IndraLab
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"Tumor suppressors such as p53, BRCA1-associated protein 1 (BAP1), and Kelch-like ECH-associated protein 1 (KEAP1) have been shown to exert their tumor-suppressive functions via inducing ferroptosis.P53 is regarded as the most critical barrier for cancer development by its cell-cycle surveillance function."
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"Intricately connected to internal environmental homeostasis, ferroptosis partakes in diverse tumor progression stages and activates various tumor suppressors, such as p53 and BRCA1-associated protein 1 (BAP1) (Jiang et al., 2015; Zhang et al., 2018; Chen et al., 2021; Zhao, Yang & Yang, 2022)."
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"Secondly, BAP1-mutated patients have been reported to develop BIMTs (multiple BAP1-inactivated melanocytic tumors), also known as BAP1-inactivated melanocytic tumors, which are multiple, skin-colored or reddish-brown, dome-shaped melanocytic tumors which tend to develop early in life (median 31 years, range 10–56 years) and increase in number with age [59]."
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"IL1RAP–xCT interactions may therefore alter xCT PTMs by affecting its association with other regulatory molecules, thereby enhancing its transporter activity or efficiency.Oncoproteins such as mutant KRAS and tumor suppressors such as p53 and BAP1 can activate or repress xCT, respectively, during tumorigenesis (36, 48, 49)."
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"BINs are highly penetrant, present in up to 90% of mutation carriers, and typically present as multiple, skin colored or reddish-brown, dome-shaped melanocytic tumors (also or previously called BAP1-inactivlated melanocytic tumors, Wiesner nevi, BAPomas, nevoid melanoma-like melanocytic proliferations, BAP1 mutant Spitz nevi, and melanocytic BAP1-mutated atypical intradermal tumors)."
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"Although the MYCN protein was elevated upon BAP1 overexpression, our results of in vitro cells assay and in vivo xenograft assay using the BAP1 overexpressed BE2C and/or SH-EP Tet21/N cells demonstrated that, BAP1 overexpression could also inhibit cell proliferation, migration, colony formation and tumor growth which is similar with the results of BAP1 knockdown."
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"In brief, in this WHO pathway I, these exceptions include some site-specific nevi, deep-penetrating/plexiform nevi, or melanocytomas; pigmented epithelioid melanocytomas; and BAP1-inactivated tumors or melanocytomas, in which atypia of the dermal component merits greater attention (as is also true in most advanced [beyond T1a] melanomas)."
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"OTUB1 overexpression is frequently found in various human cancers, which maintains high expression of SLC7A11 in cancer cells by posttranslational regulation of OTUB1.De-repression of SLC7A11 also promotes tumor development partly via inhibiting ferroptosis, e.g., genetic mutations or deletions of tumor suppressor p53 or BAP1."
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"Of note, knockdown of BAP1 promoted intrahepatic tumor metastasis, with both BAP1 knockdown groups (shBAP1#1 and shBAP1#3) showing more frequent irregular tumor borders with invasion into the adjacent liver parenchyma, more frequent tumor microsatellite formation and venous invasion (Fig. 3C, D)."
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"BAP1-inactivated melanocytic tumor (BIMT) is a group of melanocytic neoplasms with epithelioid cell morphology molecularly characterized by the loss of function of BAP1, a tumor suppressor gene located on chromosome 3p21, and a mutually exclusive mitogenic driver mutation, more commonly BRAF."
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"We postulate that, under oxidative conditions, PTEN may be promoting ferroptosis through its inhibition of AKT (1) by activating GSK3β, reducing expression of NRF2 and its target gene xCT, and depleting GSH pools and (2) through reducing mTOR activity and its downstream ferroptosis inhibitory mechanisms, as reported in other studies.Several other tumor suppressors, such as p53 and BAP1, have also been reported previously to promote ferroptosis, contributing to their tumor-suppressive properties."
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"For instance, hepatocellular carcinoma patients in the high cuprotosis-related risk score had a high mutational frequency of some tumor suppressors such as tumor protein P53 (TP53) and Breast-cancer susceptibility gene 1 (BRCA1)-associated protein 1 (BAP1) and a low frequency of catenin beta 1 (CTNNB1) [9]."
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"Consequently, our findings indicate that Bap1 deletion in cancer cells stimulates an anti-tumor response that relies on cDC1-CD8 T cell activation.Having observed a significant increase in antigen-specific CD8 T cells in Bap1-KO tumors, we sought to investigate the role of tumor antigen presentation in Bap1-KO tumor clearance."
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"BAP1 loss is crucial for the diagnosis of BAP1-inactivated melanocytic tumors, while PRKR1A1 loss supports the diagnosis of PEM.For predicting prognosis in melanomas, several GEP assays have been developed for risk stratification.For predicting response to systemic therapy in high-stage melanomas, BRAF mutation status must be assessed, either using IHC specific for the V600E mutant protein or using BRAF gene mutation analysis before BRAF-inhibitor and MEK-inhibitor therapy can be initiated.Overall, the role of molecular assays in characterizing melanocytic lesions is expanding, particularly for the purpose of differentiating between benign and malignant tumors."
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"The homozygous loss of tumor suppressors BAP1 and PBRM1, found in both tumor samples may also contribute to cancer progression, because defective chromatin remodeling and HR repair over time will give rise to genomic instability (Thompson and Schild 2001; Hopson and Thompson 2017) and increased mutation rate, consistent with the findings in our study."
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"Re-mapping the mouse LUAD genome onto the human LUAD genome revealed that, in all samples investigated, oncogenes, such as AKT1 and tumor suppressors, such as PBRM1, SETD2, BAP1, and SMAD3, were recurrently affected by copy-number gains (pink) and losses (blue) respectively in both human and mouse tumors irrespective of E or EP status (Fig. 2a)."