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Cell Anaplastic Lymphoma - Crossref

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Last Updated: 15 January 2023

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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

The authors explore the case of an 11-year-old immunocompetent boy with primary CNS CD30-positive anaplastic large-cell lymphoma that was also positive for anaplastic lymphoma kinase-1. CT scan results were normal. In the left parietal lobe, a newly developed edema with concomitant edema was discovered. No standard therapy has been established for ALCL, which is extremely rare and difficult to diagnose. This review shows that systemic HD-MTX monotherapy can be a safe and cost-effective therapeutic option for pediatric primary CNS ALCL.

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


The First Reported Case of Gluteal Implant-Associated Anaplastic Large Cell Lymphoma (ALCL)

Abstract - Anaplastic large-cell lymphoma is a very unusual but life-threatening disease that has mainly been linked to breast implants. Patients are vulnerable to BIA-ALCL with breast implant placement for either cosmetic or reconstructive purposes, with the most risk associated with textured breast implants. About a year before her diagnosis of GIA-ALCL, the patient underwent bilateral textured silicone gluteal implants. The patient was later discovered to the Plastic and Reconstructive Surgery Department at our hospital with ulceration at the site of her gluteal implants. A left lung mass biopsy revealed u201challmarku201d cells of ALCL. This case report seeks to establish that all patients undergoing implantation of textured silicone implants are at risk of developing ALCL, as well as providing evidence for the possibility of a new diagnosis of GIA-ALCL.

Source link: https://doi.org/10.1093/asj/sjz044


How to Diagnose Anaplastic Large Cell Lymphoma on Cytological Samples? A Series with Emphasis on Diagnostic Clue and Pitfalls

aplastic large cell lymphoma is a rare mature T-cell non-Hodgkin lymphoma characterized by large and pleomorphic neoplastic T cells with a slew of neoplastic T cells. ALCL has a variety of subtypes with different clinical and biological characteristics: systemic ALCL, primary cutaneous ALCL, and breast implant-associated ALCL are among the breast implant-associated ALCL. In several systemic cases, an anatomic lymphoma kinase is overexpressed and reorganized. In eight cases, and in 1 case, FNAC was performed on lymph nodes in eight cases and on skin lesion. In three cases, breast periprosthetic fluids were tested. In each case, a large immunocytochemical panel was used, as well as FISH in three cases, demonstrating ALK rearrangement in a case of ALK+ ALCL. The difference between systemic ALCL and primary cutaneous ALCL was possible in the case of skin lessions. Conclusion: ALCL's cytological diagnosis may be difficult, and proper monitoring of the collected samples is required. FISH may be useful in evaluating ALK rearrangements.

Source link: https://doi.org/10.1159/000528533


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: CD30 and JunB are both present in tumor cells in anaplastic large cell lymphoma and Hodgkin lymphoma. In both ALCL and HL, Phosphorylation of ERK1/2 MAPK was confirmed in nuclei of tumor cells. These findings show a common cause of CD30 overexpression in ALCL and HL, though 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


CD26 Regulates p38 Mitogen-Activated Protein Kinase–Dependent Phosphorylation of Integrin β1, Adhesion to Extracellular Matrix, and Tumorigenicity of T-Anaplastic Large Cell Lymphoma Karpas 299

Abstract CD26 is an antigen with a vital role in T-cell biology and is expressed on selected subsets of aggressive T-cell malignancies. To elucidate the role of CD26 in tumor formation, we review the impact of CD26 depletion by small interfering RNA transfection of T-anaplastic large cell lymphoma Karpas 299. We then evaluate the CD26-integrin u03b21 association because antiu2013integrin u03b21 blocking antibodies also prevents binding of Karpas 299 to fibronectin and collagen I. Depletion of integrin u03b21 does not reduce integrin'u3b21 expression, but it does lead to dephosphorylation of both integrin u03b21 and p38 mitogen-activated protein kinase. Also, our results showing that the p38MAPK inhibitor SB203580 dephosphorylates integrin u03b21 and the integrin anti-CD26 antibody 202. 36binds both p38MAPK and integrin 202. 36 dephosphorylates integrin u03b21 on Karpas 299, dephosphorylates cell adhesion to the extracellular matrix, indicating that CD26 mediates cell adhesion by p38MAPK-dependent u03b21.

Source link: https://doi.org/10.1158/0008-5472.can-05-0647


Aberrant Expression of and Cell Death Induction by Engagement of the MHC-II Chaperone CD74 in Anaplastic Large Cell Lymphoma (ALCL)

Systemic anaplastic large cell lymphoma is found in 50 percent of cases, as shown by the t or one of its variants, which are believed to be responsible for anaplastic lymphoma kinase-positive ALCL. Deregulation of oncogenic genes surrounding the chromosomal breakpoints on 2p and 5q has been demonstrated before in ALK+ and ALK-U2212 ALCL, showing that the invariant chain of the MHC-II complex CD74 or li, which is encoded in 5q32, is often restricted to B cells, is aberrantly expressed in T cell-derived ALCL. According to ALCL, the CD74 locus has an altered DNA methylation pattern compared to benign T cells. In vitro, we show that the CD74-targeting antibody conjugate STRO-001 efficiently and specifically kills CD74-positive ALCL cell lines.

