereafter. Complete remissions were again achieved for the first two relapses and the leukemic infiltration of the gingiva disappeared after another irradiation. The third relapse was refractory to an intensive chemotherapy and the gingival swelling also recurred in July, 1989. The patient died of pneumonia in October, 1989. The gingiva may be more common site of extramedullary relapse. Careful observation of this organ would be necessary throughout the course of leukemias.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1993

Graft versus leukemia effect after transplantation with interleukin-2-activated bone marrow. Correlation with eradication of residual disease.

IL-2 has been used after autologous BMT (ABMT) with the aim of inducing graft versus leukemia (GVL) effect. Our studies in mice have shown that IL-2 therapy induces GVL effect when employed after BMT with bone marrow (BM) that has been activated with IL-2 in vitro (ABM). The present study was carried out to define the time of optimal GVL effect after BMT so that the immunomodulatory approaches could be concentrated at the time of maximum GVL effect. Our data show that GVL effect was induced if IL-2 was instituted immediately after BMT with ABM in mice with acute myeloid leukemia; institution of IL-2 1 week after BMT with ABM did not induce GVL effect. IL-2 therapy instituted immediately or 1 week after BMT with fresh bone marrow (FBM) did not induce any GVL effect. A significant increase in the NK activity was noticed whether IL-2 was instituted immediately or 1 week after BMT, either with FBM or with ABM. To evaluate the ability of IL-2 in the eradication of residual disease from the autograft and the host, BM with variable infiltration with leukemia was activated with IL-2 and used for BMT in leukemic mice. The GVL effect of BM with minimal leukemic infiltration (absence of morphologically demonstrable disease) was comparable to the GVL effect of normal BM. These findings suggest that: (a) maximum GVL effect after BMT with ABM is concentrated in the early post-transplant period possibly because of minimal residual disease during this time; (b) an increase in the NK activity induced by IL-2 therapy may not predict for an improved GVL effect; and (c) for optimum GVL effect, BM with minimal leukemic infiltration should be activated with IL-2 before BMT.

Animals↗
PubMed2006

Dual-color split signal fluorescence in situ hybridization assays for the detection of CALM/AF10 in t(10;11)(p13;q14-q21)-positive acute leukemia.

We developed dual-color split fluorescence in situ hybridization (FISH) assays to detect AF10 and/or CALM rearrangements. Among nine cases of acute leukemia with translocation breakpoints at 10p13 and 11q14-21, a CALM/AF10 rearrangement was found in seven and was confirmed by reverse transcriptase polymerase chain reaction (RT-PCR) in all. In 2/7 cases, FISH detected CALM/AF10 in extramedullary leukemic infiltrations in the mediastinum and breast. As expected, FISH was less sensitive than RT-PCR for disease monitoring of CALM-AF10 positive cases. This new FISH assay reliably discriminates between MLL/AF10 and CALM/AF10 genomic rearrangements, identifies variant and complex CALM/AF10 translocations and detects the CALM/AF10 rearrangement in extramedullary leukemic infiltrations.

Acute Disease↗
PubMed1977

An electron microscopic study of the spleen of the rat in an acute myelogenous leukemia.

The spleens of rats were studied by light and electron microscopy during the course of an acute myelogenous leukemia, with special reference to infiltration of leukemic myeloblasts in the spleens and to the correlation of leukemic cell infiltration with splenic hematopoiesis and splenomegaly. Leukemic myeloblasts infiltrated the cordal space of the red pulp. Many of them appeared in groups. Even in spleens which were heavily infiltrated, leukemic myeloblasts did not penetrate the while pulp. Massive infiltration and proliferation of the leukemic myeloblasts in the red pulp resulted in splenomegaly. The spleen increased its hematopoietic activity, while the medullary hematopoiesis diminished due to the invasion of leukemic myeloblasts in the bone marrow. Compensatory splenic hematopoiesis occurred in most of the leukemic spleens, but diminished in spleens which were very heavily infiltrated with leukemic myeloblasts. Thus, the degree of splenomegaly and splenic hematopoiesis did not necessarily correspond to the percentage of leukemic myeloblasts in the bone marrow, but rather related to the number of leukemic myeloblasts present in the spleen. A possible role for the splenic sinus walls in promoting compensatory hematopoiesis in the spleen is discussed. A consistent association of type "C" virus particles with leukemic myeloblasts was observed.

Animals↗
PubMed1977

Pathogenesis of central nervous system infiltration in acute leukemia.

