Biology subjects

Dyson, G.

Publications and source records attributed to Dyson, G..

13 recordsLinked to original sources

bioRxiv2026

Novel biologically relevant small RNA-sequencing alignment tool LevenMap for alignment to database of non-coding RNAs

A crucial aspect of the bioinformatics workflow in small RNA-sequencing is the alignment of reads to a database of reference ncRNAs. Alignment algorithms such as Bowtie, Burrows-Wheeler Aligner (BWA), and Spliced Transcripts Alignment to a Reference (STAR) - which are designed for aligning reads to a reference genome - are typically used. Aligning short RNA-sequenced reads to a database of non-coding RNAs (ncRNAs) is fundamentally a different task than aligning longer reads to a genome due to ncRNAs (i) having roughly the same number of nucleotides as the reads being aligned and (ii) being subsequences of other ncRNAs. To account for these differences, we developed the novel alignment algorithm LevenMap. Of all reads which exactly matched a reference ncRNA in a publicly available dataset, LevenMap aligned 100.0% of them to their respective ncRNA while all other aligners mapped less than 40% of these reads to their corresponding ncRNA. Furthermore, the mean ratio (length of read) / (length of corresponding reference ncRNA) of all aligned reads was 1.0 and 0.998 for LevenMap with at most zero and one mismatch(es) allowed, respectively; this ratio was no more than 0.51 for all other aligners. Overall, LevenMap is designed to account for the nuances of aligning small RNA-sequencing data to a database of reference ncRNAs and yields more biologically relevant counts compared to traditional aligners in this context. LevenMap is free and publicly available on GitHub: https://github.com/hdlugas/LevenMap.

bioinformatics↗

bioRxiv2026

S100A9-Dependent CXCR2hi Neutrophils Mediate Systemic Immune Suppression and Checkpoint Resistance in Metastatic TNBC

Most high-dimensional studies of tumor-immune interactions focus on metastatic models, limiting insight into how immune remodeling in primary tumors shapes metastatic competence. Here, integrating single-cell RNA sequencing, CyTOF, and functional studies across metastatic (4T1) and non-invasive (EMT6) triple-negative breast cancer (TNBC) murine models, we define tumor state-specific immune programs that distinguish metastatic competence. Tumors with metastatic capacity uniquely drive early bone marrow expansion of CXCR2 neutrophils, which infiltrate primary tumors acquiring a CXCL2-producing phenotype that promotes EMT-associated cancer stem cell (CSC) plasticity. This program depends on TGF-{beta}/CEBPD-mediated induction of S100A9. Elevated CXCL2, together with G-CSF, establishes a feed-forward circuit that drives systemic neutrophil mobilization and recruitment to distant organs, where neutrophil-derived S100A8/A9 (calprotectin) promotes MET-driven CSC outgrowth and metastatic colonization. Clinically, gene signatures associated with CXCR2 neutrophils predict poor survival in TNBC patients, whereas monocyte/macrophage (CX3CR1) and T cell activation signatures correlate with improved outcomes. S100A9 ablation disrupts this cascade and enhances immunotherapy responsiveness, defining a TGF-{beta}/S100A9/CXCR2 axis linking immune remodeling, CSC plasticity and metastasis. HighlightsO_LIMetastatic TNBC engages a TGF-{beta}/C/EBP{delta}/S100A9 axis that expands CXCR2 neutrophils C_LIO_LINon-invasive EMT6 tumors retain a CX3CR1 monocyte/macrophage and T-cell landscape C_LIO_LICXCR2+ neutrophils in pre-metastatic niches suppress T cell response while promoting tumor cell proliferation C_LIO_LIS100A9 loss redirects myelopoiesis and potentiates anti-PD-L1 in TNBC models C_LI In BriefAlkan et al. dissect how tumor state programs the myeloid compartment in TNBC. Metastatic 4T1 tumors uniquely engage a TGF-{beta}/C/EBP{delta}/S100A9 axis driving CXCR2 neutrophil expansion and CXCL2/G-CSF-dependent systemic mobilization, coupling immune remodeling to EMT/MET cancer-stem-cell plasticity, while S100A9 loss restores CX3CR1 myeloid identity and unlocks checkpoint-inhibitor responsiveness.

