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Koneru, B.

Publications and source records attributed to Koneru, B..

4 recordsLinked to original sources

Biomineralized Surface-Enhanced Raman Scattering Nanotags Encode Biomolecular Identity into Machine Learning-Resolvable Plasmonic Fingerprints

Surface-enhanced Raman scattering (SERS) nanotags provide highly sensitive platforms for in vitro diagnostics but often require complex, disease-specific customization that limits clinical translation. Biomineralization, in which biomolecules mediate inorganic material synthesis, offers a versatile yet underexplored strategy for generating functional SERS nanotags. Here, we demonstrate that biomolecule-directed biomineralization of gold nanoparticles (AuNPs) using amino acids and exosomes generates distinct nano-bio interfacial architectures that encode biomolecular identity into machine learning-resolvable SERS fingerprints through modulation of plasmonic coupling and Raman reporter organization. As a proof-of-concept system, amino acid-biomineralized AuNPs were synthesized using biomolecules with diverse physicochemical properties, including differences in size, polarity, and charge. The resulting nanotags were characterized using UV-Vis spectroscopy, SERS, fluorescence spectroscopy, dynamic light scattering (DLS), and transmission electron microscopy (TEM). Random forest and support vector machine (SVM) models successfully differentiated amino acid-dependent SERS signatures with near-perfect classification performance. Extending this approach to a biologically complex preclinical cancer model, exosome-biomineralized AuNP nanotags were generated using exosomes derived from clinically relevant pediatric patient-derived osteosarcoma and neuroblastoma tumors. Distinct exosome-dependent spectral fingerprints enabled SVM classification with 93.9% accuracy, while Shapley Additive exPlanations (SHAP) and t-distributed stochastic neighbor embedding (t-SNE) analyses identified diagnostically relevant spectral regions and visualized clustering between tumor classes. Collectively, this work establishes biomineralization as a strategy for transforming complex biomolecular and cellular information into computationally resolvable optical fingerprints, enabling scalable and label-free diagnostic classification of patient-derived biomolecular samples.

bioengineering↗

Tabular foundation model predicts alternative lengthening of telomeres (ALT) and identifies SMARCAL1 as a target in ALT-driven cancers

Alternative lengthening of telomeres (ALT) is a telomerase-independent pathway used by aggressive cancers to maintain their replicative immortality. Because ALT is absent from normal human cells, it is an appealing target for cancer therapy, but the lack of ability to determine ALT status at scale has hindered discovery. Here, we developed ALTitude, a machine learning method from a tabular foundation model that infers ALT from cell line whole genome sequencing data, without need for paired germline analysis. We deployed ALTitude across the DepMap, doubling the number of known ALT+ cancer models. Systematic integration of ALTitude with CRISPR-Cas9 screens yielded the selective dependency on SMARCAL1 in ALT+ cell lines, where we show it stabilizes the ALT phenotype. Acute depletion of SMARCAL1 leads to G2/M arrest, mitotic catastrophe, and cell death. These data provide a valuable resource for studying ALT-related genomic features and present SMARCAL1 as a therapeutic target for ALT+ malignancies.

cancer biology↗

DNA2 variant analysis supports the nuclease activity as a preferred therapeutic target

DNA2 is a combined nuclease and helicase that processes long 5 flaps and other structures that occur during DNA replication and repair. Current models invoke an essential function of DNA2 in processing stalled replication forks to dampen toxic recombination based restart. As an essential replication stress response factor, DNA2 has been proposed as an anti-cancer drug target with several tool compounds developed. Here we sought to model inhibited DNA2 states using dominant genetics with separation-of-function alleles to identify the optimal mechanisms for DNA2 targeting. We find that expression of DNA2 nuclease-dead alleles exert dominant effects on fitness and DNA damage repair that are dependent on its helicase and RPA binding activities. Furthermore, we find an imperfect link wherein a subset of ALT+ models are hypersensitive to the presence of DNA2-nuclease dead protein. These results were replicated with a nuclease-specific inhibitor of DNA2. Together, our data suggests that DNA2 targeting in cancer should be nuclease focused and will rely on identification of specific biomarker subsets within ALT+ or other tumor cell states.

cell biology↗

ALT Neuroblastoma Chemoresistance due to ATM Activation by Telomere Dysfunction is Reversible with the ATM Inhibitor AZD0156

Cancers overcome replicative immortality by activating either telomerase or an alternative lengthening of telomeres (ALT) mechanism. ALT occurs in [~] 25% of high-risk neuroblastomas and relapse or progression in ALT neuroblastoma patients during or after front-line therapy is frequent and almost uniformly fatal. Temozolomide + irinotecan is commonly used as salvage therapy for neuroblastoma. Patient-derived cell-lines and xenografts established from relapsed ALT neuroblastoma patients demonstrated de novo resistance to temozolomide + irinotecan (as SN-38 in vitro, P<0.05) and in vivo (mouse event-free survival (EFS) P<0.0001) relative to telomerase-positive neuroblastomas. We observed that ALT neuroblastoma cells manifest constitutive ATM kinase activation due to spontaneous telomere dysfunction while telomerase- positive tumors lacked constitutive ATM activation or spontaneous telomere DNA damage. We demonstrated that induction of telomere dysfunction resulted in ATM activation that in turn conferred resistance to temozolomide + SN-38 (4.2 fold-change in IC50, P<0.001). ATM kinase shRNA knock-down or inhibition using a clinical-stage small molecule inhibitor (AZD0156) reversed resistance to temozolomide + irinotecan in ALT neuroblastoma cell-lines in vitro (P<0.001) and in 4 ALT xenografts in vivo (EFS P<0.0001). AZD0156 showed modest to no enhancement of temozolomide + irinotecan activity in telomerase-positive neuroblastoma cell lines and xenografts. ATR inhibition using AZD6738 did not enhance temozolomide + SN-38 activity in ALT neuroblastoma cell lines. Thus, resistance to chemotherapy in ALT neuroblastoma occurs via ATM kinase activation and was reversed with the ATM inhibitor AZD0156. Combining AZD0156 with temozolomide + irinotecan warrants clinical testing in neuroblastoma. One Statement SummaryATM activation at telomeres confers resistance to DNA damaging chemotherapy in ALT neuroblastoma that was reversed with ATM knockdown or inhibition.

cancer biology↗