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Figure S1. AAUC distribution by D100 post HCT.
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Fig 1. (a) 2D PLE maps of unsorted and (6,5)-enriched SWCNT materials dispersed in aqueous SC solution. (b) Corresponding optical absorption spectra.
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Fig. 2. Fold changes from baseline to 12 hr post-plerixafor in white blood cells (WBC) and cell activation markers in the two patients mobilized at 320 μg/kg.
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Fig. 4: Transcriptional landscape that underlies coordinated diversification of epithelial lineages and stem cell induction in the developing hair follicle.
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Fig 2. Proportion of patients who received a sarcoma care at academic/research center, comprehensive community cancer center, community cancer center, and other institutions, according to the travel distance.
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Fig. 2: Dose escalation and dose expansion carried out concurrently prior to determination of the maximum-tolerated dose (MTD).
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Fig. 3: Relative ALT-associated telomere focus size based on ATRX or SMARCAL1 status.
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Figure 1. Gender, Race, and Ethnicity in Cancer Leadership.
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Fig 2. Detection of tumor-derived mutations in plasma by cf-IMPACT as a function of cfDNA tumor fraction.
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Fig 2. Genome-wide LOH in TCGA-BLCA dataset and tumor tissue samples.
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Fig 1. Selected CAR T cell constructs currently in use or in development.
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Graphical abstract
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Fig 4. Resistance to lorlatinib with a ROS1 L2086F mutation and subsequent treatment with cabozantinib.
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Fig 1. Bispecific antibody platform has profound effects on the antitumor activity of bispecific antibody armed T cell immunotherapy. (A) BsAb structural platform.
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Figure 2. Lifetime Number of Colonoscopies and Life-Years Gained for a Cohort of 40-Year-Olds for Colonoscopy Screening Strategies.
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Fig. 6: Cancer site specific odds ratios of most effective individual predictors in the hidden genome model applied to the PCAWG whole genome data.
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Figure 5. Proposed mechanism of increased CCND1 presentation after CDK4/6i treatment.
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Figure 4: Common network visualization.
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Fig 2. Fig. 2: Melphalan mutational signatures.
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Fig 3. Clinical and pathological associations of breast cancer mutation profile.
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Fig 2. Activity of the eIF4A inhibitor [±]CR-1–31B against PDAC cells and organoids.
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Fig. 1. The autoantigenome from A549 cells identified by DS-affinity.
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Graphical Abstract.
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Figure 1. Radiation treatment plan with isodose lines for a prescribed dose of 24 Gy in 1 fraction delivered to the L2 and L3 vertebral bodies.
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Fig. 3. Cryo-EM structure of the Nse5/Nse6 complex.
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Fig. 3: Repertoire of non-synonymous somatic mutations identified in metaplastic breast cancers.
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Figure 1 Transcriptomic similarities across carcinomas with mucinous differentiation from different cancer types.
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Fig 2. Reflectance confocal microscopy features seen across time in the study patients.
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Figure 3: Germline and somatic causes of neurodegeneration.
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Fig. 1 RIF1 controls RT by reducing cell-to-cell variation in replication timing.
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Figure 1: Mouse NK cell development and maturation.
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Fig 1. Terminal elongation-defective phenotypes for TS-EL mutants after L4 and late upshifts.
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Fig 2. Mutational signature landscape in first responders and recovery workers exposed to the WTC disaster.
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Fig 1. Waterfall plots of best response to entrectinib in patients with ROS proto-oncogene 1 (ROS1) fusion–positive lung cancers, shown as the maximum percent improvement in the sum of longest diameters of identified target lesions compared with baseline, as assessed by BICR.
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Figure 1 Dose‐normalized plasma galunisertib concentrations at steady state (following treatment on day 14) with monotherapy (Part A) and combination with ramucirumab (Part D).
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Fig. 2: Common primary cancers metastasizing to the liver.
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QSER1 safeguards DNA methylation valleys from de novo methylation.
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Figure 1. SNPs in high LD of the index SNP (rs35418111) in Asians (rs8134832, rs57385578, rs8126917, and rs2078203) and Europeans (rs57385578) were prioritized using HaploReg v4.1 annotation.
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Figure 2. Subgroup analysis of 90-day mortality and survival after ICU admission
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Fig. 2: Best RECIST response, PTEN, and broader mutation profiling in patients with PTEN-mutant ER+ MBC treated with capivasertib and fulvestrant.
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Fig 1. KRAS mutation subtypes and baseline pathologic and molecular characteristics.
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Graphical abstract.
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Fig 1. Burnout versus burnout syndrome. High risk for burnout is classified as reaching threshold levels of either emotional exhaustion and/or depersonalization
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Graphical Abstract.
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Fig. 1. Arsenic usage and temporal association with herpes zoster infection.
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Graphical abstract.
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Figure 1. Estimated probabilities of developing metastatic disease (A) and prostate cancer specific survival (B) after definitive treatment of localized prostate cancer stratified by MRI category.
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Fig. 2. Representative examples.
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Fig 1. Progression-free and Overall Survival in the Intention-to-Treat Population.
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Figure 5. Genome wide changes in H3K27me3 parallel changes identified at the HoxA9 locus.
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FIGURE 2: Landscape of solid tumor CAR trials.
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Fig. 1 a Distribution of factors for not recommending cytoreductive nephrectomy.
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Fig. 2 Photomicrographs for which participants were asked to provide PNI ratings.
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Fig. 1: Mutational profiles and copy number alterations of cervical mesonephric carcinomas and mesonephric-like carcinomas of the ovary and endometrium.
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Figure 1. Timeline of the strategic mitigation planning for the management of patients during the COVID-19 pandemic, and data on the Cumulative incidence of COVID-19 positivity in MSK pediatric patients, MSK caregivers, and the pediatric population in NYC.
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Figure 2. Human and mouse memory NK cell traits.
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Fig 2. Penicillin Allergy Testing Procedure
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Fig 1. Smart-ORF cell-free system for imaging both uORF and mORF translation on single mRNA molecules.
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Fig 1. Information needed to determine harms of overused services.
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Fig. 1. Distribution of Added Path Length (APL) across volumes of interest, as represented by kernel density plots.
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Figure 5. Downstream effectors of human airway basal cell EV–mediated survival of HUVECs.
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Graphical Abstract
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Figure 2. Adjusted total reimbursements within 1 year of undergoing allo-HCT for patients with and without virus-associated HC, stratified by GVHD.
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Figure 3: Blood counts (cells/μl) of CD27+ IgD− memory B cells (A) and CD16hi NK cells (B) in patients, stratified by relapse and maraviroc treatment.
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![Fig 2. Activity of the eIF4A inhibitor [±]CR-1–31B against PDAC cells and organoids.](https://library.mskcc.org/sparks/sparksimgs/5053/Singh2021.jpg)
