17 research outputs found
Towards a Visual-Language Foundation Model for Computational Pathology
The accelerated adoption of digital pathology and advances in deep learning
have enabled the development of powerful models for various pathology tasks
across a diverse array of diseases and patient cohorts. However, model training
is often difficult due to label scarcity in the medical domain and the model's
usage is limited by the specific task and disease for which it is trained.
Additionally, most models in histopathology leverage only image data, a stark
contrast to how humans teach each other and reason about histopathologic
entities. We introduce CONtrastive learning from Captions for Histopathology
(CONCH), a visual-language foundation model developed using diverse sources of
histopathology images, biomedical text, and notably over 1.17 million
image-caption pairs via task-agnostic pretraining. Evaluated on a suite of 13
diverse benchmarks, CONCH can be transferred to a wide range of downstream
tasks involving either or both histopathology images and text, achieving
state-of-the-art performance on histology image classification, segmentation,
captioning, text-to-image and image-to-text retrieval. CONCH represents a
substantial leap over concurrent visual-language pretrained systems for
histopathology, with the potential to directly facilitate a wide array of
machine learning-based workflows requiring minimal or no further supervised
fine-tuning
ΠΠ»ΠΈΡΠ½ΠΈΠ΅ Π°Π½ΠΈΠ·ΠΎΡΡΠΎΠΏΠΈΠΈ Π½Π° ΡΡΠ°Π½ΡΠΏΠΎΡΡΠ½ΡΠ΅ ΡΠ²ΠΎΠΉΡΡΠ²Π° ΡΠ»ΠΎΠΈΡΡΠΎΠ³ΠΎ Π²ΡΡΠΎΠΊΠΎΡΠ΅ΠΌΠΏΠ΅ΡΠ°ΡΡΡΠ½ΠΎΠ³ΠΎ ΡΠ²Π΅ΡΡ ΠΏΡΠΎΠ²ΠΎΠ΄Π½ΠΈΠΊΠ° Ρ ΠΌΠ°Π³Π½ΠΈΡΠ½ΡΠΌΠΈ ΠΈ Π½Π΅ΠΌΠ°Π³Π½ΠΈΡΠ½ΡΠΌΠΈ ΠΏΡΠΎΡΡΠΆΠ΅Π½Π½ΡΠΌΠΈ Π΄Π΅ΡΠ΅ΠΊΡΠ°ΠΌΠΈ
Transport properties of anisotropic superconductor with point, columnar and columnar tilted defects have been analyzed using Monte-Carlo method. It was shown that for columnar tilted defects the critical current dependence on anisotropy weakens as increases and vanishes at certain . The S-type nonlinearity of current-voltage characteristics has been shown for three-dimensional vortex system in presence of ferromagnetic defects.ΠΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΠΎΠ½ΡΠ΅-ΠΠ°ΡΠ»ΠΎ ΠΏΡΠΎΠ°Π½Π°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π½Ρ ΡΡΠ°Π½ΡΠΏΠΎΡΡΠ½ΡΠ΅ ΡΠ²ΠΎΠΉΡΡΠ²Π° Π°Π½ΠΈΠ·ΠΎΡΡΠΎΠΏΠ½ΠΎΠ³ΠΎ ΡΠ²Π΅ΡΡ
ΠΏΡΠΎΠ²ΠΎΠ΄Π½ΠΈΠΊΠ° Ρ ΡΠΎΡΠ΅ΡΠ½ΡΠΌΠΈ, ΠΊΠΎΠ»ΡΠΌΠ½Π°ΡΠ½ΡΠΌΠΈ ΠΈ ΠΊΠΎΠ»ΡΠΌΠ½Π°ΡΠ½ΡΠΌΠΈ Π½Π°ΠΊΠ»ΠΎΠ½Π½ΡΠΌΠΈ Π΄Π΅ΡΠ΅ΠΊΡΠ°ΠΌΠΈ. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ Π² ΡΠ»ΡΡΠ°Π΅ ΠΊΠΎΠ»ΡΠΌΠ½Π°ΡΠ½ΡΡ
Π½Π°ΠΊΠ»ΠΎΠ½Π½ΡΡ
Π΄Π΅ΡΠ΅ΠΊΡΠΎΠ² Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΡ ΠΊΡΠΈΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΡΠΎΠΊΠ° ΠΎΡ Π°Π½ΠΈΠ·ΠΎΡΡΠΎΠΏΠΈΠΈ ΠΎΡΠ»Π°Π±Π΅Π²Π°Π΅Ρ Ρ ΡΠΎΡΡΠΎΠΌ ΠΈ ΠΏΡΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½Π½ΠΎΠΌ ΠΈΡΡΠ΅Π·Π°Π΅Ρ ΡΠΎΠ²ΡΠ΅ΠΌ. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ Π½Π°Π»ΠΈΡΠΈΠ΅ S-ΠΎΠ±ΡΠ°Π·Π½ΠΎΠΉ Π½Π΅Π»ΠΈΠ½Π΅ΠΉΠ½ΠΎΡΡΠΈ Π²ΠΎΠ»ΡΡ-Π°ΠΌΠΏΠ΅ΡΠ½ΠΎΠΉ Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΡΡΠΈΠΊΠΈ Π΄Π»Ρ ΡΡΠ΅Ρ
ΠΌΠ΅ΡΠ½ΠΎΠΉ Π²ΠΈΡ
ΡΠ΅Π²ΠΎΠΉ ΡΠΈΡΡΠ΅ΠΌΡ Ρ ΡΠ΅ΡΡΠΎΠΌΠ°Π³Π½ΠΈΡΠ½ΡΠΌΠΈ Π΄Π΅ΡΠ΅ΠΊΡΠ°ΠΌΠΈ