cancer biology↗

bioRxiv2025

Genomic and Transcriptomic Landscapes of MEN1-Wild-Type Low-Grade Metastatic Pancreatic NETs Uncover Key Oncogenic Drivers and Targetable Pathways

Sporadic pancreatic neuroendocrine tumors (pNETs) with wild type MEN1 represent a major yet largely ignored subset whose biology and metastatic potential remain poorly understood. Because metastasis can occur despite low histologic grade and modest mutational burden, we hypothesized that metastatic competence in MEN1-wild-type pNETs reflects quantitative reinforcement of shared oncogenic pathways rather than distinct mutational processes. We profiled 75 primary low-grade pNETs by whole-exome and RNA sequencing, including 25 percent with lymph node and/or liver metastasis, and integrated genomic and transcriptomic data to connect pathway lesions with expression state. Metastatic tumors showed a slight increase in mutation frequency but conserved base-substitution spectra relative to non-metastatic cases, and adverse clinicopathologic features were enriched in Grade 2 disease. Aggregating alterations to pathways revealed broad convergence on canonical networks, with transcriptomic analyses demonstrating cohort-wide enrichment of Calcium, WNT, and KRAS/PI3K-AKT programs in metastasis. Intersection of significantly mutated genes with differentially expressed genes identified a focused 29-gene overlap, including RYR1 and ZNF273, that marks these convergent axes and distinguishes metastatic from non-metastatic tumors. Gene set enrichment confirmed preferential activation of Calcium, WNT, and PI3K-AKT signaling in metastatic tumors, consistent with a network-intensity model of progression. Finally, upstream-regulator analysis (iPathwayGuide) and gene-centric perturbation mapping (Gene2Drug) nominated candidate targeted and repurposable agents predicted to reverse the metastatic expression phenotype and flagged drugs unlikely to provide benefit, yielding a prioritized, testable therapeutic shortlist which includes fasudil and spaglumic acid. Convergent, domain-specific mutational patterns in highly mutated genes such as ZNF273 and CLCA1 define a molecular signature that could stratify metastatic risk in low-grade pNETs. Collectively, our data reframe metastasis in MEN1-wild-type low-grade pNETs as a property of pathway state rather than mutation quantity and provide a translational blueprint for biomarker-guided therapy development focused on Calcium, WNT, and KRAS/PI3K hubs.

cancer biology↗

bioRxiv2025

Co-targeting KRAS and Exportin1 as an effective therapeutic strategy for KRASG12D mutant pancreatic ductal adenocarcinoma

BackgroundSeveral KRASG12D inhibitors (KRASG12Di) are under clinical evaluation for pancreatic ductal adenocarcinoma (PDAC). However, as seen with other first generation KRAS inhibitors, resistance may limit their long-term efficacy, necessitating combination strategies to enhance therapeutic outcomes. Exportin 1 (XPO1), a nuclear transport protein overexpressed in PDAC, represents a therapeutic vulnerability in KRAS-mutant cancers. Here, we demonstrate that the second-generation XPO1 inhibitor Eltanexor synergizes with MRTX1133 to enhance its efficacy in multiple PDAC models. MethodsWe generated KRASG12Di-resistant PDAC cells and assessed their response to Eltanexor. The antiproliferative effects of MRTX1133 and Eltanexor combinations were evaluated in 2D and 3D in vitro PDAC models. The in vivo efficacy of the combination was tested in KRASG12D-mutant human and murine PDAC xenograft and allograft models. ResultsEltanexor sensitized MRTX1133-resistant PDAC cells to growth inhibition. In both 2D and 3D culture models, the combination of Eltanexor and MRTX1133 significantly reduced cell viability. Mechanistically, the combination treatment suppressed key KRAS downstream signaling molecules, including p-ERK, mTOR, p-4EBP1, DUSP6, and cyclin D1. Kinome analysis further revealed reduced MAPK-related kinase activity. Combining subtherapeutic doses of Eltanexor and MRTX1133 resulted in significant tumor regression and prolonged survival in PDAC xenograft and immunocompetent orthotopic allograft models. Moreover, maintenance therapy with Eltanexor prevented tumor relapse, yielding a durable antitumor response. ConclusionThis study demonstrates that Eltanexor overcomes resistance to MRTX1133 and enhances its efficacy in PDAC. The combination regimen may provide a durable therapeutic response while reducing the required dose of KRASG12D inhibitors, potentially delaying resistance and improving patient outcomes. Statement of Translational RelevancePDAC remains one of the deadliest malignancies, with limited effective therapies and dismal survival rates. The emergence of KRASG12D-selective inhibitors, such as MRTX1133, marks a critical advance for nearly 40% of PDAC patients harboring this oncogenic driver. However, inevitable emergence of adaptive or acquired resistance to KRAS inhibitors remains a major barrier to achieving durable clinical benefit. This study uncovers XPO1 inhibition as a rational and synergistic strategy to augment the antitumor efficacy of MRTX1133. By enhancing KRASG12D inhibitor activity and potentially reducing the required therapeutic dose, this combination approach offers a novel means to delay or overcome resistance. These findings provide a strong preclinical rationale for clinical trials evaluating KRAS inhibitors in combination with XPO1 inhibitors and may significantly improve outcomes for a substantial subset of PDAC patients who currently lack effective targeted treatment options.

