PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “hematologic neoplasms”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 253 records · Page 14Linked to original sources
PubMed1994

Cytotoxic activity of topoisomerase II inhibitors in primary cultures of tumor cells from patients with human hematologic and solid tumors.

BACKGROUND: Little is known about the in vitro activity and cross-resistance patterns of topoisomerase II (topo II) inhibitors in primary cultures of tumor cells from patients with different diagnoses. METHODS: The in vitro activity of the topo II inhibitors daunorubicin, doxorubicin, idarubicin, epirubicin, amsacrine, mitoxantrone, and etoposide was determined using the fluorometric microculture cytotoxicity assay. Four hundred seventy-six samples from patients with various diagnoses were tested with continuous drug exposure. RESULTS: Hematologic samples were more sensitive than solid tumors to all tested drugs. Etoposide was the most active drug in solid tumors followed by epirubicin, with amsacrine the least active. The anthracyclines doxorubicin, daunorubicin, and epirubicin showed similar in vitro activity. Conversely, idarubicin showed low to moderate cross-resistance with all tested topo II inhibitors. Mitoxantrone and amsacrine showed high in vitro activity and displayed cross-resistance to the anthracyclines in the hematologic neoplasms. In the solid tumor group, mitoxantrone and amsacrine had lower activity and weak correlations with the anthracyclines. Etoposide had intermediate to weak correlations with the other drugs. CONCLUSIONS: There is a marked difference in tumor-type specificity and cross resistance patterns among the different topo II inhibitors tested. This may indicate that minor differences in topo II interaction and/or other mechanisms of drug action may substantially determine the cytotoxic activity of topo II-targeted drugs.

Antineoplastic Agents↗
PubMed2001

Tumor growth pattern and thymidine phosphorylase expression are related with the risk of hematogenous metastasis in patients with Astler Coller B1/B2 colorectal carcinoma.

BACKGROUND: The benefit of adjuvant chemotherapy appears to be limited for patients with Astler Coller B1/B2 colorectal carcinoma but may be better in a subgroup of patients with a high recurrence risk. In the current case-control analysis, the authors evaluated whether patients with a high risk of hematogenous metastasis could be identified by means of a thorough histologic and immunohistochemical examination of the resection specimens. METHODS: A database was built for all patients treated in a general teaching hospital for colorectal carcinoma between 1985 and 1995. From this database, all patients with an Astler Coller B1 or B2 tumor who subsequently had developed hematogenous metastases were taken as cases. For each case, three matched controls (age, Astler Coller, year of diagnosis) without metachronous metastases were selected. The resection specimens of cases and controls were blindly examined by two observers for the following: World Health Organization (WHO) classification; differentiation grade; growth pattern; lymphocytic, fibroblastic, and eosinophilic reaction; angioinvasion; number of lymph nodes examined; expression of E-cadherin, vascular endothelial growth factor and thymidine phosphorylase (TP); P53; microvessel density. RESULTS: Twenty-two cases and 65 controls were included in the analysis. Tumor growth pattern and tumor TP expression both independently contributed to recurrence risk. With these 2 variables, 4 subgroups could be identified with a recurrence risk ranging from 0% to 42%. CONCLUSIONS: Tumor growth pattern and degree of TP expression both appear to be related to the recurrence risk. Prospective trials should point out whether these variables can be implemented in the decision making concerning adjuvant chemotherapy.

Biomarkers, Tumor↗
PubMed2000

Cancer risk in laboratory workers: an emphasis on biological research.

BACKGROUND: At the end of the 1980s, several cancer clusters were observed in biological research laboratories. Over time, biological research and the technologies used have been diverse and have involved a wide range of mutagenic or carcinogenic chemical, physical and biological agents. METHODS: We reviewed 45 published studies on cancer risk among biological research personnel and workers in closely related fields, and numerous reports based on routinely collected data. RESULTS: Biological research could be associated with an elevated risk for pancreatic cancer, brain tumors, and certain hemopathies. A common limitation of available studies was low statistical power and the absence or inaccuracy of data on individual past exposure. CONCLUSIONS: Overall, this study suggests a low overall risk of cancer, albeit a higher risk may be suggested for cancers of the pancreas (risk ratios ranging from 0.5 to 6.3) and brain (0.7-9.4), and for non-Hodgkin's lymphoma (0.6-51.5). We suggest ways in which multiple past exposures could be assessed more precisely and emphasize a pressing need to take into account known confounders.