ΠΠ»ΠΈΡΠ½ΠΈΠ΅ Π°Π½ΠΈΠ·ΠΎΡΡΠΎΠΏΠΈΠΈ Π½Π° ΡΡΠ°Π½ΡΠΏΠΎΡΡΠ½ΡΠ΅ ΡΠ²ΠΎΠΉΡΡΠ²Π° ΡΠ»ΠΎΠΈΡΡΠΎΠ³ΠΎ Π²ΡΡΠΎΠΊΠΎΡΠ΅ΠΌΠΏΠ΅ΡΠ°ΡΡΡΠ½ΠΎΠ³ΠΎ ΡΠ²Π΅ΡΡ ΠΏΡΠΎΠ²ΠΎΠ΄Π½ΠΈΠΊΠ° Ρ ΠΌΠ°Π³Π½ΠΈΡΠ½ΡΠΌΠΈ ΠΈ Π½Π΅ΠΌΠ°Π³Π½ΠΈΡΠ½ΡΠΌΠΈ ΠΏΡΠΎΡΡΠΆΠ΅Π½Π½ΡΠΌΠΈ Π΄Π΅ΡΠ΅ΠΊΡΠ°ΠΌΠΈ
Transport properties of anisotropic superconductor with point, columnar and columnar tilted defects have been analyzed using Monte-Carlo method. It was shown that for columnar tilted defects the critical current dependence on anisotropy weakens as increases and vanishes at certain . The S-type nonlinearity of current-voltage characteristics has been shown for three-dimensional vortex system in presence of ferromagnetic defects.ΠΠ΅ΡΠΎΠ΄ΠΎΠΌ ΠΠΎΠ½ΡΠ΅-ΠΠ°ΡΠ»ΠΎ ΠΏΡΠΎΠ°Π½Π°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°Π½Ρ ΡΡΠ°Π½ΡΠΏΠΎΡΡΠ½ΡΠ΅ ΡΠ²ΠΎΠΉΡΡΠ²Π° Π°Π½ΠΈΠ·ΠΎΡΡΠΎΠΏΠ½ΠΎΠ³ΠΎ ΡΠ²Π΅ΡΡ
ΠΏΡΠΎΠ²ΠΎΠ΄Π½ΠΈΠΊΠ° Ρ ΡΠΎΡΠ΅ΡΠ½ΡΠΌΠΈ, ΠΊΠΎΠ»ΡΠΌΠ½Π°ΡΠ½ΡΠΌΠΈ ΠΈ ΠΊΠΎΠ»ΡΠΌΠ½Π°ΡΠ½ΡΠΌΠΈ Π½Π°ΠΊΠ»ΠΎΠ½Π½ΡΠΌΠΈ Π΄Π΅ΡΠ΅ΠΊΡΠ°ΠΌΠΈ. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ Π² ΡΠ»ΡΡΠ°Π΅ ΠΊΠΎΠ»ΡΠΌΠ½Π°ΡΠ½ΡΡ
Π½Π°ΠΊΠ»ΠΎΠ½Π½ΡΡ
Π΄Π΅ΡΠ΅ΠΊΡΠΎΠ² Π·Π°Π²ΠΈΡΠΈΠΌΠΎΡΡΡ ΠΊΡΠΈΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΡΠΎΠΊΠ° ΠΎΡ Π°Π½ΠΈΠ·ΠΎΡΡΠΎΠΏΠΈΠΈ ΠΎΡΠ»Π°Π±Π΅Π²Π°Π΅Ρ Ρ ΡΠΎΡΡΠΎΠΌ ΠΈ ΠΏΡΠΈ ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½Π½ΠΎΠΌ ΠΈΡΡΠ΅Π·Π°Π΅Ρ ΡΠΎΠ²ΡΠ΅ΠΌ. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ Π½Π°Π»ΠΈΡΠΈΠ΅ S-ΠΎΠ±ΡΠ°Π·Π½ΠΎΠΉ Π½Π΅Π»ΠΈΠ½Π΅ΠΉΠ½ΠΎΡΡΠΈ Π²ΠΎΠ»ΡΡ-Π°ΠΌΠΏΠ΅ΡΠ½ΠΎΠΉ Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΡΡΠΈΠΊΠΈ Π΄Π»Ρ ΡΡΠ΅Ρ
ΠΌΠ΅ΡΠ½ΠΎΠΉ Π²ΠΈΡ
ΡΠ΅Π²ΠΎΠΉ ΡΠΈΡΡΠ΅ΠΌΡ Ρ ΡΠ΅ΡΡΠΎΠΌΠ°Π³Π½ΠΈΡΠ½ΡΠΌΠΈ Π΄Π΅ΡΠ΅ΠΊΡΠ°ΠΌΠΈ
Strong reflection of a series of pulses from a four-wave mirror with thermal nonlinearity under parametric feedback conditions
Recommended from our members
Vepafestinib is a pharmacologically advanced RET-selective inhibitor with high CNS penetration and inhibitory activity against RET solvent front mutations
Acknowledgements: This work was supported by funding from Helsinn Healthcare (to R.S. and M.L.) and grants from the National Institutes of Health to E.d.S. (U54 D020355) and the MSKCC (Cancer Center Support grant P30 CA008748 and Summer Research Experiences Supervised by Faculty Mentors grant 5R25CA020449).Funder: Helsinn Healthcare, SARET receptor tyrosine kinase is activated in various cancers (lung, thyroid, colon and pancreatic, among others) through oncogenic fusions or gain-of-function single-nucleotide variants. Small-molecule RET kinase inhibitors became standard-of-care therapy for advanced malignancies driven by RET. The therapeutic benefit of RET inhibitors is limited, however, by acquired mutations in the drug target as well as brain metastasis, presumably due to inadequate brain penetration. Here, we perform preclinical characterization of vepafestinib (TAS0953/HM06), a next-generation RET inhibitor with a unique binding mode. We demonstrate that vepafestinib has best-in-class selectivity against RET, while exerting activity against commonly reported on-target resistance mutations (variants in RETL730, RETV804 and RETG810), and shows superior pharmacokinetic properties in the brain when compared to currently approved RET drugs. We further show that these properties translate into improved tumor control in an intracranial model of RET-driven cancer. Our results underscore the clinical potential of vepafestinib in treating RET-driven cancers
