tbuckley/cabot-search huggingface dataset:
Tumor shrinkage and increased overall survival are associated with improved albumin, neutrophil lymphocyte ratio (NLR) and decreased durvalumab clearance in NSCLC and UC patients receiving durvalumab.
Authors: Thomas Powles, Chaoyu Jin, Yanan Zheng, Paul Baverel, Rajesh Narwal, Pralay Mukhopadhyay, Xiaoping Jin, Phillip A. Dennis, Ashok Kumar Gupta, Yong Ben, Tony W. Ho, Lorin Roskos
Journal: Journal of Clinical Oncology (2017)

3035 Background: Progression of cancer is often associated with biomarkers of cancer inflammation, cachexia, and increased protein catabolism. Anti-PD1 and PD-L1 therapy have demonstrated durable responses across a number of tumor types. Durvalumab is a human monoclonal antibody that binds to PD-L1 and blocks its interaction with PD-1 and CD80. The primary objective of this analysis was to prospectively assess potential correlations of longitudinal changes in ALB and NLR and durvalumab clearance (CL) rate to maximum decrease in tumor size and overall survival (OS) in patients (pts) with NSCLC and UC receiving durvalumab. Methods: Longitudinal target lesion size, serum chemistry, hematology and pharmacokinetic data were obtained from 3L+ NSCLC pts (n = 418) in study ATLANTIC and 2L+ UC pts (n = 182) in study 1108 during durvalumab treatment. Nonparametric correlations (Spearman’s rho) were evaluated between OS, maximum percent change in target lesion size, and the maximum percent change from baseline observed in ALB, NLR, and CL. Results: In NSCLC, maximum decrease in tumor size was correlated with increased ALB (r = 0.46, p &lt; 0.0001), decreased NLR (r = 0.44, p &lt; 0.0001), and decreased CL (r = 0.66, p &lt; 0.0001). OS was similarly correlated with increased ALB (r = 0.47, p &lt; 0.0001), decreased NLR (r = 0.41, p &lt; 0.0001), and decreased CL (r = 0.76, p &lt; 0.0001). In UC, decreased tumor size also correlated with increased ALB (r = 0.43, p &lt; 0.0001), decreased NLR (r = 0.38, p &lt; 0.0001), and decreased CL (r = 0.65, p &lt; 0.0001). OS in UC also correlated with increased ALB (r = 0.50, p &lt; 0.0001), decreased NLR (r = 0.33, p &lt; 0.0001) and decreased CL (r = 0.82, p &lt; 0.0001). Conclusions: In NSCLC and UC pts receiving durvalumab, tumor shrinkage and longer survival are associated with increased ALB, decreased NLR and decreased clearance of durvalumab. These findings support the hypothesis that durvalumab may be associated with a decrease in protein catabolism, inflammation and cachexia among pts who benefited from therapy. Additional biomarkers of cancer, inflammation and cachexia will be evaluated for relationships to clinical outcomes.
