PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 353670

Acute nonlymphoid leukemia.

T F Necheles
View original source ↗Export metadata ↓

Abstract

Acute nonlymphoid leukemia (ANLL) is not an uncommon form of leukemia in children. The differential diagnosis is sometimes difficult, but there are a number of laboratory tests that can contribute useful information. Despite the introduction of several newer chemotherapeutic agents, only 50 to 60 percent of children with ANLL achieve complete remissions, and the median survival at this time is only about 14 to 18 months. Immunotherapy and bone-marrow transplantation may offer important future avenues of therapy. CNS leukemia has recently evolved as an important complication in this group of leukemias.

Explore related subjects

Antineoplastic AgentsBone MarrowBone Marrow TransplantationChildFemaleHumansInfant, NewbornInfant, Newborn, DiseasesInfectionsLeukemia, Myeloid, AcuteMaleRemission, SpontaneousTime FactorsTransplantation, HomologousJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

T F Necheles. 1978. Acute nonlymphoid leukemia.. https://pubmed.ncbi.nlm.nih.gov/353670/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2021

Deep generative neural network for accurate drug response imputation.

Drug response differs substantially in cancer patients due to inter- and intra-tumor heterogeneity. Particularly, transcriptome context, especially tumor microenvironment, has been shown playing a significant role in shaping the actual treatment outcome. In this study, we develop a deep variational autoencoder (VAE) model to compress thousands of genes into latent vectors in a low-dimensional space. We then demonstrate that these encoded vectors could accurately impute drug response, outperform standard signature-gene based approaches, and appropriately control the overfitting problem. We apply rigorous quality assessment and validation, including assessing the impact of cell line lineage, cross-validation, cross-panel evaluation, and application in independent clinical data sets, to warrant the accuracy of the imputed drug response in both cell lines and cancer samples. Specifically, the expression-regulated component (EReX) of the observed drug response achieves high correlation across panels. Using the well-trained models, we impute drug response of The Cancer Genome Atlas data and investigate the features and signatures associated with the imputed drug response, including cell line origins, somatic mutations and tumor mutation burdens, tumor microenvironment, and confounding factors. In summary, our deep learning method and the results are useful for the study of signatures and markers of drug response.

Antineoplastic Agents↗
PubMed1992

[Economic evaluation of prophylaxis with recombinant granulopoiesis stimulating factor].

BACKGROUND: The aim of the study was to economically evaluate the prophylactic use of the recombinant factor of the stimulation of granulocyte colonies (rG-CSF) for the prevention of episodes of febrile neutropenia (EFN) following antineoplasic chemotherapy. METHODS: The methods of economic evaluation used were those of cost analysis and cost-effectivity analysis. The probability of occurence of EFN was estimated by the application of the Delphi method and the costs were calculated. RESULTS: The costs of EFN for the patients with solid tumors is situated between 236,000-377,000 pesetas according to hospitalary centers. For patients with acute leukemia the value was estimated as between 391,000-667,000 pesetas. The results of the cost analysis indicate that the net cost per patient prophylactically treated is between 4,000-64,000 pesetas. The results of the cost-effectivity analysis indicate that the cost per case of no incidence of EFN is between 20,000-320,000 pesetas. CONCLUSIONS: Episodes of febrile neutropenia carry expansive hospital and antibiotic clinical treatment. The prophylactic use of new medication for patients between the first and second cycle of chemotherapy, in agreement with the estimates calculated, does not save health care costs but may improve the quality of life in these patients and permit the continuation of a therapeutic schedule without interruption which may improve the life expectancy of the patient.

Antineoplastic Agents↗
PubMed1992

Template-directed interference footprinting of cytosine contacts in a protein-DNA complex: potent interference by 5-aza-2'-deoxycytidine.

In the template-directed interference (TDI) footprinting method (Hayashibara & Verdine, 1990), analogs of the naturally occurring DNA bases are incorporated into DNA enzymatically and assayed for interference of sequence-specific binding by a protein. Here we extend this method to include analysis of contacts of amino acid residues to the major groove surface of cytosine residues (TDI-C footprinting). The base analog 5-aza-2'-deoxycytidine, in which the hydrophobic 5-CH of cytosine is replaced by a hydrophilic aza nitrogen, was incorporated into DNA via the corresponding 5'-triphosphate. The analog was found to base pair with guanine during polymerization, resulting in substitution of 2'-deoxycytidine residues. TDI-C footprints of the lambda repressor-OL1 operator complex revealed apparent contacts to the cytosines at operator positions 7 and 8. Inspection of the high-resolution X-ray crystal structure of the lambda-OL1 complex (Clarke et al., 1992; Beamer & Pabo, 1992) revealed that C8 makes a hydrogen binding contact with the Lys3; C7, on the other hand, makes a previously unnoticed hydrophobic contact with the alkane side chain of Lys3. In only the consensus operator half-site was cytosine interference observed, suggesting that the nonconsensus arm binds DNA very differently if at all. The N-terminal arm represents the archetypal case of a sequence-specific peptide-DNA complex characterized at high resolution; thus, the present studies suggest strategies for design and screening of DNA binding peptides. The finding that 5-aza-2'-deoxycytidine inhibits sequence-specific DNA binding proteins may suggest an alternative rationale for the biological activities of this and related azapyrimidine nucleosides.

Antineoplastic Agents↗