cancer biology↗

bioRxiv2025

Habitat suitability modeling growth and cover trends of staghorn coral (Acropora cervicornis) outplants in the lower Florida Keys

The decline of important reef building corals has motivated the development of habitat suitability models used to identify optimal locations for coral restoration. In the Florida Keys habitat suitability models incorporate coarse spatial data sampled over large areas, resulting in recommended outplant sites at distant locations, making it logistically difficult and expensive to access and regularly monitor. Restoration efforts to date show that outplanting success can vary widely within a limited space, necessitating improved predictive abilities of coral outplant success at high spatial resolutions within a restoration site. With the advent of Structure-from-Motion image reconstruction, fine-scale, site specific, digital terrain models can be created to support habitat suitability model development. In this study, generalized linear mixed models used extracted seafloor terrain attributes and environmental variables to identify within site locations of high Acropora cervicornis growth and healthy coral cover of long-term outplants. Percent healthy coral cover significantly decreased after two years of outplantation. The submodel of corals exclusively less than two years old was unable to identify environmental conditions associated with higher healthy cover. For all corals, outplant recommendations for higher healthy cover are in deeper waters, away from the coast, in less rough terrain, and closer to the reef edge. Model results for growth support these recommended outplant sites, in addition to concave locations near high slope relief. Finally, our results also indicate that marine heat waves, but especially marine cold waves negatively correspond with coral growth, and high wind events positively correspond with coral growth. These model results provide a basis for further endeavors in modeling endangered organismal success, which are vulnerable to minute differences in local environmental conditions.

ecology↗

bioRxiv2024

Transcutaneous Vagus Nerve Stimulation Reduces Pain and OA Progression in Mouse Models of Post-Traumatic Osteoarthritis

Currently, there are no disease-modifying osteoarthritis (OA) drugs (DMOAD) to prevent OA progression and there are limitations on pain relieving therapeutics. Vagus nerve stimulation (VNS) delivered by an implantable device is FDA-approved for refractory epilepsy and severe depression. Here, we investigated the efficacy of transcutaneous VNS (tVNS) for preventing OA progression and providing pain relief in two mouse models of post-traumatic OA (PTOA): the surgical destabilized medial meniscus (DMM) and the non-surgical forced tibial compression anterior cruciate ligament rupture (ACLR). Here, we show that 2 weeks of tVNS significantly reduced histological OA scores in male and female mice after ACLR compared to sham stimulation. In female, but not male, mice, tVNS reduced hyperalgesia and mechanical allodynia. In the slower DMM model, 8 weeks of tVNS improved weight bearing in male and female mice, but only female mice had improved hyperalgesia. Male mice had lower OA histological scores. Serum proinflammatory cytokines were significantly reduced by tVNS in both models but differed by gender and model. Overall, these results provide strong pre-clinical evidence that tVNS reduces OA progression, improves pain, and suppresses pro-inflammatory cytokines, making it a promising DMOAD.

physiology↗

bioRxiv2023

The Hippo kinases control inflammatory Hippo signaling and restrict bacterial infection in eukaryotic phagocytes

