If this can be experimentally proven, then MERTK would represent a good therapeutic target against which a specific tyrosine kinase inhibitor could be developed. The importance of diagnostic cytogenetics on outcome in AML: Distinct types of diffuse large B-cell lymphoma identified by gene expression profiling. Multiple endogenous antagonists of the Caspase-activation pathways have been discovered, and examples of dysregulation of their expression or function in lymphoma, leukemia, and solid tumors have been obtained. The class discriminating genes again provide a view into the molecular pathology of these leukemias and a number of testable hypotheses can be generated. It is recognized that with improvements in therapy, certain variables might lose their prognostic value; therefore, risk assignment plans should be routinely reassessed.

Although a number of groups are pursuing these types of studies, it is likely to be years before this type of analysis moves into the clinic. Simultaneous characterization of glutathione S-transferase M1 and T1 polymorphisms by polymerase chain reaction in American whites and blacks. The enzyme 5,methylenetetrahydrofolate reductase MTHFR , which catalyzes the reduction of 5,methylenetetrahydrofolate to 5-methyltetrahydrofolate, is crucial to folate metabolism. Patients with MLL do not respond well to conventional therapy. A childhood acute lymphoblastic leukemia genome-wide association study identifies novel sex-specific risk variants. Methodological Considerations Expression microarray platforms, either cDNA- or oligonucleotide-based, result in the collection of expression values for a large number of genes, varying from several hundred up to 33, genes depending on the specific microarray platform being used.

acute lymphoblastic leukemia case study hesi

Appropriate statistical methods were applied. Received Dec 12; Accepted Jan The patient was discharged and followed-up with no further treatment needed. Homocysteine, pharmacogenetics, and neurotoxicity in children with leukemia.

Lgmphoblastic features and treatment outcome of children with myeloid antigen positive acute lymphoblastic leukemia: The class discriminating genes again provide a view into the molecular pathology of these leukemias and a number of testable hypotheses can be generated.


In normal lymphocytes, none of the studied parameters changed significantly compared to cells treated with doxorubicin only. Contribution of the cystathionine beta-synthase gene ins68 polymorphism to the risk of early-onset venous and arterial occlusive disease and of fasting lymphoblastc.

Pharmacokinetics of vincristine in children and lynphoblastic with acute lymphocytic leukemia. Autophagy is essential for the regulation of cell survival in the harsh environment.

Pediatric Acute Lymphoblastic Leukemia

A phase I dose-finding study of combined treatment with an antisense Bcl-2 oligonucleotide Genasense and mitoxantrone in patients with metastatic hormone-refractory prostate cancer. However, Yeoh et al first used supervised learning algorithms primarily support vector machines to identify expressed genes that were associated with each recurrent cytogenetic abnormality in ALL.

Acute and chronic leukemia are severe malignant cancers worldwide, and can occur in pediatric patients. Host genetics of infectious diseases: In studies performed by a number of different laboratories, expression leuksmia have been obtained on a large number of diagnostic pediatric ALL samples.

Unfortunately, this is a difficult and expensive process requiring a variety of laboratory studies including morphology, immunophenotyping, cytogenetics, and molecular diagnostics.

acute lymphoblastic leukemia case study hesi

Thus, to translate these lists into biological information, it is essential to develop testable hypotheses from these gene lists, and then perform direct experiments to either validate or disprove these hypotheses. Since individual T-cell receptor and immunoglobulin genes undergo a unique clonal rearrangement, they can be used as specific targets for residual tumor detection. The analysis of the class discriminating genes can also provide new insights into the pathogenesis of the different leukemia subtypes.

The enzyme 5,methylenetetrahydrofolate reductase MTHFRwhich catalyzes the reduction of 5,methylenetetrahydrofolate to 5-methyltetrahydrofolate, is crucial lymphoblasstic folate metabolism. A novel protein complex distinct from mismatch repair binds thioguanylated DNA.

AKT plays a central role in tumorigenesis. Class specific genes can studdy selected using a variety of different statistical approaches, including t-statistics, a chi-squared metric, weighted average, etc. In reality, the bulk of tumor burden is below this limit of detection. Although the magnitude of this difference may be less apparent on recent studies, intensified therapy has failed to abrogate this difference.


Am J Pediatr Hematol Oncol. First, strategies for attacking the Bcl-2 and Bcl-X L proteins using small-molecule drugs have emerged from an understanding of how our own cells keep these anti-apoptotic proteins under control.

Recent genome wide association and replication studies have highlighted specic polymorphisms contributing to childhood ALL predispositions mostly in European populations. Higher frequency of glutathione S-transferase deletions in black children with acute lymphoblastic leukemia.

Pediatric Acute Lymphoblastic Leukemia

Almost a third of adult patients have a specific chromosome translocation; “Philadelphia Positive” ALL. In the subgroup of children who received at least one p53 dependent drug, patients could be segregated into two groups, one group that showed up-regulation of p53 protein and stydy target p21, and another group that showed no increase following therapy, thus identifying at least two distinct pathways leading to apoptosis. This site is for educational purposes only; it can not leuemia used in diagnosis or treatment.

In vivo response to the therapy would be predicted to be one of the most useful predictors of outcome and studies in ALL and other tumors show this to be the case.

Genetic lesions in a preleukemic aplasia phase in a child with acute lymphoblastic leukemia. In contrast, levels of most T lymphocyte subsets decreased only transiently and returned to leeukemia levels by days 78 to