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Cell Anaplastic Lymphoma - Crossref

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Last Updated: 15 August 2022

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High-dose methotrexate monotherapy followed by radiation for CD30-positive, anaplastic lymphoma kinase-1–positive anaplastic large-cell lymphoma in the brain of a child

Primary CNS CD30-positive anaplastic large-cell lymphoma with primary CNS CD30-positive anaplastic lymphoma that was also positive for anaplastic lymphoma kinase-1. The authors explore the case of an 11-year-old immunocompetent boy with primary CNS CD30-positive anaplastic large-cell lymphoma. The findings on CT scanning were normal. In the left parietal lobe, subsequent MRI revealed newly developed lesions and concomitant edema. Because ALCL is inherited in the brain and difficult to identify, no standard treatment has been developed. Pediatric primary CNS ALCL can be a safe and cost-effective therapeutic option for systemic HD-MTX monotherapy, according to this study.

Source link: https://doi.org/10.3171/2014.6.peds1492


Primary Central Nervous System Anaplastic Large Cell Lymphoma, ALK Positive

Abstract Objectives A key component of the primary central nervous system Anaplastic large cell lymphoma, anaplastic lymphoma kinase positive, is a rare CNS lymphoma whose description is limited to case reports. With observational results, we have the most comprehensive case series to date of primary CNS ALCL, ALK+, with observational results. Methods A retrospective review of multiple academic centers was carried out to find instances of primary CNS ALCL, ALK+. ALK+, the primary CNS ALCL, ALK+ was also researched by a team of researchers. Primary CNS ALCL, ALK+ from our databases We found three instances of primary CNS ALCL, ALK+ from our databases. An ALK rearrangement was demonstrated by fluorescence in situ hybridization, assay demonstrated an NPM1-ALK gene fusion in one case, according to genetic studies. Conclusions We present the most comprehensive case series to date of a rare primary CNS lymphoma with more diagnostic and clinical data.

Source link: https://doi.org/10.1093/ajcp/aqac046


Quantitative Acetylomics Uncover Acetylation-Mediated Pathway Changes Following Histone Deacetylase Inhibition in Anaplastic Large Cell Lymphoma

Histone deacetylases attack acetylated lysine residues in histone and non-histone proteins. In addition, HDACs regulate T-cell differentiation, and HDAC inhibitors have been licensed for use in some T-cell malignancies. However, the exact targets and mechanisms of HDAC inhibition in cancer are understudied. HDAC deficionation of Hdac1 has been isolated from a transgenic mouse model of anaplastic large cell lymphoma, a rare T-cell lymphoma, and acute HDAC involvement by transplanting tumor cell lines from a transgenic mouse model of anaplastic large cell lymphoma with abrogated HDAC activity. Following Hdac1 deletion or pharmacological inhibition using label-free liquid chromatography mass chromatography, changes in total protein expression, as well as histone and protein acetylation were determined as well as protein acetylation. HDAC inhibition in malignant T cells has broad applicability and could have translational implications for the treatment of ALCL with HDACis alone or in combination therapy.

Source link: https://doi.org/10.3390/cells11152380


Anaplastic large T-cell lymphoma: 10-year experience at the National Institute of Neoplastic Diseases, Lima – Peru

Methods: Descriptive, retrospective review of patients with Anaplastic Large T-Cell Lymphoma of the National Institute of Neoplastic Diseases between 2006 and 2016. 48 of the patients were found in CDI and II, and 36 between stages III and IV. In the case of patients with ALK+, it was 67. 4%, while in the group with ALK+ it was 42. 2%, and in the group with ALK+ it was predicted at 30. 2%.

Source link: https://doi.org/10.25176/rfmh.v22i3.5027


Anaplastic lymphoma kinase rearrangements in non-small-cell lung cancer: novel applications in diagnostics and treatment

For this reason, molecular diagnostic testing for dysregulated ALK expression is a vital component of finding the right NSCLC treatment options. We review the molecular pathology of ALK-positive NSCLC, ALK molecular diagnostic methods, ALK-targeted NSCLC treatments, and drug resistance mechanisms to ALK-targeted therapies.

Source link: https://doi.org/10.2217/pgs-2017-0098


JunB Induced by Constitutive CD30–Extracellular Signal-Regulated Kinase 1/2 Mitogen-Activated Protein Kinase Signaling Activates the CD30 Promoter in Anaplastic Large Cell Lymphoma and Reed-Sternberg Cells of Hodgkin Lymphoma

Abstract: High expression of CD30 and JunB in anaplastic large cell lymphoma and Hodgkin lymphoma is typical of tumor cells in anaplastic large cell lymphoma. In both ALCL and HL, Phosphorylation of ERK1/2 MAPK was confirmed in nuclei of tumor cells. These results reveal a common mechanism of CD30 overexpression in ALCL and HL, but the results of CD30 signaling differs between NPM-positive ALCL and NPM-negative ALCL, cutaneous ALCL, and HL, as we recently reported.

