Crucial transitions in cancer-including tumor initiation, local expansion, metastasis, and therapeutic resistance-involve complex interactions between cells within the dynamic tumor ecosystem. Transformative single-cell genomics technologies and spatial multiplex in situ methods now provide an opportunity to interrogate this complexity at unprecedented resolution. The Human Tumor Atlas Network (HTAN), part of the National Cancer Institute (NCI) Cancer Moonshot Initiative, will establish a clinical, experimental, computational, and organizational framework to generate informative and accessible three-dimensional atlases of cancer transitions for a diverse set of tumor types. This effort complements both ongoing efforts to map healthy organs and previous largescale cancer genomics approaches focused on bulk sequencing at a single point in time. Generating single-cell, multiparametric, longitudinal atlases and integrating them with clinical outcomes should help identify novel predictive biomarkers and features as well as therapeutically relevant cell types, cell states, and cellular interactions across transitions. The resulting tumor atlases should have a profound impact on our understanding of cancer biology and have the potential to improve cancer detection, prevention, and therapeutic discovery for better precision-medicine treatments of cancer patients and those at risk for cancer.Cancer forms and progresses through a series of critical transitions-from pre-malignant to malignant states, from locally contained to metastatic disease, and from treatment-responsive to treatment-resistant tumors (Figure 1). Although specifics differ across tumor types and patients, all transitions involve complex dynamic interactions between diverse pre-malignant, malignant, and non-malignant cells (e.g., stroma cells and immune cells), often organized in specific patterns within the tumor
1829 patients underwent radical prostatectomy with pelvic lymph node dissection (RP+PLND) (241 high-risk, 943 intermediate-risk, 645 low-risk). Positive margin rates were 17.8%, 14.8%, and 11.9% in the high, intermediate-and lowrisk groups. Five-year overall survival was 92.5% in lymph node-positive patients and 94.9% in lymph node-negative patients (p = 0.8). Age, prebiopsy prostatespecific antigen, and clinical stage were associated with positive surgical margins in patients with lymph node metastasis (LNM). Recipients of RP+PLND with LNM and positive surgical margins required adjuvant treatment.
Background: Low dietary intakes and low plasma concentrations of lutein and zeaxanthin are associated with an increased risk of agerelated macular degeneration (AMD). No studies have challenged AMD patients with a diet high in lutein and zeaxanthin. Objective: The objective was to examine the effect of diets low or high in lutein and zeaxanthin on plasma carotenoids and their transport in AMD patients. Design: Seven AMD patients and 5 control subjects were fed a low-lutein, low-zeaxanthin diet (Ȃ1.1 mg/d) for 2 wk, which was followed by a high-lutein, high-zeaxanthin diet (Ȃ11 mg/d) for 4 wk. Ten subjects continued the diet for 8 wk. Plasma and lipoprotein carotenoids were measured by HPLC. Results: The high-lutein, high-zeaxanthin diet resulted in 2-to 3-fold increases in plasma concentrations of lutein and zeaxanthin and other carotenoids, except lycopene, in the AMD patients and the control subjects. With this diet, 52% of the lutein and 44% of the zeaxanthin were transported by HDL; Ȃ22% of lutein and zeaxanthin was transported by LDL. Only 20 -25% of ␣-carotene, -carotene, and lycopene was transported by HDL; 50 -57% was transported by LDL. Conclusions:The AMD patients and control subjects responded similarly to a diet high in lutein and zeaxanthin; plasma carotenoid concentrations increased greatly in both groups, and the transport of carotenoids by lipoproteins was not significantly different between the groups. This finding suggests that abnormalities in the metabolism of lutein and zeaxanthin in AMD may reside in the uptake of lutein and zeaxanthin from the plasma and transport into the retina.Am J Clin Nutr 2007;85:762-9.
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