Recommended from our members
Vepafestinib is a pharmacologically advanced RET-selective inhibitor with high CNS penetration and inhibitory activity against RET solvent front mutations.
RET receptor tyrosine kinase is activated in various cancers (lung, thyroid, colon and pancreatic, among others) through oncogenic fusions or gain-of-function single-nucleotide variants. Small-molecule RET kinase inhibitors became standard-of-care therapy for advanced malignancies driven by RET. The therapeutic benefit of RET inhibitors is limited, however, by acquired mutations in the drug target as well as brain metastasis, presumably due to inadequate brain penetration. Here, we perform preclinical characterization of vepafestinib (TAS0953/HM06), a next-generation RET inhibitor with a unique binding mode. We demonstrate that vepafestinib has best-in-class selectivity against RET, while exerting activity against commonly reported on-target resistance mutations (variants in RETL730, RETV804 and RETG810), and shows superior pharmacokinetic properties in the brain when compared to currently approved RET drugs. We further show that these properties translate into improved tumor control in an intracranial model of RET-driven cancer. Our results underscore the clinical potential of vepafestinib in treating RET-driven cancers
Recommended from our members
Vepafestinib is a pharmacologically advanced RET-selective inhibitor with high CNS penetration and inhibitory activity against RET solvent front mutations
Acknowledgements: This work was supported by funding from Helsinn Healthcare (to R.S. and M.L.) and grants from the National Institutes of Health to E.d.S. (U54 D020355) and the MSKCC (Cancer Center Support grant P30 CA008748 and Summer Research Experiences Supervised by Faculty Mentors grant 5R25CA020449).Funder: Helsinn Healthcare, SARET receptor tyrosine kinase is activated in various cancers (lung, thyroid, colon and pancreatic, among others) through oncogenic fusions or gain-of-function single-nucleotide variants. Small-molecule RET kinase inhibitors became standard-of-care therapy for advanced malignancies driven by RET. The therapeutic benefit of RET inhibitors is limited, however, by acquired mutations in the drug target as well as brain metastasis, presumably due to inadequate brain penetration. Here, we perform preclinical characterization of vepafestinib (TAS0953/HM06), a next-generation RET inhibitor with a unique binding mode. We demonstrate that vepafestinib has best-in-class selectivity against RET, while exerting activity against commonly reported on-target resistance mutations (variants in RETL730, RETV804 and RETG810), and shows superior pharmacokinetic properties in the brain when compared to currently approved RET drugs. We further show that these properties translate into improved tumor control in an intracranial model of RET-driven cancer. Our results underscore the clinical potential of vepafestinib in treating RET-driven cancers