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Fig 2. Steady state plasma concentration of perifosine at weeks 2, 3, and 4.
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Fig 8. Model for 6-ETI’s mechanism of action.
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Fig 1. VEOX decreased DNA methylation and induced reexpression of TSGs in tumor cells.
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Fig 2. The Siewert–Stein classification of gastroesophageal region cancers.
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Fig 1. Infectious and noninfectious pulmonary complications of hematopoietic cell transplantation.
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Fig 3. ASXL2 target genes overlap with those of RUNX1 and AML1-ETO.
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Fig 3. Therapeutic T cell design: goals and strategies.
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Fig 1. BRD4 Silencing Enhances Autophagic Flux.
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Fig 1. Physical characterization of the surface-converting nanoparticles.
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Fig 2. ChIP-Seq Experiments Reveal Distinct but Overlapping Patterns of H3K27 Acetylation on Asynchronous and Mitotic ESCs.
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Fig 1. Best response of target lesions (RECIST 1.1) in all patients with a radiographic assessment of response.
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Fig 1. Expression of a deconjugation-resistant NEDD8 mutant (L73P) stabilizes neddylation of cullins and other non-cullin substrates.
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Fig 1. Current strategies of gut microbiota modulation.
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Fig 1. Risk stratification for small nodules.
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Fig 3. Deuteration profile of myrMA at pH 7.4 (left) and pH 8.0 (right) after 30 min of incubation in D2O.
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Fig 3. The figure in Adobe Illustrator after expanding via Image Trace.
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Fig 6. Administration of a Four-Bacteria Consortium Clears VRE from Densely Colonized Mice.
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Fig 2. Relative precision of a domain score by number of items.
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Fig 2. Representative slices of the proton therapy plan for the patient with a mean liver dose of 22 Gy and with 1,100 cm3 of the liver receiving <25 Gy.
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Fig 2. Onset of diagnosis of neurologic morbidity compared with onset of subsequent meningiomas among childhood cancer survivors exposed to cranial radiation.
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Fig 2. Requirement of RNA splicing factor mutations in disease initiation vs maintenance.
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Fig 5. Frequencies of CD8+, CD4+, and TAM Clusters for Each ccRCC Sample.
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Fig 1. Examples of challenging diagnostic features of oncocytic renal cell neoplasms.
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Fig 1. The EML4–ALK rearrangement and downstream signaling.
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Fig 3. Top alignments to full-length L1 loci from HEK293 cells.
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Fig 4. Model for proposed mechanism of nanoprobe translocation to the nucleus.
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Fig 1. High-level comparison of target enrichment workflow for amplicon and capture hybridization NGS assays.
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Fig 1. Convergent Extension of the Ventral Nerve Cord.
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Fig 1. Algorithm for detection of mismatch repair deficiency in colorectal cancer.
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Fig 2. Immune checkpoint inhibitors: releasing the brakes on the immune system. MHC, major histocompatibility complex; PD-1, programmed death 1; PD-L1, programmed death ligand-1; TCR, T-cell receptor.
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Fig 6. Interphase fluorescent in situ hybridization detection of NTRK3 gene rearrangement.
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Fig 1. Structure of chimeric antigen receptors (CAR).
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Fig 4. Model for proposed mechanism of nanoprobe translocation to the nucleus.
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Fig 2. MAVS signaling in nonhematopoietic cells maintains intestinal barrier function.
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Fig 5. (A) Anion exchange chromatography profile of induced culture supernatant on a HiTrap Q Sepharose XL column. Elution was done in a linear gradient from 0 to 190 mM NaCl using 20 mM Tris-Cl/1 M NaCl pH 8. (B) Silver-stained SDS-PAGE shows fractions 1–12 (numbered lanes).
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Fig 4. IFT54 co-localizes with microtubular structures during cell division.
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Fig 1. Characterization of the SN-38-loaded unmodified and antibody-modified NPs, as determined by DLS and HR-SEM.
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Fig 5. Gene expression changes in Tailor and Dis3L2 single and double mutants.
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Fig 3. A 70‐year‐old patient with metastatic breast cancer who developed an asymptomatic atypical femoral fracture (AFF) following classic prodromal symptoms and who also developed an atypical stress reaction on the contralateral femur.
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Fig 2. Consensus somatic SVs and CNVs.
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Fig 2. Actual and intended use of screening in BSD users.
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Fig 8. Model summarizing the trafficking defects in Mks1krc/krc mutants as well as double mutants with Bbs and Ift.
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Fig 9. Resected scapula after tumor recurred, cut in the coronal plane.
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Fig 1. Characterization of mutations, copy number, clinical data, and survival in HSTL cases.
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Fig 10. Patient induced susceptibility distortions in the MRCAT source MR images.
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Fig 2. Differences in response assessment depending on the number of lesions analyzed.
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Fig 1. PLB labeling schemes.
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Fig 3. Kaplan-Meier analysis comparing overall survival in patients treated with upfront stereotactic radiosurgery (SRS), upfront whole-brain radiotherapy (WBRT), and upfront epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI), stratified by disease specific Graded Prognostic Assessment (GPA).
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Fig 1. The four basic morphologic features to diagnose tumors of follicular cell derivation: (i) papillary growth pattern; (ii) follicular growth pattern; (iii) presence of a tumor capsule and of its invasion, in the form of capsular or vascular invasion; (iv) alterations of nuclear morphology typical of papillary carcinoma.
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Fig 2. BCAP is expressed within BM HSPCs.
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Fig 1. The stepwise activation of ERK signaling results in the transcriptional activation of genes responsible for cell-cycle progression and feedback regulation.
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Fig 1. Venetoclax induces response in several non-Hodgkin lymphoma histologies.
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Fig 5. PD-1 expression among case and control patients displayed as heatmap.
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Fig 6. Vhl and Pbrm1 Doubly Deficient Clear Cell Kidney Tumors Display Hyperactive mTORC1 Signaling.
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Fig 1. TIRR is a novel partner of 53BP1.
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Fig 2. Heat map showing hierarchical clustering analysis of the gene expression profiles of the ClearCode34 genes in metastatic renal cell carcinoma TCGA tumors (n = 54).
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Fig 2. SmD2 and SmD1 structures and contacts with U4 snRNA.
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Fig 1. Intestinal damage and dysbiosis linked to GVHD.
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Fig 1. Histologic image of a hairy cell.
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Fig 2. PTEN expression in primary OCCCs.
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Fig 3. ProteoModlR computes exact and approximate abundance and PTM stoichiometry based on the available set of peptides for a given protein.
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