Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Leukemic Infiltration”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed1989

[Dyspnea, cough, febrile state].

A 71-year old man was admitted because of increasing dyspnea and fever. Myelomonocytic leukemia was diagnosed on blood films. Diffuse bilateral pulmonary infiltrates detected on chest radiographs were related to the febrile state. Because leukemic infiltrates as well as pneumonia were possible causes for the pulmonary lesions antibiotic therapy followed by prednisone on the same day was initiated. An unusually rapid improvement of the pulmonary infiltrates within 4 days was indicative of a leukemic infiltrate. The patient died a few days later and the diagnosis of diffuse leukemic pulmonary infiltrates was confirmed at autopsy.

Aged↗
PubMed1985

Leukemic iris infiltration as the only site of relapse in a child with acute lymphoblastic leukemia: temporary remission with high-dose chemotherapy.

A 12-year-old Caucasian boy developed leukemic hyphema with iris infiltration as the only relapse site during the third complete remission of his acute lymphoblastic leukemia. With high-dose methotrexate, high-dose cytosine-arabinoside plus teniposide, and a 5-week course of vincristine, prednisolone, and L-asparaginase, a complete remission could be achieved. Maintenance treatment was reinstituted for 1 year. However, after stopping the treatment, the iris infiltrate reappeared, and this time the eye was irradiated after chemotherapeutic reinduction. Seven months later, the boy remains in complete remission. The pathogenesis of leukemic iris infiltration is discussed briefly.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1978

Chronic lymphocytic leukemia showing pituitary tumor with massive leukemic cell infiltration, and special reference to clinicopathological findings of CLL.

An autopsy case of a 33 years old doctor with chronic lymphocytic leukemia (CLL) was reported. Two remissions were noted with chemotherapy and irradiation. The special characteristic of this case was the tumor formation in the sellar fossa similating a pituitary tumor which was considered as a type of meningeal leukemia, showing visual disturbance. Leukemic cell infiltration was hardly observed in any other organs. From the analysis of five cases of CLL, the author proposes that CLL may be classified into two types: the one is the severe type showing a short clinical course and the other is a mild one, showing a long clinical course. Details such as histopathological findings, cause of death and clinical findings were discussed.

Adult↗
PubMed1986

Sequential testicular biopsies in childhood acute lymphocytic leukemia.

Between August 1978 and November 1981, 33 boys with acute lymphocytic leukemia (ALL) (26 non-T, 7 T-cell) younger than 16 years underwent bilateral wedge testicular biopsies at the time of initial diagnosis. Seven (4 non-T, 3 T-cell) demonstrated focal leukemic infiltrates. Rebiopsy after successful induction therapy without testicular irradiation showed eradication of leukemic infiltrates in five, persistent focal infiltrates in one, and a diffuse infiltrate in one. The two patients who had persistent leukemic involvement had a T-cell phenotype, and in one of them overt testicular disease developed 2 years later. All 33 patients were followed prospectively for a minimum of 3 years. Fifteen (14 non-T, 1 T-cell) remained in remission for 3 years and underwent another testicular biopsy before the cessation of therapy. Two patients, both non-T and both of whom were free of testicular involvement at diagnosis, showed testicular infiltrates at that time. Of the seven boys with positive specimens at diagnosis, only two remained disease-free for 3 years and showed no testicular involvement upon the completion of chemotherapy. In this study, microscopic testicular involvement by lymphoblasts occurred in 21% of newly diagnosed boys with ALL; this occurred only if the leukocyte count exceeded 25,000/microliter. These patients in general had a poor prognosis, probably reflecting the overall heavy tumor burden. However, it was not possible to predict accurately those patients who would have leukemic testicular infiltrates at the cessation of chemotherapy by performing biopsy of the testes at the time of initial diagnosis or after induction therapy.

Adolescent↗
PubMed1995

Perforin-positive leukemic cell infiltration in the heart of a patient with T-cell prolymphocytic leukemia.

Here we report a rare case of T-cell prolymphocytic leukemia in whom leukemic killer cells, expressing a cytolytic factor perforin, infiltrated the heart. Perforin may have directly injured myocardial cells which showed marked expression of human leukocyte antigens (HLAs) and intercellular adhesion molecule-1 (ICAM-1) as well as costimulatory molecules B7 and B70, which are ligands for CD28 expressed on T-cells. In spite of chemotherapy against leukemic cells, this autoimmune process finally caused fatal congestive heart failure.

Adult↗
PubMed1996

[Infiltration of the testes in acute lymphoblastic leukemia in childhood--personal experience].

