SMARCB1-Deficient Cancers: Novel Molecular Insights and Therapeutic Vulnerabilities

Cooper, Garrett W.; Hong, Andrew L.

doi:10.3390/cancers14153645

Cited by 30 publications

(24 citation statements)

References 159 publications

(207 reference statements)

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“…The SWI/SNF related, matrix-associated, actin-dependent regulator of chromatin, subfamily B, member 1 (SMARCB1) protein is a subunit of the BAF complex. SMARCB1 deficiency resulted in the miss-localization of the BAF complex, which leads to the inhibition of gene expression [ 127 ]. However, residual BAF complex can still maintain abnormal gene expression required for cancer progression.…”

Section: Cgas-sting and Baf Complexmentioning

confidence: 99%

Inflammatory Networks in Renal Cell Carcinoma

Kruk

Mamtimin

Braun

et al. 2023

Cancers

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Cancer-associated inflammation has been established as a hallmark feature of almost all solid cancers. Tumor-extrinsic and intrinsic signaling pathways regulate the process of cancer-associated inflammation. Tumor-extrinsic inflammation is triggered by many factors, including infection, obesity, autoimmune disorders, and exposure to toxic and radioactive substances. Intrinsic inflammation can be induced by genomic mutation, genome instability and epigenetic remodeling in cancer cells that promote immunosuppressive traits, inducing the recruitment and activation of inflammatory immune cells. In RCC, many cancer cell-intrinsic alterations are assembled, upregulating inflammatory pathways, which enhance chemokine release and neoantigen expression. Furthermore, immune cells activate the endothelium and induce metabolic shifts, thereby amplifying both the paracrine and autocrine inflammatory loops to promote RCC tumor growth and progression. Together with tumor-extrinsic inflammatory factors, tumor-intrinsic signaling pathways trigger a Janus-faced tumor microenvironment, thereby simultaneously promoting or inhibiting tumor growth. For therapeutic success, it is important to understand the pathomechanisms of cancer-associated inflammation, which promote cancer progression. In this review, we describe the molecular mechanisms of cancer-associated inflammation that influence cancer and immune cell functions, thereby increasing tumor malignancy and anti-cancer resistance. We also discuss the potential of anti-inflammatory treatments, which may provide clinical benefits in RCCs and possible avenues for therapy and future research.

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Section: Cgas-sting and Baf Complexmentioning

confidence: 99%

Inflammatory Networks in Renal Cell Carcinoma

Kruk

Mamtimin

Braun

et al. 2023

Cancers

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“…Different subunits are associated with different tumors: for example, SMARC1 loss is seen in atypical teratoid/rhabdoid tumors (ATRTs), among others [380,381], whereas AIRD1A loss has been described in endometrioid EC (~40%), endometrioid (~30%), clear-cell (46-57%) OCs, etc., with up to ~20% of all human cancers harboring AIRD1A-inactivating mutations [337,372,[382][383][384][385]. In addition, the loss of ARID1A has been demonstrated in patient samples with atypical endometriotic lesions contiguous to clear-cell OC, raising the possibility that the loss of ARID1A may contribute to an early cancer-promoting event in endometriosis that leads to clear-cell OC [337].…”

Section: Arid1amentioning

confidence: 99%

The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies

Czegle

Huang

Soria

et al. 2023

Life

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There is an increasing understanding of the molecular and cytogenetic background of various tumors that helps us better conceptualize the pathogenesis of specific diseases. Additionally, in many cases, these molecular and cytogenetic alterations have diagnostic, prognostic, and/or therapeutic applications that are heavily used in clinical practice. Given that there is always room for improvement in cancer treatments and in cancer patient management, it is important to discover new therapeutic targets for affected individuals. In this review, we discuss mitochondrial changes in breast and gynecological (endometrial and ovarian) cancers. In addition, we review how the frequently altered genes in these diseases (BRCA1/2, HER2, PTEN, PIK3CA, CTNNB1, RAS, CTNNB1, FGFR, TP53, ARID1A, and TERT) affect the mitochondria, highlighting the possible associated individual therapeutic targets. With this approach, drugs targeting mitochondrial glucose or fatty acid metabolism, reactive oxygen species production, mitochondrial biogenesis, mtDNA transcription, mitophagy, or cell death pathways could provide further tailored treatment.

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“…The mechanism of action of SMARCB1 as a tumor suppressor relies on the intersection with several pathways, including cell proliferation and survival [ 71 ] ( Figure 2 ).…”

Section: Smarcb1 Loss An Es Molecular Hallmarkmentioning

confidence: 99%

Beyond SMARCB1 Loss: Recent Insights into the Pathobiology of Epithelioid Sarcoma

Savio

Maestro

2022

Cells

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Epithelioid sarcoma (ES) is a very rare and aggressive mesenchymal tumor of unclear origin and uncertain lineage characterized by a prevalent epithelioid morphology. The only recurrent genetic alteration reported in ES as yet is the functional inactivation of SMARCB1 (SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily B member 1), a key component of the SWI/SNF (SWItch/Sucrose Non-Fermentable) chromatin remodeling complexes. How SMARCB1 deficiency dictates the clinicopathological characteristics of ES and what other molecular defects concur to its malignant progression is still poorly understood. This review summarizes the recent findings about ES pathobiology, including defects in chromatin remodeling and other signaling pathways and their role as therapeutic vulnerabilities.

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SMARCB1-Deficient Cancers: Novel Molecular Insights and Therapeutic Vulnerabilities

Cited by 30 publications

References 159 publications

Inflammatory Networks in Renal Cell Carcinoma

Inflammatory Networks in Renal Cell Carcinoma

The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies

Beyond SMARCB1 Loss: Recent Insights into the Pathobiology of Epithelioid Sarcoma

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