Biological Science Disciplines↗
PubMed1985

Immunofluorescent plasma cell labeling indices (LI) using a monoclonal antibody (BU-1).

Tritiated thymidine labeling indices (LI), although useful in diagnosis and prognosis of multiple myeloma, have not found wide-spread application because autoradiographic analysis is difficult and time consuming. Using a monoclonal antibody (BU-1) reactive with 5-bromo-2-deoxyuridine (BrdUrd), we have developed an immunofluorescent procedure that allows DNA S-phase measurements to be determined in 4 hr. Plasma cells are easily identified by reactivity with a fluorescein isothiocyanate-conjugated antihuman immunoglobulin, and cells in DNA S phase are detected via BU-1 and a rhodamine-conjugated antimouse immunoglobulin. Results using this method on 12 patients with multiple myeloma compare favorably (correlation coefficient 0.84), with those obtained by tritiated thymidine. This immunofluorescent slide method will facilitate application of labeling indices as a clinical test to measure disease activity in patients with multiple myeloma and other hematologic neoplasms.

Antibodies, Monoclonal↗
PubMed1992

Prognostic value of cytogenetic analysis in human cerebral astrocytomas.

Cytogenetic analysis has become an important part of the diagnostic evaluation of most hematological neoplasms. However, there is limited information on the value of cytogenetic analysis in most solid tumors, including cerebral astrocytomas. This report summarizes a prospective cytogenetic study of 99 human cerebral astrocytomas, 16 mixed oligoastrocytomas, and 2 gliosarcomas. The cytogenetic procedure involved in situ culture and robotic harvesting techniques. Correlative clinical and survival data were available on all patients. We successfully cultured and obtained suitable metaphases in 107 of the 117 tumors. One or more chromosomally abnormal clones were observed in 72 tumors, and nonclonal or normal karyotypes were observed in 35 tumors. In a multivariate analysis, survival time was significantly better in patients whose tumors had normal or nonclonal karyotypes on cytogenetic analyses than in those whose tumors had clonal abnormalities (p = 0.0071). Our study demonstrates that cytogenetic analysis provides independent prognostic information in patients with cerebral astrocytomas.

Astrocytoma↗
PubMed2004

Soluble vascular endothelial growth factor receptor 1, and not receptor 2, is an independent prognostic factor in acute myeloid leukemia and myelodysplastic syndromes.

BACKGROUND: Vascular endothelial growth factor (VEGF) and its receptors (VEGFRs) are major regulators of angiogenesis, which plays a key role in the growth and dissemination of solid tumors and hematologic neoplasms. METHODS: The authors measured the plasma concentrations of soluble VEGFR1 (sVEGFR1) and sVEGFR2 in 133 patients with acute myeloid leukemia (AML) and in 80 patients with myelodysplastic syndromes (MDS) at the time of initial presentation and compared clinical behaviors. RESULTS: A reverse correlation was observed between plasma sVEGFR1 levels and the rate of complete remission (CR) in patients with AML, but not in patients with MDS. In contrast, increased plasma levels of sVEGFR2 were correlated with a lower CR rate in patients with MDS, but not in patients with AML. Cox regression model analysis demonstrated that plasma levels of sVEGFR1, but not sVEGFR2, were independent prognostic factors in both patients with AML and patients with MDS. CONCLUSIONS: The findings suggest that different mechanisms are involved in the pathophysiology of AML and MDS. The concentration of sVEGFR1 and sVEGFR2 in plasma should be considered a significant factor in guiding antiangiogenic therapy for AML and MDS. They may play a role in the pharmacodynamics of therapeutic agents that are supposed to bind directly to these receptors.

Adolescent↗
PubMed2006

Amplified, lost, and fused genes in 11q23-25 amplicon in acute myeloid leukemia, an array-CGH study.