The Hippo kinases MST1 and MST2 initiate a highly conserved signaling cascade called the Hippo pathway that limits organ size and tumor formation in animals. Intriguingly, pathogens hijack this host pathway during infection, but the role of MST1/2 in innate immune cells against pathogens is unclear. In this study, we generated Mst1/2 knockout macrophages to investigate the regulatory activities of the Hippo kinases in immunity. Transcriptomic analyses identified differentially expressed genes (DEGs) that are enriched in biological pathways, such as systemic lupus erythematosus, tuberculosis, and apoptosis. Surprisingly, pharmacological inhibition of the downstream components LATS1/2 in the canonical Hippo pathway did not affect expression of a set of immune DEGs, suggesting that MST1/2 control these genes via alternative inflammatory Hippo signaling. Moreover, MST1/2 may affect immune communication by influencing the release of cytokines, such as TNF, CXCL10, and IL-1ra. Comparative analyses of the single- and double-knockout macrophages revealed that MST1 and MST2 differentially regulate TNF release and expression of the immune transcription factor, MAF, demonstrating that the two homologous Hippo kinases individually play a unique role in innate immunity. Notably, MST1 and MST2 are both required for macrophages to activate apoptosis. Lastly, we demonstrated that the Hippo kinases are critical factors in mammalian macrophages and single-cell amoebae to restrict infection by Legionella pneumophila, Escherichia coli, and Pseudomonas aeruginosa. Together, these results uncover non-canonical inflammatory Hippo signaling in macrophages and the evolutionarily conserved role of the Hippo kinases in anti-microbial defense of eukaryotic hosts.

microbiology↗

bioRxiv2023

The relationships between genetic ancestry, somatic mutation frequency, and histologic subtypes in high-grade endometrial cancer

High-grade endometrial cancer, like numerous other cancer types, exhibits clear racial disparities in the United States for both the incidence and outcomes of the disease. While institutional factors are likely the primary contributor to these disparities, other underlying causes cannot be ignored (i.e., molecular, genetic, and histopathologic factors). This study seeks to interrogate the role that germline genetic influences, specifically genetic ancestry, may play in contributing to characteristics of high-grade endometrial cancer. This is mainly accomplished by examining the relationship between local ancestry inferences and somatic mutation frequency as well as histologic subtypes. An association between clinical characteristics and patient survival was also interrogated, and while global ancestry was seen to have no significant effect, tumor mutation burden (TMB) did impact patient survival. Here, we identify associations between local ancestry segments on chromosomes 1 and 14 and an increased TMB in self-described (SD) Black patients. We also highlight a complex relationship between heterozygous ancestry combinations within genomic regions (i.e., [European/African] vs. [African/African]) and an increase in local somatic mutation frequency. Furthermore, we explore the relationship between local ancestry and histologic subtype. We identify one region (chr9q32) wherein the African/European local ancestry diplotype was associated with a higher incidence of serous carcinoma. We also underline a difference in somatic mutation frequency between endometrioid and serous carcinoma. While highly exploratory, these findings begin to characterize the complex relationship between genetic ancestry and characteristics of high-grade endometrial cancer, which may impact patient survival.

genomics↗

bioRxiv2023

Host genetic background regulates the capacity for anti-tumor antibody-dependent phagocytosis

BackgroundAntitumor antibody, or targeted immunotherapy, has revolutionized cancer treatment and markedly improved patient outcomes. A prime example is the monoclonal antibody (mAb) trastuzumab, which targets human epidermal growth factor receptor 2 (HER2). However, like many targeted immunotherapies, only a subset of patients benefit from trastuzumab long-term. In addition to tumor-intrinsic factors, we hypothesize that host genetics may influence subsequent immune activation. MethodsTo model the human population, we produced F1 crosses of genetically heterogeneous Diversity Outbred (DO) mice with BALB/c mice (DOCF1). Distinct DOCF1 mice were orthotopically implanted with the BALB/c-syngeneic TUBO mammary tumor line, which expresses the HER2 ortholog rat neu. Treatment with anti-neu mAb clone 7.16.4 began once tumors reached [~]200 mm3. Genetic linkage and quantitative trait locus (QTL) effects analyses in R/qtl2 identified loci associated with tumor growth rates. Locus validation was performed with BALB/c F1 crosses with recombinant-inbred Collaborative Cross (CC) strains selected for therapy-associated driver genetics (CCxCF1). The respective roles of natural killer (NK) cells and macrophages were investigated by selective depletion in vivo. Ex vivo macrophage antibody-dependent phagocytosis (ADCP) assays were evaluated by confocal microscopy using 7.16.4-opsonized E2Crimson-expressing TUBO tumor cells. ResultsWe observed a divergent response to anti-tumor antibody therapy in DOCF1 mice. Genetic linkage analysis detected a locus on chromosome 10 that correlates to a robust response to therapy, which was validated in CCxCF1 models. Single-cell RNA sequencing of tumors from responder and non-responder models identified key differences in tumor immune infiltrate composition, particularly within macrophage (M{varphi}) subsets. This is further supported by ex vivo analysis showing M{varphi} ADCP capacity correlates to in vivo treatment outcomes in both DOCF1 and CCxCF1 models. ConclusionsHost genetics play a key regulatory role in targeted immunotherapy outcomes, and putative causal genes are identified in murine chromosome 10 which may govern M{varphi} function during ADCP.

cancer biology↗

bioRxiv2022

Hyperglycemic O-GlcNAc transferase activity drives cancer stem cell induction in TNBC

Enhanced glucose metabolism is a feature of almost all cancers, but downstream functional effects of aberrant glucose flux are difficult to mechanistically determine. The objective of this study is to characterize a mechanism by which elevated glucose level drives a tumorigenic pathway in triple negative breast cancer (TNBC). We used chemical biology methods to track how a metabolite of glucose, N-acetylglucosamine (GlcNAc), is linked to the transcriptional regulatory protein tet-methylcytosine dioxygenase 1 (TET1) as an O-linked GlcNAc post translational modification (O-GlcNAc). In this work, we revealed that intracellular protein glycosylation by O-GlcNAc is driven by high glucose levels in TNBC models, including on TET1. A single enzyme, O-GlcNAc transferase (OGT), is responsible for catalyzing protein modification of O-GlcNAc. We showed that OGT activity is higher in TNBC cell lines compared to non-tumor breast cell lines and is associated with hyperglycemia. Furthermore, enhanced OGT activity activated a pathway for cancer stem-like cell (CSC) reprogramming in TNBC cells. In our model, O-GlcNAcylated TET1 upregulated expression of splicing factor TAR-DNA binding protein (TARDBP), which drives CSC induction as well as higher OGT levels. We show that this OGT-TET1-TARDBP axis "feeds-forward" in hyperglycemic conditions both in cell lines and diet-induced obese mice, which displayed higher blood glucose levels and tumor O-GlcNAc levels than lean littermates. This data converges on a novel pathway whereby hyperglycemia drives aberrant OGT activity, activating a pathway for CSC induction in TNBC. Our findings partially explain a key aspect of how obesity is associated with TNBC risk and negative outcomes. Statement of ImplicationThis work presents a novel mechanism to explain how obesity is a risk factor for triple-negative breast cancer via elevated sugar-transfer activity by O-GlcNAc transferase in hyperglycemia, leading to the induction of a cancer stem-like cells and revealing a targetable pathway in obesity-associated tumors.

cancer biology↗

bioRxiv2022

Molecular profiling of XPO1 inhibitor and gemcitabine-nab-paclitaxel combination in cellular and LSL-Kras G12D/+; Trp53 fl/+; Pdx1-Cre (KPC) pancreatic cancer model

The majority of pancreatic ductal adenocarcinoma (PDAC) patients experience disease progression while on treatment with gemcitabine and nab-Paclitaxel (GemPac) treatment indicating the need for more effective combinations for this recalcitrant disease. Earlier we showed that nuclear exporter protein exportin 1 (XPO1) is a valid therapeutic target in PDAC and the selective inhibitor of nuclear export (SINE) selinexor (Sel), synergistically enhances the efficacy of GemPac in pancreatic cancer cells, spheroids, patient derived tumors and had promising activity in a phase I study in patients with PDAC. Here we investigated the mechanisms of synergy by molecular profiling of Sel or Sel-GemPac treated PDAC cells, in vitro and by utilizing genetically modified LSL-Kras G12D/+; Trp53 fl/+; Pdx1-Cre (KPC) mouse model. In KPC model, Sel given with GemPac at a sub-MTD dose enhanced the survival compared to controls (p < 0.05). Molecular analysis of residual KPC tumors showed re-organization of tumor stromal architecture, suppression of proliferation and nuclear retention of tumor suppressors. Single cell nuclear RNA sequencing (snRNAseq) revealed significant loss of cellular clusters in the Sel-GemPac treated mice including CD44 stem cell population. RNA-seq, Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA) analysis showed inhibition of several tumor promoting molecules. Prioritized RNA-seq identified molecules were validated in in vitro or in the PDAC patient samples through siRNA mediated silencing, quantitative gene expression, cytotoxicity assays and confirmed their role in observed synergy. Sel or Sel-GemPac caused broad penetration in PDAC supporting signaling networks.

cancer biology↗

bioRxiv2021

A Diversity Outbred F1 mouse model identifies host-intrinsic genetic regulators of response to immune checkpoint inhibitors

Immune checkpoint inhibitors (ICI) have improved outcomes for a variety of malignancies; however, many patients fail to benefit. While tumor-intrinsic mechanisms are likely involved in therapy resistance, it is unclear to what extent host genetic background influences response. To investigate this, we utilized the Diversity Outbred (DO) and Collaborative Cross (CC) mouse models. DO mice are an outbred stock generated by crossbreeding 8 inbred founder strains, and CC mice are recombinant inbred mice generated from the same 8 founders. We generated 207 DOB6F1 mice representing 48 DO dams and demonstrated that these mice reliably accept the C57BL/6-syngeneic B16F0 tumor and that host genetic background influences response to ICI. Genetic linkage analysis from 142 mice identified multiple regions including one within chromosome 13 that associated with therapeutic response. We utilized 6 CC strains bearing the positive (NZO) or negative (C57BL/6) driver genotype in this locus. We found that 2/3 of predicted responder CCB6F1 crosses show reproducible ICI response. The chromosome 13 locus contains the murine prolactin family, which is a known immunomodulating cytokine associated with various autoimmune disorders. To directly test whether prolactin influences ICI response rates, we implanted inbred C57BL/6 mice with subcutaneous slow-release prolactin pellets to induce mild hyperprolactinemia. Prolactin augmented ICI response against B16F0, with increased CD8 infiltration and 5/8 mice exhibiting slowed tumor growth relative to controls. This study highlights the role of host genetics in ICI response and supports the use of F1 crosses in the DO and CC mouse populations as powerful cancer immunotherapy models. One Sentence SummaryUsing germline genetic analysis in Diversity Outbred and Collaborative Cross models, we identify prolactin as a host-intrinsic regulator of response to combined immune checkpoint inhibitors.

immunology↗

bioRxiv2018

Novel immune cell subtypes linked to survival among African American women with triple-negative breast cancer

Triple negative breast cancer (TNBC) is an aggressive disease that is twice as likely to be diagnosed in African American (AA) women compared to white women, with poor clinical outcomes. Tumor infiltrating lymphocytes (TILs) are associated with improved survival for TNBC, but the relevance of TILs and immune cell subtypes to survival in AA women with TNBC is unknown. We evaluated histopathologic TIL counts and molecular characteristics among 60 AA women diagnosed with TNBC with linkage to clinical outcomes using data from the Metropolitan Detroit Cancer Surveillance System. We utilized whole genome expression profiling of TN tumors and cell type deconvolution analysis to evaluate the underlying mechanisms and immune cell subtypes associated with survival patterns in the context of TILs. TILs were significantly associated with improved survival [1-10% Hazard Ratio (HR)=0.32, 95% Confidence Interval (CI) 0.12-0.90, p=0.031; >10% HR=0.18, 95% CI 0.05-0.67, 9.9x10-3]. 524 transcripts (326 coding, 198 non-coding) were associated with TIL levels, 34 of which were associated with both TILs and survival (p<0.05). While only naive B cells were associated with survival when considering individual cell types [Median HR=2.43, 95% CI 1.07-5.55, p=0.035], increased naive B cells, plasma cells, and activated NK cells, and decreased resting mast cells, M1 macrophages, and monocytes were associated with transcripts that predicted worse survival. These data provide evidence for novel roles for these immune cells types in TNBC, and further studies are needed to validate these findings and identify determinants of patterns of immune response in TNBC relevant to the AA population.\n\nSummaryWe found that increased naive B cells, plasma cells, and activated natural killer cells, and decreased resting mast cells, M1 macrophages, and monocytes were associated with expression biomarkers of worse survival among African American women with triple negative breast cancer.

epidemiology↗