How does rara work

By contrast, rare genetic rearrangements may also contribute to leukemogenesis but are less summarized. Inhibition of cancer stem cell like cells by a synthetic retinoid. Nat Commun. Developing novel drugs that can abrogate the growth and metastasis of malignant tumors is a major challenge for cancer researchers.

Here we describe a novel synthetic retinoid, namely WYC, which inhibits proliferation of malignant murine melanoma tumor-repopulating cells TRCs , known to resist conventional drug treatment, with an IC.

Anaplastic thyroid cancer ATC is a highly lethal undifferentiated malignancy without reliable therapies. Retinoic acid RA has been employed to promote redifferentiation of thyroid cancers by increasing their I. Related: Thyroid Cancer. Breast Cancer Res Treat. Alternative probes may be used in equivocal cases. We present a single community-based institution's experience in further evaluating these cases. However, Because almost half of FISH equivocal cases converted to HER2 amplified upon alternative testing, clinical studies to determine the benefit of anti-HER2 therapy in these patients are urgently needed.

Cell Physiol Biochem. Numerous studies have found that methylation of the RAR beta promoter contributed to the occurrence and development of malignant tumors. However, the connection between RAR beta promoter methylation and prostate cancer PCa remains unknown.

The rates of RAR beta promoter methylation in the PCa and control groups including benign prostatic hyperplasia and normal prostate tissues were summarized. In addition, we evaluated the source region of available samples and the methods used to detect methylation. Additional studies with sufficient data are essential to further evaluate the clinical features and prognostic utility of RAR beta promoter methylation in PCa. Hum Pathol. As this mutation involved the region of interaction with DNA methyltransferases, we speculate an epigenetic alteration of genes involved in the APL-like phenotype.

Coupling the core of the anticancer drug etoposide to an oligonucleotide induces topoisomerase II-mediated cleavage at specific DNA sequences. Nucleic Acids Res. Etoposide and other topoisomerase II-targeted drugs are important anticancer therapeutics. Unfortunately, the safe usage of these agents is limited by their indiscriminate induction of topoisomerase II-mediated DNA cleavage throughout the genome and by a lack of specificity toward cancer cells.

Therefore, as a first step toward constraining the distribution of etoposide-induced DNA cleavage sites and developing sequence-specific topoisomerase II-targeted anticancer agents, we covalently coupled the core of etoposide to oligonucleotides centered on a topoisomerase II cleavage site in the PML gene. The initial sequence used for this 'oligonucleotide-linked topoisomerase inhibitor' OTI was identified as part of the translocation breakpoint of a patient with acute promyelocytic leukemia APL.

OTIs increased levels of enzyme-mediated cleavage by inhibiting DNA ligation, and cleavage complexes induced by OTIs were as stable as those induced by free etoposide. Finally, OTIs directed against the PML-RARA breakpoint displayed cleavage specificity for oligonucleotides with the translocation sequence over those with sequences matching either parental gene.

These studies demonstrate the feasibility of using oligonucleotides to direct topoisomerase II-mediated DNA cleavage to specific sites in the genome. Related: Etoposide.

Am J Hematol. Recent work has identified distinct molecular subgroups of acute myeloid leukemia AML with implications for disease classification and prognosis. It remains unclear whether these genetic alterations are associated with distinct immunophenotypic findings or affect prognosis. We identified cases of NPM1-mutated AML and correlated sequencing data with immunophenotypic and clinical findings.

Related: Apoptosis Signal Transduction. Multiplex fusion gene testing in pediatric acute myeloid leukemia. Pediatr Int. Karyotyping is generally performed to enable risk stratification, but the results are not always consistent with those of reverse transcription-polymerase chain reaction RT-PCR , and more accurate and rapid methods are required.

Fusion genes were confirmed on fluorescence in situ hybridization FISH in 11 of these 19 patients. In contrast, fusion genes were detected in 37 of 39 patients There were discrepancies in four patients Sci Rep. Acute myeloid leukemia AML is a malignancy of myeloid progenitor cells that are blocked in differentiation.

Autophagy is a lysosomal degradation pathway for the removal of cytoplasmic content and recycling of macromolecules. Retinoic acid RA has broad clinical applications for the treatment of various cancers, particularly acute promyelocytic leukemia.

However, RA-based therapy is limited by relapse in patients associated with RA resistance, the mechanism of which is poorly understood. RaRF was highly expressed in RA-resistant leukemia cells and its expression was strongly correlated with RA sensitivity. Collectively, we propose that RaRF may be a factor in the resistance mechanism and thus a potential target for leukemia therapy using RA. Related: MCL1.

Medicine Baltimore. Acute promyelocytic leukemia is characterized by an accumulation of promyelocytes in the bone marrow. A rearrangement translocation of genetic material between chromosomes 15 and 17, written as t 15;17 , fuses part of the RARA gene on chromosome 17 with part of another gene on chromosome 15 called PML. The PML protein blocks cell growth and division proliferation and induces self-destruction apoptosis in combination with other proteins.

As a result, excess promyelocytes accumulate in the bone marrow and normal white blood cells cannot form, leading to acute promyelocytic leukemia. Genetics Home Reference has merged with MedlinePlus. Learn more. The information on this site should not be used as a substitute for professional medical care or advice.

Maci S. Terrell, BS , Maci S. Terrell, BS. Joanna S. Yi, MD Joanna S. Yi, MD. Cite Icon Cite. View large Download slide. Add comment Close comment form modal. Submit a comment. Comment title. You have entered an invalid code. Submit Cancel. Thank you for submitting a comment on this article.