According to various literature data testicular leukemic infiltration occurs in 5-40%, while the mean time for testicular recurrence is 36 months. Hematologic recurrence usually occurs in the interval from 1-6 months. Although testicular leukemic infiltration clinically occurs as an isolated recurrence of leukemia, it usually presents only a clearly marked spot in the general recurrence of the disease. It is a painless enlargement of one or both testes. The diagnosis is made ultrasonographically and by histopathologic examination of the biopsied testicle tissue. This paper deals with 4 patients with acute lymphoblastic leukemia and testicular recurrence. In 2 patients the testicular recurrence occurred as a part of the general recurrence of the disease, while in the other 2 at the time of testicular recurrence diagnosis, the bone marrow was regular. All 4 patients were treated with combined radiotherapy and chemotherapy, in 3 cases successfully.

Child↗
PubMed1983

Pathology of the mononuclear cell leukemia of Fischer rats. I. Morphologic studies.

Pathological evaluations were done in 205 rats with mononuclear cell leukemia. Leukemia was diagnosed in 22.2% of males and 20.4% of females with significant risk beginning at 20 months of age. Mononuclear cell leukemia was responsible for 50% of early deaths in two-year studies. Clinically, rats became depressed, pale, icteric and had palpably enlarged spleens. Gross lesions included splenomegaly, enlarged mesenteric lymph nodes, and mottled livers. Hemorrhages occurred in the lungs, brain, and lymph nodes. Histological examination demonstrated that spleen and liver were most consistently and seriously involved, although numerous other organs contained leukemic infiltrates of variable severity. Spleens exhibited diffuse leukemic infiltration of the red pulp, follicular lymphoid depletion, and decrease in both extramedullary hematopoiesis and hemosiderin. Liver lesions consisted of diffuse centrilobular degeneration and necrosis. Erythrophagocytosis by tumor cells was common in the spleen and observed in liver, lymph nodes, and adrenals. The disease appeared to originate in the spleen. Bone marrow infiltration occurred late relative to spleen involvement and was present in less than half of the rats.

Animals↗
PubMed1996

Perforin-positive leukemic cell infiltration in the aortic tissue of a patient with T-cell prolymphocytic leukemia.

Here we report a rare case of T-cell prolymphocytic leukemia in which leukemic killer cells, expressing a cytolytic factor perforin, infiltrated the aorta as well as the heart and may have directly injured aortic vascular cells which strongly expressed human leukocyte antigens (HLAs) and intercellular adhesion molecule-1 (ICAM-1) as well as costimulatory molecules B7 and B70, which are ligands for CD28 expressed on T-cells. In spite of chemotherapy against leukemic cells, this autoimmune process finally caused fatal multi-organ failure.

Adult↗
PubMed1980

Leukemic iris infiltration.

A 7-year-old boy with acute lymphocytic leukemia developed iris infiltration, blood-streaked hypopyon, and high intraocular pressure. A diagnostic anterior chamber paracentesis was performed, which provided a cytologic diagnosis. The aspirate was studied by both the millipore filter technique with Papanicolaou stain and a dried smear using the Wright's stain. Wright's stain provided more distinct cellular details. Irradiation of the anterior segment resulted in clearing of leukemic iris infiltration, hypopyon, and glaucoma.

Adrenal Cortex Hormones↗
PubMed1997

OX40 expressed on fresh leukemic cells from adult T-cell leukemia patients mediates cell adhesion to vascular endothelial cells: implication for the possible involvement of OX40 in leukemic cell infiltration.

We demonstrated previously that OX40 and its ligand, gp34, directly mediate adhesion of activated normal CD4+ T cells, as well as human T-cell leukemia virus type I (HTLV-I)-transformed T cells to vascular endothelial cells. In the present study, we examined expression of OX40 on fresh leukemic cells from patients with adult T-cell leukemia (ATL) and its possible involvement in cell adhesion. Flow cytometric analysis showed that peripheral blood mononuclear cells (PBMC) or lymph node tumor cells from 15 of 17 cases expressed significant levels of OX40 without stimulation. On the other hand, gp34 was not expressed on these cells, although its expression is also known to be associated with HTLV-I-infection. In Western blot analysis, a 50-kD protein band was detected by anti-OX40 monoclonal antibody (MoAb) in two ATL cases examined, as well as phytohemagglutinin (PHA) blasts and Hut102, an HTLV-I-infected T-cell line, but not in resting PBMC or Jurkat. Expression of OX40 mRNA was shown by reverse transcriptase-polymerase chain reaction in all ATL cases tested, PHA-blasts, and Hut102, but not in resting PBMC or Jurkat. We could not detect expression of HTLV-I viral mRNA in any of the cases tested. Cell adhesion assay was performed and in at least three cases, fresh ATL cells exhibited adhesion to human umbilical vein endothelial cells that could be considerably inhibited by either anti-OX40 MoAb or anti-gp34 MoAb. Immunohistochemical staining of skin biopsy specimens indicated that infiltrating mononuclear cells express OX40 in vivo. Taken together, these data indicate that leukemic cells from most, but not all, ATL patients constitutively express OX40, which may play a role in leukemic cell infiltration in addition to cell adhesion in vivo.

