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Results for “Leukemic Infiltration”

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At least 1,315 records · Page 73Linked to original sources
PubMed1993

Endothelial activation antigens in pulmonary leukostasis in leukemia.

Adhesion between leukemic cells and the vascular endothelium has been suggested to play a role in the development of leukostasis in myelocytic leukemia. To define the role of adhesion molecules on the surface of endothelial cells in leukostasis, we used immunohistochemistry to study the expression of endothelial leukocyte adhesion molecule-1 (ELAM-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in lung tissue of 4 patients with pulmonary leukostasis. Lung tissue of 2 patients with myelocytic leukemia without leukostasis and 4 patients with irrelevant nonpulmonary disease was used as a negative control. Positive control tissues included a lymph node with angioimmunoblastic lymphadenopathy and a hyperplastic tonsil. Weak positive staining for ELAM-1 was found in 1 patient in vessels, both with and without leukostasis. Expression of VCAM-1 and ICAM-1 in all patients tested was similar to that in the negative controls. The results of this study suggest that activation of endothelium, with increased expression of the endothelial adhesion molecules under study, is not a prerequisite for the development of pulmonary leukostasis in leukemia.

Adolescent↗
PubMed1992

Central nervous system expression of a monoclonal paraprotein in a chronic lymphocytic leukemia patient.

An unusual complication of chronic lymphocytic leukemia (CLL) is reported. The patient, a 79-year-old man, had a long standing history of CLL, that had been complicated by the development of a Guillain-Barré-like syndrome and a peripheral biclonal gammopathy. The biclonal immunoglobulins identified in the serum were IgM lambda and IgG lambda. The patient's condition progressed and he eventually developed ophthalmologic complications. Cerebrospinal fluid (CSF) obtained during evaluation of his visual dysfunction contained numerous small, mature lymphocytes consistent with the presence of CLL cells in the central nervous system (CNS); immunoperoxidase staining of these cells revealed a monoclonal population. Protein electrophoretic evaluation of the patient's CSF showed a single monoclonal band and immunofixation electrophoresis of the CSF revealed that the immunoglobulin present was IgG lambda. No evidence for the monoclonal IgM paraprotein identified in serum could be appreciated in the CSF by immunofixation. Taken together, these findings strongly implied that there was CNS involvement by the leukemia and this process caused the patient's neurologic symptoms. Furthermore, this study demonstrates that chronic lymphocytic leukemia should also be considered as one of the hematopoietic malignancies associated with monoclonal gammopathies involving the CNS.

Aged↗
PubMed1985

Predominant T cells in pleural effusion of a patient with B-cell CLL.

Pleural effusion is a relatively rare complication of chronic lymphatic leukemia (CLL). It can be the result of primary pleural involvement, central lymphatic blockage, infection or changes induced by previous irradiation or chemotherapy. When the effusion is caused by leukemic pleural infiltration, the lymphocytes are identical to those in the peripheral blood. We have recently treated a splenectomized patient with B-cell CLL who developed pleural effusion with predominant T cells. It is suggested that this might be due to a redistribution of the T cells in the recirculating lymphocytic pool in a patient who had undergone splenectomy in the past. The possible source of these cells in the pleural effusion is discussed.

B-Lymphocytes↗
PubMed1998

Diffuse alveolar hemorrhage with underlying pulmonary capillaritis in the retinoic acid syndrome.

All-trans-retinoic acid (ATRA) can induce a clinical remission in patients with acute promyelocytic leukemia. An adverse condition called "retinoic acid syndrome" limits this therapy. It is characterized by fever and respiratory distress, along with weight gain, pleural or pericardial effusions, peripheral edema, thromboembolic events, and intermittent hypotension. The lung disease has been previously ascribed to an infiltration of leukemic or maturing myeloid cells into lung parenchyma, which is sometimes associated with pleural effusions and diffuse alveolar hemorrhage. We report a case of retinoic acid syndrome in an 18-yr-old woman who developed diffuse alveolar hemorrhage while being treated with ATRA for acute promyelocytic leukemia. An open lung biopsy revealed pulmonary capillaritis.

Adolescent↗
PubMed1987

Burkitt-like lymphoid malignancy presenting as a breast tumor.

The authors describe a case of a female patient, who presented with a rapidly expanding mass of the right breast as the first clinical sign of a Burkitt-like lymphoproliferative disorder. Massive bone marrow infiltration with leukemic spillover and limited lymph node involvement were subsequently detected. The difficulties encountered in classifying, according to current schemes, the observed lymphoid neoplasm are emphasized. Moreover, an evaluation of the true rarity of mammary localizations at the onset of lymphoid malignancies, based on a review of the literature, suggests, especially for the most malignant varieties, a higher frequency than supposed.

Bone Marrow↗
PubMed2002

Mediastinal immature teratoma with yolk sac tumor and myelomonocytic leukemia associated with Klinefelter's syndrome.

A 14-year-old male presenting with a short history of right subclavicular chest pain was found to have a mediastinal tumor. Hematologic investigations and bone marrow examination showed features of myelomonocytic leukemia. The mediastinal tumor was excised, but the surgery was complicated by massive hemorrhage. The patient's condition deteriorated postoperatively and he died a week later. The histology of the mediastinal tumor showed the typical features of an immature teratoma with a yolk sac tumor. A prominent infiltrate of leukemic blast cells was present within blood vessels and in close proximity to the yolk sac component. The karyotypic analysis of leukemic cells isolated and cultured from the bone marrow showed 50XXY, +8, +21, +iso G-group marker chromosome karyotype.

Adolescent↗
PubMed2003

Inhibition of acute lymphoblastic and myeloid leukemias by a novel kinase inhibitor.

In recent years, synthetic tyrosine kinase inhibitors have made a rapid transition from basic research to therapeutic application. These compounds represent a major clinical advance in the approach to cancer in their relative specificity of action and decreased toxicity. We report here the effects of a novel tyrosine kinase inhibitor CR4 that interferes with growth-promoting pathways to markedly inhibit the growth and survival of both Philadelphia-positive and -negative acute lymphoblastic leukemia (ALL) as well as acute myeloid leukemia (AML). While efficiently ablating leukemic cell growth, normal cell growth and differentiation remain unaffected by CR4. CR4 demonstrates an ability to inhibit the function of multiple growth-critical kinases and yet exhibits a low level of cytotoxicity. These findings suggest that CR4 may prove to be highly effective as a therapeutic agent.

Acute Disease↗
PubMed2003

Possible link between unique chemokine and homing receptor expression at diagnosis and relapse location in a patient with childhood T-ALL.

Childhood acute lymphoblastic leukemia (ALL) is often associated with extramedullary infiltration by leukemic cells at diagnosis or at relapse. To understand the mechanisms behind the dissemination of T-cell ALL (T-ALL) cells this study investigated the homing receptor expression on the blast cells of 11 pediatric T-ALL patients at diagnosis. One patient revealed a unique profile with high expression of the chemokine receptor CCR9 and the integrin CD103 on the T-ALL cells. Both of these molecules are specifically associated with homing to the gut. This finding was clinically significant as the patient later suffered a relapse that was confined to the gut. Immunohistochemistry revealed that the leukemic cells in the gut still expressed CCR9 and colocalized with a high expression of the CCR9 ligand, CCL25. These findings suggest that the original expression of CCR9 and CD103 on the leukemic cells contributed to the relapse location in the gut of this patient.

Calcium Signaling↗
PubMed2004

Infant acute lymphoblastic leukemia with MLL gene rearrangements: outcome following intensive chemotherapy and hematopoietic stem cell transplantation.

Forty-four infants with acute lymphoblastic leukemia (ALL) characterized by MLL gene rearrangements were treated on a protocol of intensive chemotherapy followed by hematopoietic stem cell transplantation (HSCT) between November 1998 and June 2002. The remission induction rate was 91.0%, and the 3-year overall survival and event-free survival (EFS) rates, with 95% confidence intervals, were 58.2% (43.5%-72.9%) and 43.6% (28.5%-58.7%), respectively. Univariate analysis of EFS by presenting features indicated a poorer outcome in patients younger than 6 months of age with high white blood cell counts (>/= 100 x 10(9)/L; EFS rate, 9.4% versus 55.1% for all others, P = .0036) and in those with central nervous system invasion (EFS rate, 10.0% versus 56.9% for all others, P = .0073). The 3-year posttransplantation EFS rate for the 29 patients who underwent HSCT in first remission was 64.4% (46.4%-82.4%). In this subgroup, only the timing of HSCT (first remission versus others) was a significant risk factor by multivariate analysis (P < .0001). These results suggest that early introduction of HSCT, possibly with a less toxic conditioning regimen, may improve the prognosis for infants with MLL(+) ALL. Identification of subgroups or patients who respond well to intensified chemotherapy alone should have a high priority in future investigations.

