Autophagy and cellular senescence in classical Hodgkin lymphoma

Kyriazopoulou, Lydia; Karpathiou, Georgia; Hatzimichael, Eleftheria; Péoc’h, Michel; Papoudou‐Bai, Alexandra; Kanavaros, Panagiotis

doi:10.1016/j.prp.2022.153964

Cited by 5 publications

(8 citation statements)

References 49 publications

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“…Expression of EBER1/2 transcripts was detected in variable proportions of malignant HRS cells in 19/62 studied cases of cHL (31%). The results for the 52 cases were reported previously (17). No statistically significant correlation between GATA3 expression patterns (positive vs negative cases) and the status of EBV (EBER1/2 positive vs EBER1/2 negative cases) was found.…”

Section: Ebv Statussupporting

confidence: 56%

“…Immunohistochemical studies were performed in formalin-fixed paraffin embedded tumor tissue sections (4 μm thick) using an automated immunostaining system (OMNIS, Dako-Agilent, Santa Clara, CA, USA) [ 17 ]. The following antibodies were used: GATA3: clone L50-823, mouse monoclonal, ZETA corporation, 1:100; CD20: clone L26, mouse monoclonal, Abcam, 1:100; CD3: clone PS1, mouse monoclonal, Novocastra/Leica Biosystems, 1:200; CD68: clone KP-1, mouse monoclonal, Abcam, 1:3000; CD56: clone 123C3, mouse monoclonal Dako, 1:50; CD30: clone Ber-H2, mouse monoclonal, Dako, 1:30; and CD15: clone MMA (LeuM1), mouse monoclonal, Diagnostic BioSystems, 1:150.…”

Section: Methodsmentioning

confidence: 99%

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Expression Patterns of GATA3 in Classical Hodgkin Lymphoma: A Clinico-Pathological Study

Papoudou-Bai,

Koumpis,

Karpathiou

et al. 2024

Diseases

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GATA3 is a transcription factor involved in T-cell maturation and has been previously shown to be aberrantly overexpressed in malignant Hodgkin and Reed–Sternberg (HRS) cells of classical Hodgkin lymphoma (cHL). However, the immunophenotypes of the cell types expressing GATA3 have not been precisely characterized so far in cHL tissues. In this single-center retrospective cohort study we analyzed the expression patterns of GATA3 alone and in combination with B, T, NK or macrophage-associated markers in 73 cases with newly diagnosed cHL and investigated for a possible correlation with clinical and laboratory parameters. Immunohistochemistry (single and double) was performed using GATA3 alone and in combination with CD20, CD3, CD56, CD68, CD30 or CD15. Clinical and laboratory parameters were collected and correlated with the expression of GATA 3. GATA3 nuclear expression was found in HRS cells in 39/73 (54%) cases of cHL. The Nodular Sclerosis (NS) subtype showed the highest positivity rate (35/56, 63%), followed by mixed cellularity (MC; 4/14, 29%) and lymphocyte rich (LR; 0/3). Double immunostainings showed that GATA3 was expressed by CD30+ or CD15+ HRS cells and a few CD3+ T-cells, whereas GATA3 expression was not detected in CD20, CD56 or CD68+ cells. GATA3-negative cHL was significantly associated with unfavorable prognostic factors such as older age at diagnosis and increased levels of serum β2-microglobulin. The heterogenous expression patterns of GATA3 in HRS cells that were observed in a substantial proportion of cHL, mainly in the NS subtype, further support the biological heterogeneity of cHL.

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Section: Ebv Statussupporting

confidence: 56%

Section: Methodsmentioning

confidence: 99%

Expression Patterns of GATA3 in Classical Hodgkin Lymphoma: A Clinico-Pathological Study

Papoudou-Bai,

Koumpis,

Karpathiou

et al. 2024

Diseases

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“…Remarkably, p62 is a diagnostic biomarker for early stage melanomas (Tang et al, 2016) and p62 is emerging as a possible therapeutic target in melanoma (Karras et al, 2019;Fei et al, 2022). Further, high p62 expression in lymphoma shows significant positive correlation with disease relapse (Kyriazopoulou et al, 2022). We have previously demonstrated high p62 expression in primary sclerosing cholangitis (PSC) representing a chronic inflammatory cholangiopathy frequently complicated by CCA (Carpino et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Autophagy impairment in human bile duct carcinoma cells

Petrungaro,

de Franchis,

Filippini

et al. 2023

Front. Physiol.