Adult↗
PubMed1989

In vitro and in vivo killing of acute lymphoblastic leukemia cells by L-asparaginase.

L-Asparaginase (ASNase) is a potent antileukemic enzyme routinely used in the treatment of children with acute lymphoblastic leukemia. As part of investigations of the biological activity of ASNase, we have developed techniques which measure the in vitro and in vivo cell killing ability of ASNase. To study the effect of ASNase on in vitro survival of primary lymphoblasts, bone marrow mononuclear cells obtained from untreated patients with acute lymphoblastic leukemia were cultured with and without ASNase. After 5 days, viable cells were counted using trypan blue exclusion to calculate total cell kill due to ASNase. Propidium iodide exclusion, leukemia cell surface antigens, and flow cytometry were used to determine leukemia cell kill due to ASNase. Comparison of leukemia cell kill and total cell kill showed a direct linear relationship (n = 24, r = 0.7), preferential killing of leukemia cells by ASNase (slope = 0.66), and that use of leukemia cell surface markers yielded a more accurate measurement of leukemia cell killing. ASNase at concentrations from 0.0001 to 0.1 IU/ml had equal effects on extent of leukemia cell killing (P = 0.3 to 0.7), suggesting the absence of a dose response at the ASNase concentrations tested. As a measure of the in vivo response to ASNase treatment, the number of viable bone marrow leukemia cells in the patient prior to and 5 days after treatment with ASNase was measured as the product of (% of rhodamine 123 fluorescent [viable] cells) x (absolute leukemic infiltrate). The change which occurred in the viable leukemic infiltrate was the same for patients whether they received 25,000 or 2,500 IU/m2 of ASNase as a single drug. There was a linear correlation (n = 8, r = 0.9) between in vivo and in vitro leukemia cell killing by ASNase. Thus, the in vitro assay described here can be used to predict in vivo sensitivity to ASNase in acute lymphoblastic leukemia.

Asparaginase↗
PubMed1996

Optic nerve head infiltration in acute leukemia in children: an indication for emergency optic nerve radiation therapy.

Two pediatric patients with acute leukemia who developed optic nerve head leukemic infiltration are presented. In one patient both eyes were involved at diagnosis as well as her central nervous system. Despite systemic and intrathecal chemotherapy she lost her vision within a few weeks. Cranial irradiation at that point could not reverse this outcome. In the second patient optic nerve head infiltration was found a few months after diagnosis, treated promptly with cranial irradiation and her vision was saved. Her central nervous system (CNS) was not involved at any time. It is stressed that ocular complaints including eye pain or blurred vision in the pediatric patient with leukemia should be investigated without delay by an ophthalmologist. In the young child these complaints may be absent and change in the visual behavior should then alert the pediatric oncologist for possible ocular problems. If optic nerve head leukemic infiltration is diagnosed and promptly treated with emergency radiation, vision can be salvaged.

Adolescent↗
PubMed1994

Analysis of mast cell subpopulations (MCT, MCTC) in cutaneous inflammation using novel enzyme-histochemical staining techniques.

In order to gain insights into the dynamics of mast cell subpopulations in normal and diseased skin, a novel enzyme-histochemical double and triple staining method was employed that allowed the detection of metachromasia (toluidine blue) and the mast cell proteases tryptase and chymase within the same cell. Cryostat sections were used of skin biopsies from the following specimens: normal skin (N = 4), psoriasis (N = 13), atopic eczema (N = 7), lichen planus (N = 6), interferon alpha 2a injection sites (N = 1) of a leukemic infiltrate and corresponding normal skin of the same patient before and after treatment. (i) Equal numbers of tryptase- and chymase-positive mast cells (MCTC) were obtained in all normal and diseased specimens in papillary and reticular dermis, with threefold increases around appendages. (ii) Tryptase-positive mast cells (MCT) were absent in normal skin, but were markedly increased in a disease-specific pattern within the papillary dermis, the inflammatory infiltrate and around appendages. (iii) Marked increases of MCT were also noted at interferon injection sites within the leukemic infiltrate, but not in the normal skin of the same patient. These data suggest that disease-dependent mast cell dynamics involve only MCT in cutaneous inflammation and that MCT numbers are controlled by distinct, disease-specific local tissue factors.

Amino Acid Sequence↗