Source link: https://doi.org/10.3390/cancers13195012


Reverse strategy to locally advanced breast implant-associated anaplastic large cell lymphoma: A case report

Breast implant-associated anaplastic large cell lymphoma is a rare T-cell lymphoma related to textured breast implants. More often, BIA-ALCL suffers with locally advanced mass-formed disease and a regional lymph node involvement. A modern case of a 49-year-old woman who appeared on the left side of the breast A mass-formed stage 3 BIA-ALCL 15 years after a bilateral breast augmentation with textured silicone implant. The patient was scheduled for a multidisciplinary team's u201crebase-strategyu201d sequential approach consisting of induction chemotherapy, hematopoietic stem cell mobilization, and harvest followed by autologous stem cell transplantation. The patient had a complete pathologic response and was a candidate for radical surgery after 100 days from stem cell transplantation. In some instances of advanced-stage BIA-ALCL in which it was not possible to perform an immediate radical surgery, this case study has demonstrated the effectiveness of neoadjuvant chemotherapy as part of a u201creverse project u201d.

Source link: https://doi.org/10.3389/fonc.2022.1062389


Regulation of CD45 phosphatase by oncogenic ALK in anaplastic large cell lymphoma

Although ALK+ ALCL is devoted to mature T cell lymphomas, in the majority of ALCL, a transcriptional and epigenetic repressive programme triggered by oncogenic NPM-ALK, a loss of T cell identity is observed. Most ALK+ ALCL cell lines have expressed the CD45RO isoform with limited CD45RA expression, and NPM-ALK has restricted the expression of these CD45 isoforms, according to our results. When ALK kinase expression was reduced by therapy with ALK tyrosine kinase inhibitors, it was likely that CD45RO expression was restricted to ALK kinase inhibitors that stifled NPM-ALK kinase activity. STAT3 repression was mediated by STAT3 as shown by ChIP-seq results on ALCL cells treated with the ALK-TKI crizotinib or cells treated with a STAT3 degrader, as shown by ChIP-seq results on ALCL cells treated with the ALK-TKI crizotinib or cells treated with a STAT3 degrader. We found that knocking out CD45 with the CRISPR/Cas9 system resulted in increased resistance to ALK TKI therapy, and CD45 was down-regulated in ALCL cells that developed resistance in vitro to ALK TKIs, which was resistant in vitro to ALK TKIs.

Source link: https://doi.org/10.3389/fonc.2022.1085672


A Rare Case of Cutaneous Anaplastic Large Cell Lymphoma in an Adolescent Female

Primary cutaneous anaplastic large cell lymphoma is a CD30 positive lymphoproliferative disorder that is the second most common group of cutaneous T-cell lymphoma. For a 14-year-old Caucasian female who complained of a painless, reproducing, friable, hemorrhagic nodule on her right medial buccal cheek of 2 weeks since 2019, we review her. On the 1. 7 cm x 1. 3 cm lesion, a shave biopsy was performed. Staining revealed CD30 positivity of a substantial portion of the tumor filtrate, but not generally positive. Rare cells were granzyme positive. Following the shave biopsy, the lesion began to regress spontaneously. In 20-42% of cases, rapid recovery of C-ALCL is common, in which case, aggressive therapy is not appropriate. This rare case of C-ALCL in an adolescent female is an additional example of a rare clinical presentation in unusual infant female, retelling the critical histopathological findings for diagnosis.

Source link: https://doi.org/10.25251/skin.7.1.10


Super-enhancer-based identification of a BATF3/IL-2R−module reveals vulnerabilities in anaplastic large cell lymphoma

Abstract: Anaplastic large cell lymphoma (CD30+) lymphoma with systemic anaplastic lymphoma, as well as ALK-negative, primary cutaneous and breast implant-associated ALCL, which is characterized as a robust CD30-positive T-cell lymphoma. BATF3 expression is correlated with specific and high-level IL2R expression in ALCL. Following BATF3's demise, a regulatory link, IL-2R-expression decreases, IL-2R-expression decreases, and BATF3 is recruited to IL2R regulatory regions. In line, a high IL-2Ru03b1-expression in ALCL patients has been attributed to more active clinical presentation. Our findings reveal the importance of the BATF3/IL-2R-module for ALCL biology as a promising treatment strategy for ALCL.

Source link: https://doi.org/10.1038/s41467-021-25379-9

* 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