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Bile duct epithelial cells, named cholangiocytes, may undergo a neoplastic transformation leading to cholangiocarcinoma. The role autophagy plays in cancer is still debated and few information are available in cholangiocarcinoma. We report in vitro data, at least in part validated in vivo,i ndicating that autophagy is impaired in intrahepatic cholangiocarcinoma cells, as compared to healthy cholangiocytes, evaluated through LC3II and p62 Western blot analyses. Autophagy impairment was found to be associated with low expression of TFEB protein and high expression of three proteins i.e., c-FLIP, caspase-10 and cleaved BCLAF-1, as compared to healthy cholangiocytes. We highlight biological effects of autophagy impairment in cholangiocarcinoma showing that autophagy induction, via rapamycin, as well as caspase inhibition, via Q-VD-OPh, are able to reduce proliferation marker PCNA level, colony size and protein content of cultured cholangiocarcinoma cells. The increased protein expression of p62, c-FLIP, caspase-10 observed in vitro in cholangiocarcinoma cells was paralleled by significant increase at gene expression levels in vivo; in fact, significant increase of transcript levels of p62, c-FLIP and caspase-10 was observed in 34 biopsies from human cholangiocarcinoma patients compared to 9 biopsies from 9 healthy controls, as reported in the GEPIA2 public database. The significant increase of p62 level in cholangiocarcinoma was found as a relatively uncommon finding in solid cancers, since it was also found in only 7 cancer types out of 31 cancer types investigated, including melanoma and hepatocarcinoma. In conclusion, we present data suggesting a molecular machinery controlling autophagy in cholangiocytes and autophagy impairment in cholangiocarcinoma.

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“…The SASP secretome includes a variety of proinflammatory mediators, chemokines, growth factors, angiogenic factors, bioactive lipids, and MMPs that may act in a paracrine or autocrine manner to induce senescence in vivo, triggering a positive-feedback loop that leads to the perpetuation of the inflammatory response [ 197 ]. Senescent cells have been identified in the context of human diseases, including COVID-19 [ 198 ], where senescent cells were detected in SARS-CoV-2-infected lung tissue, and Hodgkin lymphoma, where a high percentage of senescent cells were detected in the affected lymph nodes [ 199 , 200 ]. Our group has reported the presence of senescent cells in biopsy-proven GCA specimens [ 188 ].…”

Section: Chronic Inflammatory Components On the Tissue Levelmentioning

confidence: 99%

Current Insights into Tissue Injury of Giant Cell Arteritis: From Acute Inflammatory Responses towards Inappropriate Tissue Remodeling

Palamidas,

Chatzis,

Papadaki

et al. 2024

Cells

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Giant cell arteritis (GCA) is an autoimmune disease affecting large vessels in patients over 50 years old. It is an exemplary model of a classic inflammatory disorder with IL-6 playing the leading role. The main comorbidities that may appear acutely or chronically are vascular occlusion leading to blindness and thoracic aorta aneurysm formation, respectively. The tissue inflammatory bulk is expressed as acute or chronic delayed-type hypersensitivity reactions, the latter being apparent by giant cell formation. The activated monocytes/macrophages are associated with pronounced Th1 and Th17 responses. B-cells and neutrophils also participate in the inflammatory lesion. However, the exact order of appearance and mechanistic interactions between cells are hindered by the lack of cellular and molecular information from early disease stages and accurate experimental models. Recently, senescent cells and neutrophil extracellular traps have been described in tissue lesions. These structures can remain in tissues for a prolonged period, potentially favoring inflammatory responses and tissue remodeling. In this review, current advances in GCA pathogenesis are discussed in different inflammatory phases. Through the description of these—often overlapping—phases, cells, molecules, and small lipid mediators with pathogenetic potential are described.

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Autophagy and cellular senescence in classical Hodgkin lymphoma

Cited by 5 publications

References 49 publications

Expression Patterns of GATA3 in Classical Hodgkin Lymphoma: A Clinico-Pathological Study

Expression Patterns of GATA3 in Classical Hodgkin Lymphoma: A Clinico-Pathological Study

Autophagy impairment in human bile duct carcinoma cells

Current Insights into Tissue Injury of Giant Cell Arteritis: From Acute Inflammatory Responses towards Inappropriate Tissue Remodeling

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