The distribution pattern of leukemic infiltrates was studied in 31 cases of acute leukemia with CNS involvement. Dura mater involvement was found in 93% (29/31) of the cases; arachnoid, 71% (22/31); perivascular cuffing, 37% (17/31); parenchymatous, 16% (5/31). Dura matter infiltrates were the sole manifestation in nine cases; Infiltration of the arachnoid in the absence of dural infiltration was rare (9%). The anatomic evidence supports the concept that leukemic cells infiltrate by way of perivenous adventitial tissue connecting the dura mater and subarachnoid space. It is likely that this pathway leads directly from the bones of the skull into the brain parenchyma.

Brain↗
PubMed1976

[Benzene acute aleukemic leukosis, with widespread leukemic parenchymal infiltration (author's transl)].

A case is reported by the authors of a progressive benzene hemopathy with a final leukemic evolution. The leukemic pattern was an autopsy ""surprise'', inasmuch as never, even in the hours just before death, could leukemic cells be detected in the blood stream. The authors discuss some pathogenic aspects, with particular emphasis on the systemic spreading of a malignant hemopathy from very few leukemic cells in bone marrow.

Autopsy↗
PubMed1984

Central nervous system complications in childhood leukemia. Correlation between clinical and computed tomographic findings.

We used cranial computed tomography (CT) to evaluate 51 leukemic patients with or without central nervous system (CNS) symptoms. Among 17 symptomatic patients, nine had gross abnormalities on CT scans; leukemic infiltrations, infections (CNS aspergillosis), hemorrhages, and therapy-related complications were all evident. One with a leukemic infiltration showed a periventricular low density on the CT scans. The differential diagnosis of CT findings and the correlation between clinical and CT findings is described. The significance of a low-density area observed in an asymptomatic patient on long-term intrathecal methotrexate therapy for CNS leukemia is also discussed.

Brain↗
PubMed1979

[Cerebro-meningeal involvement in acute myeloblastic leukaemia and myeloproliferative syndromes in acute transformation. Cytological, histological and clinical study of 62 cases (author's transl)].

Clinical and histopathologic study of central nervous system (CNS) was performed in 46 acute myeloid leukemia (AML) and 16 chronic granulocytic leukemia in the blastic phase (CGL). Involvement of the CNS developed in 28 cases. Eighteen patients out of these 28 had neurological symptoms. The frequency of meningeal leukemia depends on the number of lumbar punctures and on the survival time. Post-mortem examination was performed on 45 patients. Eighteen had evidence of CNS leukemic infiltration (18/45 arachnoid, 10/31 dura, 5/45 brain). Hemorrhages are frequent even without CNS involvement (19/27). CNS leukemic infiltration is common enough in AML and CGL to justify agressive diagnostic, therapeutic, and prophylactic measures.

Arachnoid↗
PubMedDate not supplied

[Acute leukemia with cardiac infiltration].

A nine years old female child with malnutrition who showed, six months before admission, a number of clinical manifestations consistent with leukemia. The outstanding clinical manifestation during her hospital stay was that of pericarditis with effusion, which was found associated with pericardial leukemic infiltration. The final picture was that of cardiorespiratory failure associated, both to leukemic infiltration of these organs, as to that of postoperative hemorrhage.

Acute Disease↗
PubMed1984

Sonographic findings in leukemic renal disease.

The ultrasonic findings in 10 patients with diffuse leukemic infiltration of the kidneys are described. The findings are analogous to those seen pathologically and include enlargement of the kidneys, diffuse leukemic infiltration of the renal cortex with sparing of the adjacent medullae, loss of definition and distortion of the renal sinus echo complex and a focal mass. The ultrasound findings correlated well with those seen with intravenous urography making it the preferable screening modality for the initial detection of renal involvement, subsequent follow-up and response to therapy in leukemic patients.

Child↗
PubMed1978

Cushing's syndrome and acute lymphoblastic leukemia.

Cushing's disease developed in a 5-year-old girl with acute lymphoblastic leukemia 18 months after her last therapeutic exposure to adrenal glucocorticosteroids. Obesity, hyperpigmentation, striae, osteoporosis, and hirsutism were accompanied by elevated levels of plasma cortisol. These showed no diurnal fluctuation and they were not suppressed by dexamethasone. At autopsy, the adrenal glands were enlarged and the pituitary gland showed increased numbers of basophils of the adrenocorticotropic hormone (ACTH)/melanocyte-stimulating hormone secreting type. Leukemic infiltrates in brain tissue were prominent in the hypothalamus and in the limbic system. It is postulated that the destructive leukemic infiltrate of the limbic system removed a restraining influence on pituitary function, with basophilic hyperplasia, ACTH hypersecretion, adrenocortical hypertrophy, and clinical Cushing's disease the consequences.

Adrenal Gland Neoplasms↗