Gene amplifications occur rarely in hematologic neoplasms. We characterized two cases of acute myeloid leukemia (AML) with marker chromosomes and 11q23-25 amplicons. Case 1 was a 14-year-old male with an additional ring of chromosome 11 material as the sole karyotypic abnormality, as determined by G-banding and multicolor fluorescence in situ hybridization. Standard comparative genomic hybridization (CGH) showed amplification in 11q23-qter. However, the MLL gene, in 11q23, was not amplified by FISH. Case 2 was a 38-year-old male with the G-banding karyotype 51,XY,+8,+19,+3mar and with 11q22-qter amplification by standard CGH. This patient also had the MLL-LARG fusion gene. We used microarray-based CGH (array-CGH) to characterize the amplicons. In case 1, the amplified region in 11q24.3-25 (5.5 Mb) was continuous, and MLL was not amplified, as expected. In case 2, the amplicon was divided into two distinct parts, in 11q23.3 (1.2 Mb) and in 11q23.3-25 (13.3 Mb). It contained a loss ( approximately 1 Mb) in 11q23.3, and the amplicon breakpoint was in the middle of MLL. Although the amplicon size varied, the patients had a common amplified region in 11q24-25 that comprised 14 genes. Expression microarray of case 1 revealed that three of these genes, FLI1, NFRKB, and SNX19, were also overexpressed. The results indicate that the 11q24-q25 region may harbor new candidate oncogenes. In addition, the complex amplicon of case 2 suggests some intriguing chromosomal mechanisms.

Acute Disease↗
PubMed1992

Chromosomal in situ suppression hybridization of immunologically classified mitotic cells in hematologic malignancies.

Chromosomal in situ suppression (CISS) hybridization was performed with library DNA from sorted human chromosomes 8, 9, 15, 17, 21, and 22 on immunologically stained bone marrow cells of four patients with a hematologic neoplasm, including two patients with myelodysplastic syndrome and trisomy 8, one patient with promyelocytic leukemia bearing the translocation t(15;17)(q22;q11-12), and one patient with chronic myeloid leukemia and the translocation t(9;22)(q34;q11). In all patients, the results of conventional karyotype analysis could be confirmed by one- or two-color CISS hybridization using the appropriate chromosome-specific libraries. Our results show that CISS hybridization can detect both numerical and structural chromosome changes in immunologically classified cells with high specificity and reliability. The fact that chromosome spreads of very poor quality can now be included in such analyses is a decisive advantage of this approach. In addition, the suitability of this approach for interphase cytogenetics is discussed.

Chromosome Aberrations↗
PubMed1995

Fluorescence in situ hybridization analysis of whole-arm 7;12 translocations in hematologic malignancies.

Cytogenetic analysis of one case of acute myeloid leukemia (AML), one of acute lymphoblastic leukemia (ALL), one of refractory anemia with excess of blasts (RAEB), and one of acute mixed lineage leukemia (AMLL) with unbalanced 7;12 translocations mapped the breakpoints to the centromeres on both chromosomes. The rearrangements were interpreted as the whole-arm translocations der(7;12)(q10;q10) in the AML and ALL and der(7;12)(p10;q10) in the RAEB and AMLL. However, further analysis by metaphase and/or interphase fluorescence in situ hybridization (FISH) showed centric fusion only in the AML and ALL. In the RAEB and AMLL, centromeric material from chromosome 7 but not from 12 was present in the derivative chromosome. Whereas the t(7;12) resulted in loss of 12p in all four cases, the corresponding chromosome 7 imbalances differed--monosomy for 7q in the RAEB and AMLL and monosomy for 7p in the AML and ALL. Six hematologic neoplasms with unbalanced whole-arm or near-centromeric 7;12 translocations and seven dic(7;12) with juxtacentromeric breakpoints have been reported previously: 2 AML, 1 RAEB in transformation, and 10 ALL. All karyotypically informative cases had loss of 12p material. All but one of the cases with combined 7p and 12p deletion were ALL, whereas all cases with 7q and 12p loss showed myeloid differentiation. No particular clinical, morphologic, or immunophenotypic features seem to characterize ALLs with t(7;12). AMLs with an unbalanced t(7;12), often together with 5q deletions, might be associated with previous genotoxic exposure and poor prognosis.

Adult↗
PubMedDate not supplied

Histopathological lesions of the liver in hairy cell leukemia: a report of 14 cases.

