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Cell Anaplastic Lymphoma - Europe PMC

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Last Updated: 15 September 2022

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IL-2/IL-2R signaling and IL-2Rα-targeted therapy in anaplastic large cell lymphoma.

Tu2011cell lymphoma, a CD30-positive non-Hodgkin's Tu2011cell lymphoma, is a CD30-positive non-Hodgkin's Tu2011cell lymphoma. Despite the introduction of CD30 antibody-drug conjugate-targeted therapy into front-line therapy regimens, some subtypes of the disease persists unsatisfactory. Therefore, targeting BATF3/IL-2R signaling may be a novel therapeutic treatment for ALCL patients.

Source link: https://europepmc.org/article/MED/36094651


Efficacy of Brigatinib in Patients With Advanced Anaplastic Lymphoma Kinase-Positive Non-Small Cell Lung Cancer Who Progressed on Alectinib or Ceritinib: ALTA-2 Study.

Patients with advanced ALK+ NSCLC with no deterioratib or ceritinib were treated with brigatinib 180 mg once daily in this single-arm, phase 2 ALTA-2 trial. In 33. 3% of baseline ctDNA; 14/202R; 52% of patients with detectable ALK fusion had EML4-ALK variant 3. In ALTA-2, brigatinib demonstrated limited growth in patients receiving ALK+ NSCLC post-ceritinib or post-alectinib therapy. In patients without baseline detectable plasma ALK fusion, Median PFS' life expectancy was longer due to brigatinib.

Source link: https://europepmc.org/article/MED/36096442


Characteristics and Clinical Outcomes of Patients with ALK-positive Anaplastic Large Cell Lymphoma: Report from the Prospective International T-Cell Lymphoma Project.

The T-cell Lymphoma Project is a worldwide registry prospective research that enrolls patients with newly diagnosed peripheral T-cell lymphomas and NK-cell lymphomas. Patients diagnosed and treated at their respective centers between September 2006 and February 2018, seventy-four institutions from 14 North America, South America, Europe, and Asia collected patient records from September 2006 to February 2018. Among 1553 PTCL patients, 131 were found to have an aplastic large cell lymphoma - kinase positive - kinase positive. Both estimates indicate that OS and PFS were both 77% and 68% respectively at three years, and that PFS were relatively similar at 5 years, with 77% of OS and 64% of PFS being the same. Although the results of ALK+ ALCL are superior to that of other PTCLs, it is still deemed favourable, considering the patient's young median age. Our findings show that both IPI and PIT are effective in identifying groups of patients with mixed outcomes.

Source link: https://europepmc.org/article/MED/36083035


Special clinicopathological features of anaplastic diffuse large B-cell lymphoma: a case report and literature review

In a nodular or follicular germinating center-like growth, there are a large number of pleomorphic centroblast-like cells with anaplastic characteristics and HRS-like cells in a nodular or follicular germinating center-like growth, which is consistent with diffuse large B-cell lymphoma, a non-specific subtype, which is typical of diffuse large B-cell lymphoma. This paper provides ana In addition, CD21 showed FDC networks, and p53 was largely positive. There was no correlation with the EB virus in Tumor cells. Our case illustrates atypical morphological variation from previously reported A-DLBCL cases, which reveal a lack of morphological signs with common diffuse large B-cell lymphoma and anaplastic large cell lymphoma.

Source link: https://europepmc.org/article/PPR/PPR540714


STAT3 cooperates with the core transcriptional regulatory circuitry to drive MYC expression and oncogenesis in anaplastic large cell lymphoma

Anaplastic large cell lymphoma is a rare, CD30+ T-cell lymphoma of children and adults. The proto-oncogene MYC, which needs active STAT3 to facilitate high levels of MYC transcription, is one of the critical downstream targets of this network in ALCL cells. MYC binding to the promoter regions associated with STAT3 and each of the key regulatory transcription factors is further enhanced by the presence of this auto-regulatory transcription loop.

Source link: https://europepmc.org/article/PPR/PPR539779


Primary Cutaneous Anaplastic Large-Cell Lymphoma With Aberrant CD20 Expression: Case Report and Review of the Literature.

Differentiating cases of T-cell lymphoma with irregular expression of the B-cell marker CD20 from B-cell lymphoma may lead to misdiagnosis or delays in diagnosis. We present the first case of CD20+ primary cutaneous anaplastic large-cell lymphoma, as well as a review of published studies of CD20+ cutaneous T-cell lymphoma.

Source link: https://europepmc.org/article/MED/36066130


PDGFRβ promotes oncogenic progression via STAT3/STAT5 hyperactivation in anaplastic large cell lymphoma.

Background Antennular large cell lymphoma is a non-Hodgkin T cell lymphoma that is mainly triggered by NPM-ALK. Methods and findings In a transgenic mouse model that mimics PDGFRu03b2-driven human ALCL in vivo, we find PDGFRu03b2 as a source of rapid tumor formation. Cell viability will be severely reduced when compared to deletion of STAT5A, STAT5B, or STAT3 alone. In addition, we believe that PDGFRu03b2 or STAT3/5 inhibition can enhance existing therapies for both previously treated and refractory ALK + ALCL patients.

Source link: https://europepmc.org/article/MED/36045346


CD30 Regulation of IL-13-STAT6 Pathway in Breast Implant Associated Anaplastic Large Cell Lymphoma.

Background Anaplastic large cell lymphoma with bone graft lymphoma is a rare rarely indolent T cell lymphoma, often surrounded by eosinophils, expressing IL-13 and pSTAT6. Methods We silenced CD30 and investigated its effect on IL-13 signaling and tumor cell viability, as well as tumor cell viability. Flow cytometry and pSTAT6 detection by immunohistochemistry evaluated BIA-ALCL cell lines by flow cytometry and pSTAT6 measurement by immunohistochemistry. The effect of CD30 deletion on p38 MAPK phosphorylation was determined. In cytotoxicity assays, Tumor cell viability following CD30 deletion and treatment with a pSTAT6 inhibitor were determined. CD30 expression is required for p38 MAPK phosphorylation and activation, according to Mechanistically, and IL-13- STAT6 signaling in BIA-ALCL tumor cells is reduced by an inhibitor of p38 MAPK. Tumor cell viability was reduced by silencing of CD30 and a specific inhibitor of STAT6, which shows that STAT6 inhibition is cytotoxic to BIA-ALCL tumor cells.

Source link: https://europepmc.org/article/MED/35999655


Efficacy of lorlatinib after alectinib-induced interstitial lung disease in a patient with anaplastic lymphoma kinase-positive non-small cell lung cancer: a case report.

Background Anaplastic lymphoma kinase-positive non-small cell lung cancer patients are common therapeutic agents, and treatment with these agents has been shown to improve long-term survival in patients. Here, we present a case of a triumphant lorlatinib therapy after the onset of a drug-induced interstitial lung disease caused by alectinib. Case presentation The 57-year-old Japanese man was diagnosed with stage IVB non-small cell lung cancer by bronchoscopy, but gene mutation testing could not be carried out due to the small amount of specimens. Bronchoscopy was performed again to guide further evaluation, and the non-small cell lung cancer was found to be an aplastic lymphoma kinase positive. Conclusion Since alectinib can occasionally cause interstitial lung disease, as in the present case, lorlatinib may be a way to continue therapy in patients with no other treatment options.

Source link: https://europepmc.org/article/MED/35999557

* 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