Age Factors↗
PubMed2007

Neurologic complications associated with intrathecal liposomal cytarabine given prophylactically in combination with high-dose methotrexate and cytarabine to patients with acute lymphocytic leukemia.

Central nervous system (CNS) prophylaxis has led to a significant improvement in the outcome of patients with acute lymphocytic leukemia (ALL). Liposomal cytarabine (Enzon Pharmaceuticals, Piscataway, NJ; Skye Pharma, San Diego, CA), an intrathecal (IT) preparation of cytarabine with a prolonged half-life, has been shown to be safe and effective in the treatment of neoplastic meningitis. Liposomal cytarabine was given for CNS prophylaxis to 31 patients with newly diagnosed ALL. All patients were treated concurrently with hyper-CVAD chemotherapy (fractionated cyclophosphamide, vincristine, doxorubicin, and dexamethasone) including high-dose methotrexate (MTX) and cytarabine on alternating courses. Liposomal cytarabine 50 mg was given intrathecally on days 2 and 15 of hyper-CVAD and day 10 of high-dose MTX and cytarabine courses until completion of either 3, 6, or 10 IT treatments, depending on risk for CNS disease. Five patients (16%) experienced serious unexpected neurotoxicity, including seizures, papilledema, cauda equina syndrome (n = 2), and encephalitis after a median of 4 IT administrations of liposomal cytarabine. Toxicities usually manifested after the MTX and cytarabine courses. One patient died with progressive encephalitis. After a median follow-up of 7 months, no isolated CNS relapses have been observed. Liposomal cytarabine given via intrathecal route concomitantly with systemic chemotherapy that crosses the blood-brain barrier such as high-dose MTX and cytarabine can result in significant neurotoxicity.

Adult↗
PubMed1993

Extended triple intrathecal chemotherapy trial for prevention of CNS relapse in good-risk and poor-risk patients with B-progenitor acute lymphoblastic leukemia: a Pediatric Oncology Group study.

PURPOSE: The Pediatric Oncology Group (POG) acute leukemia in childhood (ALinC) 13 study tested two treatment regimens that used different CNS chemoprophylaxis for children older than 12 months with non-T, non-B acute lymphoblastic leukemia (ALL) and with no demonstrable CNS disease at diagnosis. PATIENTS AND METHODS: With the first regimen, standard (S), six injections of triple intrathecal chemotherapy (TIC), consisting of methotrexate (MTX), hydrocortisone (HC), and cytarabine (ara-C), were administered during intensification treatment and at every-8-week intervals throughout the maintenance phase for 17 additional doses. The second regimen, standard and MTX pulses (SAM), also specified six TICs during intensification, but substituted every-8-week pulses of intermediate-dose parenteral methotrexate (IDM; 1 g/m2) for the 17 maintenance TIC injections, with a low-dose intrathecal (IT) MTX boost administered with the first four maintenance IDM pulses. Otherwise, systemic therapy on regimen SAM was identical to regimen S. There were 1,152 patients randomized to the S and SAM regimens after stratification by risk group (age/leukocyte count) and immunophenotype. RESULTS: The 5-year probabilities (+/- SE) of an isolated CNS relapse were regimen S: good risk (n = 381), 2.8% +/- 1.3%; poor risk (n = 196), 7.7% +/- 3.2%; good + poor risk (n = 577), 4.7% +/- 1.5%; regimen SAM: good risk (n = 388), 9.6% +/- 2.2%; poor risk (n = 187), 12.7% +/- 4.2%; good + poor risk (n = 575), 10.9% +/- 2.2%. In poor-risk patients, approximately one third of the isolated CNS relapses occurred before preventive CNS therapy was begun at week 9. Hence, regimen S has provided better CNS preventive therapy for both good- and poor-risk patients (P < .001 overall). The difference is statistically significant for good-risk patients (P < .001), but not for poor-risk patients (P = .20). Neither treatment has shown a significant advantage in terms of general outcome. CONCLUSION: TIC injections extended throughout the intensification and maintenance periods are superior to IDM pulses for prevention of CNS leukemia. Our results with TIC seem comparable with those achieved with other contemporary methods of CNS preventative therapy. Thus, extended TIC affords a reasonable alternative to CNS irradiation plus upfront IT MTX for patients with B-progenitor ALL.

Antineoplastic Combined Chemotherapy Protocols↗