Laura E. Stevens's research while affiliated with Dana-Farber Cancer Institute and other places
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Publications (17)
Brain metastatic breast cancer is particularly lethal largely due to therapeutic resistance. Almost half of the patients with metastatic HER2-positive breast cancer develop brain metastases, representing a major clinical challenge. We previously described that cancer-associated fibroblasts are an important source of resistance in primary tumors. He...
Approximately 70% of patients diagnosed with non-small cell lung cancer (NSCLC) are not eligible for curative resection, often due to disseminated disease at diagnosis. Thus, the advent of novel therapeutics, especially those efficacious for metastatic disease, is of primary importance. Metastasis correlates with epigenetic alterations that drive t...
Inflammatory breast cancer (IBC) is a highly aggressive subtype of breast cancer characterized by rapidly arising diffuse erythema and edema. Genomic studies have not identified consistent alterations and mechanisms that differentiate IBC from non-IBC tumors, suggesting that the microenvironment could be a potential driver of IBC phenotypes. Here,...
Background
Patients with inflammatory breast cancer (IBC) have overall poor clinical outcomes, with triple-negative IBC (TN-IBC) being associated with the worst survival, warranting the investigation of novel therapies. Preclinical studies implied that ruxolitinib (RUX), a JAK1/2 inhibitor, may be an effective therapy for TN-IBC.
Methods
We conduc...
Triple-negative breast cancer (TNBC) is a heterogeneous disease with limited treatment options. To characterize TNBC heterogeneity, we defined transcriptional, epigenetic, and metabolic subtypes and subtype-driving super-enhancers and transcription factors by combining functional and molecular profiling with computational analyses. Single-cell RNA...
Triple-negative breast cancer (TNBC) is a subtype accounting for 20-30% all breast cancer cases and is a highly aggressive disease with inferior prognosis. The acquired resistance is a major obstacle for efficient therapy and discovery of novel clinically-actionable targets has become an urgent need. In this study, we carried out an in-depth functi...
Inflammatory breast cancer (IBC) is a difficult-to-treat disease with poor clinical outcomes due to high risk of metastasis and resistance to treatment. In breast cancer, CD44+CD24− cells possess stem cell-like features and contribute to disease progression, and we previously described a CD44+CD24−pSTAT3+ breast cancer cell subpopulation that is de...
Lineage selective transcription factors (TFs) are important regulators of tumorigenesis, but their biological functions are often context dependent with undefined epigenetic mechanisms of action. In this study, we uncover a conditional role for the endodermal and pulmonary specifying TF GATA6 in lung adenocarcinoma (LUAD) progression. Impairing Gat...
To define transcriptional dependencies of triple-negative breast cancer (TNBC), we identified transcription factors highly and specifically expressed in primary TNBCs and tested their requirement for cell growth in a panel of breast cancer cell lines. We found that EN1 (engrailed 1) is overexpressed in TNBCs and its downregulation preferentially an...
Lung cancer is a deadly treatment refractory disease that is biologically heterogeneous. To understand and effectively treat the full clinical spectrum of thoracic malignancies, additional animal models that can recapitulate diverse human lung cancer subtypes and stages are needed. Allograft or xenograft models are versatile and enable the quantifi...
Mechanisms underlying the propensity of latent lung adenocarcinoma (LUAD) to relapse are poorly understood. In this study, we show how differential expression of a network of extracellular matrix (ECM) molecules and their interacting proteins contributes to risk of relapse in distinct LUAD subtypes. Overexpression of the hyaluronan receptor HMMR in...
Lung adenocarcinoma (LUAD) is a heterogeneous and deadly subtype of non-small cell lung cancer that metastasizes rapidly to distant organs. Recent transcriptional profiling of primary LUADs by TCGA identified three molecular subgroups with unique clinical and biological features. Amongst the most aggressive LUADs are tumors classified in the proxim...
Lung cancer is the leading cause of cancer-related deaths worldwide. This poor prognosis is due to the rapid metastatic progression of this disease, yet the mechanisms that govern lung cancer dissemination and colonization are unclear. Through an integrated approach, we identified an alveolar cell-selective gene signature that stratifies lung adeno...
Molecular programs that mediate normal cell differentiation are required for oncogenesis and tumor cell survival in certain cancers. How cell-lineage-restricted genes specifically influence metastasis is poorly defined. In lung cancers, we uncovered a transcriptional program that is preferentially associated with distal airway epithelial differenti...
Citations
... 87.8% of the samples are classified as the Basal subtype, which is consistent with the reported findings[21076464, 18398844] [13] [14]. To validate the effectiveness of UBS93 in analyzing single-cell transcriptome data, we utilize two published datasets from human breast cancer cell lines (GSE173634, GSE202771) for UBS93 prediction[35361816, 38100350] [15][16]. In GSE173634, ...
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... Specific genes, such as HSPA1B, SESN2, EGR1, DNAJB1, CDKN1A, PMEPA1, DUSP1 and Coroa1 were up-regulated, while TOP2A and ASPM were down-regulated. The involvement of the MAPK and JAK/STAT pathways in cancer cell growth and proliferation is well-established, indicating that they will be prime targets for anticancer drug discovery [32,33]. ...
... Moreover, GATA6, in synergy with HOPX, regulated overlapping alveolar differentiation and the expression of aggressive target genes, collectively limiting the metastatic potential of lung cancer cells (Cheung et al. 2013). GATA6 was also implicated in the regulation of the chromatin landscape in lung cancer cells, thereby governing tumor proliferation (Arnal-Estape et al. 2020). In addition, studies have found that miR-196b can promote the progression of lung cancer by inhibiting the expression of GATA6 (Liang et al. 2020). ...
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... These two genes are located at an AA-specific risk locus identified by our recent GWAS conducted among AA participants 24 . EN1 is a transcription factor with known roles in brain 27 and dermomyotome 28 development and its downregulation significantly reduced viability and tumorigenicity in TNBC cell lines 29 . LincRNA LINC01956 is an E2F1 target gene, and its overexpression correlates with poor prognosis in basal-like breast cancer participants 30 . ...
... In this proof-of-principle study, we sought to explore the potential of utilizing exhaled miRNAs for noninvasive detection of secondary lung cancer in orthotopic animal models. For these analyses, we chose to inoculate a highly metastatic breast cancer cell line that has been well documented to rapidly establish significant pathological lung tumor burden in athymic nude mice, which provided an adequate model to test the collection and analysis of exhaled breath condensates [92][93][94][95] . -231 subline 3475 triple-negative breast cancer cells were selected because of their aggressive and targeted lung tumor growth. ...
... It is partly due to poor diagnostic techniques and treatment approaches [4,5]. In the past, the main treatment for lung cancer was surgery and radiotherapy, but for patients with metastatic lung cancer, radiotherapy alone often has limited therapeutic effects [6,7]. At present, various biomarkers have been widely discovered and applied in the treatment of various types of tumors [8], demonstrating their roles in the field of cancer. ...
... Specifically, GATA6 inhibited AKT activation by upregulating the expression of p53 and p21 mRNA, leading to p21 protein stabilization and the induction of senescence in lung cancer cells (Chen et al. 2020). Moreover, GATA6, in synergy with HOPX, regulated overlapping alveolar differentiation and the expression of aggressive target genes, collectively limiting the metastatic potential of lung cancer cells (Cheung et al. 2013). GATA6 was also implicated in the regulation of the chromatin landscape in lung cancer cells, thereby governing tumor proliferation (Arnal-Estape et al. 2020). ...