Albert Ludwig Sigesmund Neisser, MD—A Life of Discovery and Controversy in Dermatology
Authors: Kishore L. Jayakumar, Jules B. Lipoff
Journal: JAMA Dermatology (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Dermatology HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Dermatology journal
Lung Adenocarcinoma Harboring EGFR T790M and In Trans C797S Responds to Combination Therapy of First- and Third-Generation EGFR TKIs and Shifts Allelic Configuration at Resistance
Authors: Zhen Wang, Jin-Ji Yang, Jie Huang, Jun-Yi Ye, Xu-Chao Zhang, Hai-Yan Tu, Han Han-Zhang, Yi-Long Wu
Journal: Journal of Thoracic Oncology (2017)
Comparison of different sequences of combination chemotherapy and bevacizumab in patients with mKRAS colorectal cancer who received 2 lines of therapy: Results of population register of 14 regions of Russia
Authors: Mikhail Fedyanin, Alexey Tryakin, Shamai Aliyeva, Liubov Vladimirova, Sanal Erdniev, Alexander Ivanov, Alexey Katkov, Valeriy Kulik, Evgeniya Kuzmina, Elena Matyushina, Larisa Nikitina, Rashida Orlova, Anton Povyshev, Eduard Pshevlotskiy, Madina Ramazanova, Olga Shalofast, Elena Smirnova, Alexandra Tkachuk, Natalya Ulanova, Sergei Tjulandin
Journal: Annals of Oncology (2017)
Abstract 47: Loss of the Cardio Protection Inferred by S-nitrosylation of GRK2 At Cysteine 340 Leads to Decreased Cardiac Performance and a Hypertensive Phenotype With Aging
Authors: Christopher J Traynham, Ancai Yuan, Erhe Gao, Walter Koch
Journal: Circulation Research (2015)

In the next 35 years, the global population of individuals above 60 years of age will double to approximately 2 billion. In the aged population, cardiovascular diseases are known to occur at a higher prevalence ultimately leading to increased mortality. G protein-coupled receptors (GPCRs) have been identified as vital regulators of cardiac function. GPCR kinases (GRKs) are important in cardiac GPCR regulation through desensitization of these receptors. GRK2 is highly expressed in the heart, and has been widely characterized due to its upregulation in heart failure. Studies from our lab have shown that elevated GRK2 levels in ischemia-reperfusion (I/R) injury result in a pro-death phenotype. Interestingly, cardio-protection can be inferred via S-nitrosylation of GRK2 at cysteine 340. Further, we have generated a knock-in GRK2 340S mouse, in which cysteine 340 was mutated to block dynamic GRK2 S-nitrosylation. GRK2 340S mice are more susceptible to I/R injury. Given that GRK2 340S mice are more susceptible to oxidative stress, and there is a nitroso-redox imbalance in senescence, it is possible that these mice are more likely to exhibit decreased cardiac performance as they age. Therefore, we hypothesize that with age GRK2 340S knockin mice will develop an overall worsened cardiac phenotype compared to control wild-type (WT) mice. To test this hypothesis, 340S and WT mice were aged for a year, and cardiac function was evaluated via echocardiography. Aged 340S mice exhibited significantly decreased ejection fraction and fraction shortening relative to aged WT controls. Prior to tissue harvesting, in-vivo hemodynamics was conducted via Millar catheterization. At baseline, aged 340S mice exhibited increased systolic blood pressure compared to aged WT mice. At the conclusion of this protocol, mice were sacrificed and heart weight (HW), body weight (BW), and tibia length (TL) measured to evaluate cardiac hypertrophy. Aged 340S mice exhibited significantly increased HW/BW and HW/TL ratios, indicative of cardiac hypertrophy, relative to aged WT controls. Taken together, these data suggest that with age, loss of the cardio protection inferred by S-nitrosylation of GRK2 at leads to decreased cardiac performance, and an overall worsened cardiac phenotype.
Sensitive assay of tumor S-adenosyl-methionine and S-adenosyl-homocysteine
Authors: Shukuan Li, Zhijian Yang, Xinghua Sun, Xiao-Ming Li, Mingxu Xu, Huaiyu Ma, Yuying Tan, Shigeo Yagi, Robert M. Hoffman
Journal: Cancer Research (2005)

2370  Many human cancers, both cell lines and patient tumors, have been shown to have an increased requirement for methionine in order to proliferate. This increased requirement for methionine in tumors has been termed methionine dependence. Under conditions of methionine depletion, such as substitution of homocysteine for methionine in the culture medium, cancer cells selectively decrease their amount of S-adenosyl-methionine (SAM) to a much greater extent than normal cells. The bacterial protein, methioninase, has been developed to target the methionine dependence of cancer cells in vivo. We report here a sensitive assay for SAM as well as S-adenosyl-homocysteine (SAH) in order to determine the extent of SAM and SAH depletion by methioninase in tumor tissue. This method is based on high-performance liquid chromatography (HPLC) using a C18 reversed-phase column, step gradient elution and ultraviolet detection for the simultaneous determination of SAM and SAH in tumor tissues. This improved method can detect as little as 1.25 pmol/μl SAH and 2.5 pmol/μl SAM. The assay was validated over a linear range of 1.25-40 pmol/μl for SAH and 2.5-40 pmol/μl for SAM. Applying the method, we determined the level of SAM and SAH over 10 days in the H460 human lung tumor xenograft, a methionine-dependent tumor. The results demonstrated that in H460, SAM and SAH, over a 10 day period, were maintained at a relatively stable level. SAM levels were 55.7 + 6.5 nmol/gram wet tumor tissue. SAH levels were 7.5 + 0.4 nmol/gram wet tumor tissue. The high levels of SAM in the H460 xenograft may in part explain methionine-dependent growth.