Source link: https://doi.org/10.1158/0008-5472.can-05-0925


Cost-effectiveness analysis of ceritinib vs. crizotinib in previously untreated anaplastic lymphoma kinase (ALK)-positive non-small cell lung cancer (NSCLC) in Hong Kong

In 2018, lower-dose ceritinib was introduced in Hong Kong for first-line treatment of patients with anaplastic lymphoma kinase-positive advanced non-small cell lung cancer with anaplastic lymphoma kinase-positive advanced non-small cell lung cancer. From a HK healthcare service provider's or government's perspective, this report investigated the cost-effectiveness of ceritinib vs. crizotinib in the first-line treatment of ALK+ NSCLC in the first-line treatment of ALK+ NSCLC. Methods: Costs and effectiveness of first-line ceritinib vs. crizotinib over a 20-year period were determined using a partitioned survival model with three health states based on a partitioned survival model. The efficacy results for ceritinib were obtained from a phase 3 trial comparing ceritinib with chemotherapy for advanced non-small cell lung cancer as well as extrapolated using parametric survival models. From a matching-adjusted indirect comparison based on ASCEND-4 and PROFILE 1014 trials, a long-term survival associated with crizotinib was predicted using a hazard ratio of crisisotinib vs. ceritinib was estimated.

Source link: https://doi.org/10.21203/rs.3.rs-17823/v2


Cost-effectiveness of ceritinib in previously untreated anaplastic lymphoma kinase (ALK)-positive non-small cell lung cancer (NSCLC) in Hong Kong

Abstract : In 2018 in Hong Kong, a lower-dose ceritinib was approved for the first-line treatment of patients with anaplastic lymphoma kinase-positive advanced non-small cell lung cancer. From a HK healthcare service provider's or government's perspective, this report investigated the cost-effectiveness of ceritinib vs. crizotinib in the first-line treatment of ALK+ NSCLC in the first-line treatment of ALK+ NSCLC. Methods: Costs and results of first-line ceritinib vs. crizotinib over a 20-year time span were determined using a partitioned survival strategy with three health states based on a 20-year time horizon. Using a hazard ratio of crizotinib vs. ceritinib obtained from matching-adjusted indirect comparison based on ASCEND-4 and PROFILE 1014 trials, long-term survival associated with crizotinib was estimated for long-term survival following a closely monitored indirect comparison based on matching-adjusted indirect comparison based on ASCEND-4 and PROFILE 1014 trials. Patients receiving crizotinib had 2. 68 QALYs, 3. 85 LYs, and $ 150,424 total costs over the same time horizon. U2022 Certinib is the latest in a series of affordable healthcare services in Hong Kong, with 13,343. Conclusion: Ceritinib offers a cost-effective option compared to crizotinib for previously untreated ALK+ advanced NSCLC in HK. Implication for clinical practice or policy 2̆022 Ceritinib offers a cost-effective option compared to crizotinib for previously untreated ALK+ advanced NCSLC in HK with an incremental cost per QALY of 13,343 USD, significantly lower than the willingness to pay threshold. u2022 Ceritinib was a widely used treatment strategy in previously untreated adult patients with ALK+ advanced NCSLC, providing significant improvement in PFS, LYs, and QALYs in comparison to crizotinib.

Source link: https://doi.org/10.21203/rs.3.rs-17823/v1


CD30+ anaplastic large cell lymphoma: a review of its histopathologic, genetic, and clinical features

Abstract The neoplastic large cell lymphoma is a commonly recognized group of large cell lymphomas. Primary systemic anaplastic lymphoma kinase + ALCL, primary systemic ALK, U2212 ALCL, and primary cutaneous ALCL have been identified with the use of molecular and clinical methods. ALK+ ALCL is mainly caused by chromosomal translocations, most commonly t. ALK+ ALCL is mainly related to young male patients, and if treated with chemotherapy has a favorable prognosis. In contrast, large B-cell lymphomas with anaplastic morphology are thought to be not a distinct entity nor a morphologic manifestation of diffuse large B-cell lymphoma. Both Hodgkin disease and ALCL have morphological characteristics of both Hodgkin disease and ALCL and ALCL have previously been referred to as Hodgkin-like ALCL. However, new immunohistologic reports show that ALCLs Hodgkin-like represent either cases of tumor cellu2013-rich classic Hodgkin disease, ALK+ ALCL or ALK2212 ALCL.

Source link: https://doi.org/10.1182/blood.v96.12.3681


Understanding Factors Associated With Anaplastic Lymphoma Kinase Testing Delays in Patients With Non–Small Cell Lung Cancer in a Large Real-World Oncology Database

Contextu2014 (askeptile cell lung cancer) Patients with advanced non-u2013small cell lung cancer have multiple therapeutic options. The prompt ordering and return of results to determine therapy are of utmost importance. U2014 To determine the causes affecting anaplastic lymphoma kinase test ordering and result delivery, determine objectives. The ALK tests were performed on 14 197 patients with advanced nonu2013small cell lung cancer diagnosed between January 2015 and May 2019. ALK sample receipt in the laboratory was a surrogate for test order time and was a precursor to non-u2013small cell lung cancer diagnosis to ALK sample receipt. To determine factors associated with order time and turnaround time delays, Multivariable logistic regression was used to determine the causes associated with order time and turnaround time delays. Results. The result of the U2014 Median ALK test order time was 15 days, with 36. 4% of all 14 657 orders delayed. Failure of non-fluorescence in situ hybridization testing, tissue sample, and orders combining ALK with other biomarkers were associated with delayed ALK results reporting.

Source link: https://doi.org/10.5858/arpa.2021-0029-oa

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions