Biology subjects

Wang, S.

Publications and source records attributed to Wang, S..

At least 127 records · Page 7Linked to original sources

bioRxiv2026

A High-Confidence Atlas of Protein Methylation Enables AI-Driven Detection of Methylated Peptides

Lysine and arginine methylation regulate chromatin dynamics, transcription, and cellular signaling, however confident mass spectrometry (MS)-based detection and localization of this modification remain challenging. We reanalyzed eight public human methylation-enriched datasets using an open and standardized workflow that integrates database searching via the Trans-Proteomic Pipeline with a decoy-based statistical method for the independent estimation of false localization rates (FLR). This yielded a high-confidence Human Methylation Atlas of 1,828 sites (57 methyl-lysine, 1,771 methyl-arginine) across 1,021 proteins, classified into Gold, Silver, and Bronze confidence tiers. This is far fewer sites than reported in previous studies, reflecting the application of stringent FLR control, and what we hypothesise is potential high-false discovery in previous analyses. We then leveraged this resource to adapt a deep learning-based methodology for the improved detection of methylated peptides. Three mouse methylation-enriched datasets were reanalysed to augment training, and the phosphoproteomics-trained AHLF (ad hoc learning of peptide fragmentation) model was fine-tuned by transfer learning to create AHLF-Methylation. The model achieved mean ROC-AUC values of 0.824 on human spectra, and 0.829 on combined human-mouse spectra. The atlas is available through PTMeXchange and PRIDE, with curated site evidence integrated into UniProt and PeptideAtlas.

bioinformatics↗

bioRxiv2026

Internalized Components of Membrane Attack Complexes Disrupt Proteostasis and Acquire Alarmin-Like Properties

Immune effects of membrane attack complexes (MAC) have been widely attributed to their abilities to cause cell death. Here, we show that the MAC component, C9, forms non-cytolytic aggregates with pro-inflammatory effects. Intracellular aggregates of C9 are detected within inflamed tissues of patients in association with endothelial cell (EC) activation but not increased cell death. We identify NUMBL as a Rab35 effector that directly binds surface-bound C9 to promote C9 internalization and entry into the endolysosomal pathway. Within acidified endolysosomes, C9 forms insoluble aggregates that are targeted for degradative aggrephagy in a process that activates NF-{kappa}B. For C9 aggrephagy to occur, ZFYVE21, a Rab5 effector, complexes with RNF34 to bridge C9 aggregates to LC3B+ aggresome membranes. We detect C9 aggregates in vivo, and we show that a ZFYVE21-RNF34 signaling axis is required for C9 aggrephagy and NF-{kappa}B -dependent EC activation in three separate mouse models. Mice with conditional loss of ZFYVE21 in ECs show reduced aggregraphy, resulting in attenuated systemic inflammation and reduced tissue injury following skin transplantation. Our data show that the C9 component of MACs forms intracellular aggregates with alarmin-like properties.

biochemistry↗

bioRxiv2026

Microfluidic Tissue Array Platform for Personalized Drug Screening Using Tumor Explants or Biopsies

Despite major improvements in molecular characterization of breast cancer, current biomarkers still fall short in accurate treatment prediction. Interrogating tumor tissue ex-vivo in its native conformation is a direct strategy for guiding treatment of individual patients but presents a challenge. In this study, we developed a microfluidic tissue array (FTA) using small biopsy samples (< 1mm3) mimicking physiological flow for consistent exchange of nutrients and waste, retaining the tumor native stroma. Cell/patient-derived breast cancer xenograft tissues were maintained over 2 weeks in the array and their response to therapeutic agents, doxorubicin or neratinib, were interrogated. Drug response in the uFTA showed >2-fold reduction in tumor cell viability which corroborated tumor size shrinkage in mice bearing the same tumor load. EdU/Ki67 assays indicated selective retention of cells with higher proliferative capacity after drug treatment, underscoring in vivo clinical relevance . We have also developed a valved-FTA to increase throughput and variety of treatment conditions on the same chip. Together, this FTA can be staged as a powerful, low-cost benchtop theranostic tool for personalized cancer therapeutics compatible with FDAs New Approach Methods.

cancer biology↗

bioRxiv2026

A High-Quality Acetylation Dataset Reveals Modest Data Requirements for Transfer Learning to Identify Little Studied Post-Translational Modifications

Dysregulation of post-translational modifications (PTMs) is associated with severe pathologies, including cancers and Alzheimers disease. Despite their biological importance, identifying modified peptides remains challenging due to the immense combinatorial search space. While searches benefit from prior knowledge of a peptides modification status, the data scarcity for most PTMs hinders the development of accurate deep learning classifiers like AHLF (ad hoc learning of peptide fragmentation). Here, we overcome this data bottle-neck for acetylation and ubiquitination. We harmonised a dataset with about 500,000 high quality acetylated peptide-spectrum matches (PSMs) from nine publicly available acetylation-enriched datasets. We fine-tuned AHLF with the acetylation and a 2-million spectra strong ubiquitination dataset separately and assessed the minimum data requirement for training by iteratively downsampling. Training separate models on SILAC and label-free subsets also assessed the impact of data diversity. The resulting acetylation and ubiquitination models achieve an AUC of 0.87 and 0.90 respectively. Beyond 28,500 acetylated spectra, corresponding to roughly 0.3% of the original models training data, additional data just provides minor performance gains. Finally, we show that data diversity is beneficial for generalizability, while models trained on homogeneous data sources tend to overfit to their respective data type. All code, and model weights are available at https://gitlab.com/dacs-hpi/ahlf-ptmai.

bioinformatics↗

bioRxiv2026

From innovation to integration: Personality, sex, and learning drive recombination of innovative behaviours in lovebirds

Behaviour innovation plays a pivotal role in a species adaptability to dynamic environments. Investigating innovative behaviour and its underlying mechanism is therefore crucial for elucidating the development of cognitive flexibility across animals. Animal personality--which shapes how individuals perceive and engage with their surroundings--could offer insights into individual variation in this process. This study used a three-step foraging puzzle to evaluate the innovation capacity in 28 rosy-faced lovebirds (Agapornis roseicollis), specifically examining their capacity to recombine individually innovated component behaviours into integrated, more sophisticated techniques. We found that nearly half of the individuals spontaneously innovated multiple component behaviours to solve novel puzzles. Crucially, when challenged with a more sophisticated task, they recombined these behaviours into functionally dependent sequences without prior social demonstration. We further identified sex, persistence, and asocial learning capacity as key predictors of innovative problem-solving performance, with females, persistent individuals, and superior asocial learners excelled at problem-solving. Our findings demonstrate that behavioural innovation is not a static event, but a dynamic process--modulated by physical, cognitive, and personality variables--in which behaviours are flexibly transferred and recombined into increasingly complex forms to enable rapid individual adaptation.

animal behavior and cognition↗

bioRxiv2026

LDB1-dependent enhancer connectivity defines T-cell leukemia identities and masks metabolic vulnerabilities

Spatial enhancer connectivity is fundamental to proper gene regulation. Enhancer dysregulation has emerged as a hallmark of cancers, including T-cell acute lymphoblastic leukemias (T-ALL). T-ALL are aggressive malignancies characterized by marked transcriptional heterogeneity driven by distinct stages of developmental arrest and diverse noncoding alterations. How these cancers co-opt nuclear architecture to rewire enhancer connectivity remains poorly understood. Here, we report that the LDB1 chromatin architectural complex is an essential mediator of enhancer-oncogene looping that sustains oncogenic transcriptional programs across multiple T-ALL subtypes. Integrating bulk and single-cell transcriptomic data from patients with T-ALL and healthy hematopoietic controls, we show that the LDB1-dependent regulatory circuitry defines the molecular identities of distinct T-ALL subtypes while restricting plasticity toward alternative cell states. LDB1 loss dismantles chromatin looping among cell state-defining enhancers liberating them to form promiscuous interactions with nearby genes. This enhancer rewiring stimulates expression of key metabolic genes, creating a mevalonate pathway dependency exploitable with statin treatment. Our study establishes LDB1 as a central executor of T-ALL regulatory circuitry and more broadly illustrates chromatin rewiring as a source of targetable dependencies in cancer.

Cancer Biology↗

bioRxiv2026

Mammalian aging involves genome-wide splicing degeneration leading to functional decline

Alternative splicing exhibits significant changes during development and aging, affecting the composition and variance in the transcriptome. However, it is unclear whether and how age-associated splicing dysregulation leads to functional consequences. Here, an integrative analysis of transcriptome data across mouse and human tissues revealed that aging is characterized by systematic deterioration of the fidelity of RNA splicing, here termed splicing degeneration, a measure of functional alteration of reading frame and domain configuration of protein products. Genes with higher aging-associated splicing degeneration were more conserved and enriched for processes such as RNA metabolism and antigen presentation. By assessing alternative splicing events associated with functional deterioration, we quantified the degree of splicing degeneration. Its level increased with age but was alleviated following calorie restriction or rapamycin treatment, indicating that it can serve as a new molecular hallmark of aging. Mechanistically, through a comprehensive meta-data analysis, we discovered that splicing degeneration is associated with age-associated changes in specific splicing factors, which in turn showed a strong association with age-related transcriptome changes. Overall, our study demonstrates the intricate relationship between aging and genome-wide splicing degeneration, revealing a promising target for aging interventions acting to reverse splicing degeneration.

Systems Biology↗

bioRxiv2026

Doublesex- mediated regulation of insulin signaling drives sex-specific body growth

Most animals develop sex-biased body sizes driven by sexually divergent plasticity in nutrient-dependent growth. Prior work in Drosophila, implicated the sex-determination gene transformer (tra) in regulation of sex differences in body size. However, tra does not widely mediate sex determination across insects. Thus, the unifying molecular pathway governing female-biased sexual size dimorphism (SSD) remains poorly established in non-drosophilid insects. The rice stem borer Chilo suppressalis, a devastating lepidopteran crop pest, exhibits a robust SSD, offering an ideal system to dissect underlying mechanisms. We report that female-specific splice forms of the sex-determining gene doublesex (Csdsx) are master regulators of female-biased growth. Disruption of the female-specific Csdsx exon 3 via CRISPR knockout or RNA interference drastically reduces female body size and completely erases the SSD. Csilp2, encoding a key insulin-like peptide (ILP2), is selectively upregulated in late-instar female larvae, and female CsDsx proteins directly bind and activate the Csilp2 promoter to boost transcription. Loss-of-function of Csilp2 eliminates the SSD by suppressing female somatic overgrowth. Our results identify a novel regulatory cascade: female-specific Dsx directly stimulates insulin signaling via Csilp2, bridging core sex-determination circuitry and nutrient-dependent body growth control. SignificanceSexual size dimorphism (SSD), widespread across insects with larger females, strongly shapes reproductive fitness. Yet reports on the molecular connection between sex determination and dimorphic growth are scarce. Using a major agricultural pest, the rice stem borer with a prominent female-biased SSD, we show that female-specific Doublesex (dsx) splice variants directly activate the promoter of Insulin-like peptide 2 in late larvae to trigger increased growth. Knocking out either gene in females abolishes the SSD. Our findings thus establish dsx as a novel link connecting sex-determination, insulin signaling and nutrient-dependent body growth.

Developmental Biology↗

bioRxiv2026

Hippocampal-cortical coupling dynamics drive system consolidation of remote memory

System consolidation transforms temporary hippocampal representation of memory into long-term storage in cortex. The underlying neural substrate, however, remains enigmatic. Here, we tracked the spatiotemporal evolution of hippocampus (HPC)-cortex local field potentials and single-neuron spikes in behaving animals during fear memory formation. During learning, HPC fast gamma exhibited a progressive phase shift relative to PFC theta oscillations, with gamma power aligning to progressively later phases of the PFC theta cycle. Strikingly, a related phase-shifted coupling pattern re-emerged during subsequent consolidation in association with hippocampal sharp-wave ripples and transient PFC spindle events during NREM sleep. Across this process, interregional interactions evolved from HPC-driven cortical gamma coherence at recent stages to PFC-mediated cortical low-frequency coherence at remote stages. Using closed-loop optogenetic perturbations, we demonstrated a stepwise causal chain of coupling events underlying remote memory formation. Our study revealed HPC-PFC coupling phase shift as a feasible substrate mediating recent-to-remote transformation of memory.

neuroscience↗

bioRxiv2026

Regulatory co-option of a homeobox gene drives parasitoid venom evolution

How gene regulatory networks are rewired to generate phenotypic and functional innovation remains a central question in evolutionary biology. Parasitoid wasp venoms provide a powerful system for addressing this question, as their repertoires evolve rapidly through extensive lineage-specific turnover, yet the regulatory principles underlying such flexibility are largely unknown. Here we integrate tissue-resolved transcriptomic, chromatin-accessibility and histone-modification profiling to reconstruct the venom regulatory network of the parasitoid wasp Pteromalus puparum. We show that venom expression is embedded in distinct chromatin states and shaped by regulatory elements associated with venom-gland transcription. Comparative and functional analyses support a general model in which regulators related to the endoplasmic reticulum stress and unfolded protein response pathways have been repeatedly recruited to venom regulation across venomous lineages. Unexpectedly, we identify the recently co-opted homeobox gene Lbx as a lineage-specific hub that regulates more than half of venom genes and is linked to enhancer evolution. These results reveal a nested model of venom regulatory evolution, in which an ancestral secretory programme provides a reusable regulatory backbone, while newly co-opted homeobox gene specify a lineage-specific venom expression. Our study highlights regulatory co-option as a mechanism by which conserved developmental genes can acquire new physiological functions during adaptive evolution.

evolutionary biology↗

bioRxiv2026

CWF19L2 couples pre-mRNA alternative splicing with the maternal-to-zygotic transition to safeguard female fertility

The maternal-to-zygotic transition (MZT) requires precise spatiotemporal execution of pre-mRNA alternative splicing (AS), yet the core splicing machinery driving this developmental reprogramming remains incompletely understood. Here, we identify the CWF19-like protein 2 (CWF19L2) as an indispensable pre-mRNA AS regulator that safeguards against oocyte and early embryo competence defects (OECD). While murine germline-specific depletion of Cwf19l2 spares morphological folliculogenesis, oocyte maturation, or fertilization, it induces complete female sterility characterized by profound developmental arrest at the 2-cell stage. Mechanistically, maternal deficiency of CWF19L2 localized to nuclear speckles disrupts transcription-splicing-translation coupling, collapsing AS homeostasis during maternal reserves and zygotic genome activation. We further demonstrate that CWF19L2 orchestrates the pre-mRNA splicing network through directly binding to target transcripts and indirectly modulating via interacting with the core spliceosomal factor PRPF8. Importantly, exogenous Cwf19l2 mRNA partially rescues the embryonic arrest. Together, our findings establish CWF19L2 as an indispensable AS engine during the MZT, providing a mechanistic foundation for OECD and a novel molecular etiology for female infertility.

Cell Biology↗

bioRxiv2026

RNAStabFormer: Region-Aware Multi-Task Hybrid Learning for RNA Stability Prediction from Pulse-Chase Transcriptomics

RNA stability is a major post-transcriptional regulator of gene expression, yet sequence-based prediction from pulsechase transcriptomics remains difficult because labels depend on time window, quantification region, and replicate quality. We present RNAStabFormer, a controlled RNA stability framework centered on a Region-aware Multi-task Hybrid Transformer (RAMHT). RAMHT encodes 5'UTR, CDS, and 3'UTR nucleotide context, adds a CDS codon stream, upgrades engineered sequence features into a tabular interaction branch, and uses gated multi-task regression to predict four ENCODE BrU-seq/BruChase-seq stability proxies, with exon total 6 h/0 h as the primary task. Across 26 outer splits including 23 chromosome holdouts, a heterogeneous three-member RAMHT ensemble achieves 0.773 mean Pearson correlation on the primary task, statistically matching an engineered-feature XGBoost baseline (0.773; mean paired delta +0.000004; bootstrap 95% CI [- 0.003845, +0.004077]; Wilcoxon p = 0.8613). The ensemble improves over the strongest single RAMHT member (0.768 to 0.773; 23/26 split wins), while a strict nested XGBoost+RAMHT blend reaches 0.775. Same-split checks also exceed frozen full-length mRNA-LM embeddings (0.760) and public LAMAR-DR transfer (0.180). Gate, ablation, and recoding analyses show that engineered sequence grammar remains dominant, while nucleotide and codon branches provide complementary CDS-local signal. RNAStabFormer narrows the gap between neural RNA sequence modeling and strong tabular baselines while retaining an extensible architecture for interpretation and biological integration.

bioinformatics↗

bioRxiv2026

The Fas-FADD-caspase-8 axis is a cancer cell-intrinsic determinant of cytotoxic lymphocyte-mediated killing

Cytotoxic lymphocytes induce cancer cell death through death receptor-ligand interactions and the perforin-granzyme pathway. These pathways are generally thought to converge on the activation of executioner caspases to drive apoptosis. Here, we employed a reductionist approach to systematically disrupt key cell death mediators in a cytotoxic lymphocyte killing system to define their roles in determining cancer cell fate. We found that loss of executioner caspases conferred only limited resistance to cytotoxic lymphocyte-mediated killing. To identify cancer cell-intrinsic regulators that function beyond executioner caspases, we performed unbiased genome-wide CRISPR screens in executioner caspase-deficient cells. Unexpectedly, disruption of Fas or FADD--core components of the death receptor pathway-- conferred substantial resistance to cytotoxic lymphocyte-mediated killing even in the absence of executioner caspases. This resistance persisted following additional disruption of known downstream mediators of Fas-FADD-caspase-8 (CASP8) signaling. Together, these findings identify the Fas-FADD-CASP8 axis as a central cancer cell-intrinsic determinant of susceptibility to cytotoxic lymphocyte-mediated killing whose function is not fully explained by canonical apoptotic or non-apoptotic effector pathways. Our results further suggest that CASP8 engages additional downstream substrates or mechanisms to promote cytotoxic lymphocyte-induced cancer cell death.

immunology↗

bioRxiv2026

Homeobox transcription factor MSX2 down-regulates ERα action to facilitate anti-estrogensensitivity in ERα+ breast cancer

Breast cancer is the most common malignancy among women worldwide. Estrogen receptor (ER)-positive breast cancer is about 70% in the total breast cancer. It has variable prognosis and high recurrent risk, frequently developing resistance to endocrine therapies. Herein, we have identified that a homeobox transcription factor MSX2 downregulated in ER-positive breast cancer is correlated with the advanced grade and poor survival outcomes. Our results have demonstrated that MSX2 interacts with ER to inhibit ER-mediated transactivation. Mechanistically, MSX2 associates with HDAC1/HDAC2 to form a protein complex. MSX2 is required for recruitment of HDAC1/HDAC2 complex to estrogen response elements (EREs) region on ER downstream target genes, reducing histone H3K9ac and H3K27ac levels to inactivate gene transcription. Functionally, ectopic expression of MSX2 suppresses cell growth and enhances the sensitivity to anti-estrogen treatment in ER-positive breast cancer cells. Our results indicate that MSX2 as a novel co-repressor of ER is involved in suppression of ER-positive breast cancer progression. Restoring MSX2 protein may provide a promising strategy to overcome endocrine resistance in ER-positive breast cancer.

Molecular Biology↗

bioRxiv2026

Aberrant neuron-OPC synaptic transmission and deficient myelination define sex bias in major depressive disorder

Sex bias is a notable feature of major depressive disorder (MDD), yet its cellular and molecular origins remain unclear. We integrated computational analyses of human patient data with histological and biochemical validation in animal models to uncover female-specific MDD pathways. We identified female-specific mechanisms involving oligodendroglial lineage cells, especially oligodendrocyte precursor cells (OPCs), as key signal receivers with unidirectional preference in interactome networks. The neurexin (NRXN) pathway emerged as the most perturbed in MDD, with greater disruption in females. Subclustering further identified committed OPCs (cOPCs) as a disease-associated oligodendroglial subpopulation characterized by high expression of synaptic genes; cOPCs were also enriched of MDD-related transcriptional signatures revealed by trajectory analysis. High-dimensional weighted gene co-expression network analysis identified GABRG3 as an MDD-specific hub gene in cOPCs. The GABRG3 was also involved in the NRXN synaptic assembly cascade. Using Gabrg3 conditional knockout mice, we validated findings in patients and demonstrated that conditional deletion of Gabrg3 in cOPCs recapitulates MDD-like phenotypes, highlighting impaired neuron-cOPC synaptic communication, abnormal myelination, and depression-like behaviors. Together, our work defines a sex-specific cellular and molecular pathobiology of MDD, bridges clinical discovery with preclinical context, and provides a translatable framework for precision medicine targeting fundamental sex differences.

neuroscience↗

bioRxiv2026

Targeting Lysosomal MCOLN1/TRPML1 Ion Channels to Finely Alleviate Diabetes Mellitus via a Ca 2+ - CaMKKβ-AMPK pathway

Type 2 Diabetes mellitus (T2DM) is a metabolic syndrome characterized by hyperglycemia and various complications. Current drugs are limited by side effects and resistance, necessitating novel targets and therapies. Previous studies have shown that MK-83, a synthetic agonist of transient receptor potential mucolipin 1 (TRPML1/ MCOLN1), a lysosomal Ca2+ channel, activates adenosine 5'-monophosphate-activated protein kinase (AMPK), a key therapeutic target in diabetes. However, whether targeting TRPML1 can treat T2DM remains unclear. In this study, we found that transgenic overexpression or pharmacological activation of TRPML1 finely controls AMPK phosphorylation via a Ca2+-CaMKK{beta}-dependent mechanism. This activation promotes glucose transporter 4 (GLUT4) translocation and dramatically increases intracellular glucose uptake. Conversely, genetic inactivation or pharmacologically inhibition of TRPML1 blocks both AMPK activation and glucose uptake. More importantly, pharmacological activation of TRPML1 in vivo dramatically alleviates hyperglycemia in db/db mice (a T2DM model), as evidenced by random blood glucose levels, fasting blood glucose levels and HbA1c levels. Furthermore, other hallmark features of db/db mice-including impaired oral glucose tolerance, reduced insulin tolerance, and elevated ALT and AST levels- were all ameliorated upon TRPML1 activation. Hence, targeting lysosomal TRPML1 channel represents a promising therapeutic strategy for T2DM, with highly specific TRPML1 agonists as potential anti-diabetic agents.

Cell Biology↗

bioRxiv2026

oxo-flow: compiled, memory-safe bioinformatics workflow orchestration

Bioinformatics analyses depend on workflow engines to coordinate dozens of computational tools across complex dependency chains. The most widely adopted engines--Snakemake, Nextflow, the Common Workflow Language (CWL), and the Workflow Description Language (WDL)--run on interpreted or just-in-time (JIT) compiled language runtimes, incurring hundreds of milliseconds of startup latency and providing no compile-time safety guarantees from the host language. We developed oxo-flow, a workflow engine written in Rust that compiles to a single native binary. On an Apple M5 processor, oxo-flow parses, validates, and dry-runs a production-scale workflow in roughly 22 milliseconds--before Snakemake or Nextflow have finished loading their runtime environments. Peak memory usage is 16 megabytes, representing six- to seven-fold reductions relative to Snakemake and Nextflow. Dry-run latency is essentially independent of workflow size: a hundred-fold increase in rule count adds approximately 0.4 milliseconds. oxo-flow integrates 31 command-line tools, a REST interface with 60 endpoints, an embedded web application, and native cluster submission into a single 10-megabyte binary. It provides per-rule environment isolation across seven backends, checkpoint-based fault tolerance with cryptographic output verification, and a formal installation and operational qualification protocol for regulated laboratory environments. Ten curated workflows and three demonstration pipeline repositories are available. oxo-flow is freely available under Apache License 2.0 at https://github.com/Traitome/oxo-flow.

bioinformatics↗

bioRxiv2026

A multimodal foundation model linking histopathology and DNA methylation

Hematoxylin and eosin (H&E) slides are routinely available in cancer care, but molecular profiling often requires additional tissue processing and turnaround time. We introduce HistoMethyl, a DNA methylation-aware pathology foundation model that aligns whole-slide histopathology with matched genome-scale methylation beta-value profiles during pre-training while requiring only an H&E slide at inference. We evaluated HistoMethyl across four task groups: gene mutation prediction, morphology-associated classification, overall survival prediction, and direct DNA methylation beta-value recovery. Evaluation spanned TCGA cross-validation, a disease-held-out lower-grade glioma cohort, and external cohort validation in CPTAC glioblastoma and SurGen rectal adenocarcinoma, totaling 14 cancer cohorts and 81 gene mutation tasks. The best-performing configuration improved mean mutation AUROC by 5.03 percentage points. By converting DNA methylation supervision into an H&E-only representation, His-toMethyl could support an early molecular triage layer that helps prioritize cases for confirmatory sequencing, methylation profiling, immunohistochemistry, and molecular tumor board review. These image-only predictions are intended to accelerate downstream molecular testing and tissue allocation while leaving final diagnosis and treatment selection anchored in validated molecular assays.

Cancer Biology↗