Pathological lesions of the liver were studied in 14 cases of hairy cell leukemia, a rare hematologic neoplasm involving numerous organs. Tumor infiltration of hepatic parenchyma was observed in all cases. Tumor cells were easily recognized by their cytological features, namely their "halo" appearance consisting of a clear rim of abundant cytoplasm surrounding uniform round or slightly indented nuclei. Portal infiltration was observed in all cases, associated with sinusoidal infiltration in 12 cases. A peculiar change of the sinusoids, i.e., the angiomatous lesions, was noted in 9 of 14 patients. Angiomatous lesions consisted of intralobular cavities without zonal predominance which were lined by tumor cells which replaced the normal sinusoidal wall and were filled with red blood cells and tumor cells. This pattern of involvement is different from hepatic localization of other blood malignancies and is highly suggestive of hairy, cell leukemia. It might reflect the unique phenotype of the tumor cells, which express lymphocytic and monocytic features. The angiomatous lesion strongly mimics peliosis hepatis and could be, as well as in peliosis, the consequence of modification of the sinusoidal barrier. In hairy cell leukemia, sinusoidal wall abnormalities might be secondary to infiltration of the sinusoids by tumor cells.

Adult↗
PubMed2006

Abnormal methylation of the common PARK2 and PACRG promoter is associated with downregulation of gene expression in acute lymphoblastic leukemia and chronic myeloid leukemia.

The PARK2 gene, previously identified as a mutated target in patients with autosomal recessive juvenile parkinsonism (ARJP), has recently been found to be a candidate tumor suppressor gene in ovarian, breast, lung and hepatocellular carcinoma that maps to the third common fragile site (CFS) FRA6E. PARK2 is linked to a novel described PACRG gene by a bidirectional promoter containing a defined CpG island in its common promoter region. We have studied the role of promoter hypermethylation in the regulation of PARK2 and PACRG expression in different tumor cell lines and primary patient samples. Abnormal methylation of the common promoter of PARK2 and PACRG was observed in 26% of patients with acute lymphoblastic leukemia and 20% of patients with chronic myelogenous leukemia (CML) in lymphoid blast crisis, but not in ovarian, breast, lung, neuroblastoma, astrocytoma or colon cancer cells. Abnormal methylation resulted in downregulation of PARK2 and PACRG gene expression, while demethylation of ALL cells resulted in demethylation of the promoter and upregulation of PARK2 and PACRG expression. By FISH, we demonstrated that a lack of PARK2 and PACRG expression was due to biallelic hypermethylation and not to deletion of either PARK2 or PACRG in ALL. In conclusion, our results demonstrate for the first time that the candidate tumor suppressor genes PARK2 and PACRG are epigenetically regulated in human leukemia, suggesting that abnormal methylation and regulation of PARK2 and PACRG may play a role in the pathogenesis and development of this hematological neoplasm.

DNA Methylation↗
PubMed1986

Legionnaires' disease in patients with cancer.

A 4-year experience with Legionella pneumophila (LD) diagnosed in 36 patients with cancer was reviewed. Cancer patients represented 24% of the total population of patients acquiring LD during that time. Hematologic neoplasms (42%) and lung cancer (22%) accounted for the majority of afflicted patients. Nosocomial infections occurred in 42% of the patients evaluated. Several risk factors were assessed, and only neutropenia, and previous steroid therapy played a causal role (p less than .05) when assessed in a retrospective case control fashion. Overall mortality in oncology patients with LD (53%) was high and underscores the need rapidly to diagnose and treat this entity. This mortality decreased after 1977 when an effective antibiotic was utilized. Mixed infections also played a major role in outcome and occurred in 31% of the 36 patients studied. The mortality in these cancer patients was 73%, and this emphasizes the need to exclude and treat concomitant bacterial or fungal infections.

Adult↗
PubMed1996

Antitumor Functions of Natural Killer Cells and Control of Metastases

Natural killer (NK) cells have been recognized as effector cells responsible for the elimination of blood-borne metastases. Newer evidence suggests that NK cells play an important role in the control of solid tissue metastases. NK cells have the ability to kill a broad variety of fresh or cultured "NK-resistant" tumor cell targets by mechanisms that are not dependent on perforin or granzyme secretion. Also, a subset of interleukin 2 (IL-2)-activated NK cells, which are called A-NK cells, is capable of extravasation, movement in solid tissues, localization to the sites of metastases, and killing tumor cells in situ. Studies in experimental animals and in cancer patients indicate that systemic adoptive immunotherapy with A-NK cells and IL-2 is a tolerable and promising treatment for advanced solid tissue as well as hematologic neoplasms. In this article, antitumor functions of A-NK cells in vitro and in vivo are reviewed, and the mechanisms responsible for their antitumor effects are considered.

Journal Article↗