Transcriptomic analysis of purified human cortical microglia reveals age-associated changes
Authors: Thais F Galatro, Inge R Holtman, Antonio M Lerario, Ilia D Vainchtein, Nieske Brouwer, Paula R Sola, Mariana M Veras, Tulio F Pereira, Renata E P Leite, Thomas Möller, Paul D Wes, Mari C Sogayar, Jon D Laman, Wilfred den Dunnen, Carlos A Pasqualucci, Sueli M Oba-Shinjo, Erik W G M Boddeke, Suely K N Marie, Bart J L Eggen
Journal: Nature Neuroscience (2017)
Diagnostic value of plasma and urinary 2-hydroxyglutarate to identify patients with IDH-mutated glioma.
Authors: Giuseppe Lombardi, Giuseppe Corona, Patrizia Farina, Ardi Pambuku, Luisa Bellu, Alessandro Della Puppa, Pasquale Fiduccia, Roberta Bertorelle, Marina Paola Gardiman, Giuseppe Toffoli, Vittorina Zagonel
Journal: Journal of Clinical Oncology (2014)

2037 Background: Mutation of IDH1 gene is a prognostic factor and a diagnostic hallmark of gliomas. Mutant IDH1 enzyme can convert α-KG into 2-Hydroxyglutarate(2HG); mutated gliomas have elevated amounts of intracellular 2HG. We analyzed 2HG concentration in plasma and urine in glioma patients(PTS) to identify a biomarker of IDH1 gene mutation Methods: All PTS had a prior histological confirmation of glioma, a recent brain MRI (within 2 weeks) showing the neoplastic lesions. The exclusion criteria were any chemotherapy performed within 28 days prior, other neoplastic and metabolic diseases. Plasma and urine samples were taken from all PTS and 2HG concentrations determined by liquid chromatography tandem mass spectrometry; Mann-Whitney test was used to test for differences in metabolite concentrations. ROC curve was used to evaluate the cut off value of 2HG biomarker. Results: 84 PTS were enrolled: 38 with IDH1 mutated and 46 IDH1 wild-type. Among PTS with mutant IDH1 we had 21 high-grade gliomas (HGG) and 17 low-grade gliomas (LGG); among PTS with IDH1 wild-type we had 35 HGG and 11 LGG. In all PTS we analyzed the mean 2HG concentration in plasma (P_2HG), in urine (U_2HG) and the ratio between P_2HG and U_2HG (R_2HG). The results are shown in Table. We found an important significant difference in R_2HG between PTS with and without IDH1 mutation. The optimal cut-off value of R_2HG to identify glioma PTS with and without IDH1 mutation was 19 with sensitivity (S) 63%, specificity (SP) 76% and accuracy (A) 70%.; in only PTS with HGG the optimal cut-off value was 20 (S 76%, SP 89%, A 84%, PPV 80%, NPV 86%). No association between the grade or size of tumor and R_2HG were found. In 7 out of 7 HGG PTS, we found a correlation between R_2HG value and response to treatment. Conclusions: By analyzing the R_2HG derived from individual plasma and urine 2HG levels is possible discriminate glioma PTS with and without IDH1 mutation. A larger samples need to be analyzed to investigate this method to monitor treatment efficacy. IDH1 wt IDH1 mut P P_2HG (ng/mL) 97.0 97.2 0.9 U_2HG(mg/mg)* 7.3 4.6 0.002 R_2HG (all gliomas) 15.6 22.2 <0.0001 R_2HG (only HGGs) 15.3 24.9 <0.0001 * Concentration of 2HG (mg/mL) normalized by creatinine concentration (mg/mL).
Diagnostic accuracy and safety of coaxial core-needle biopsy (CNB) system in a predominanty gastrointestinal oncology patient population, treated at the Royal Marsden (RM) Hospital
Authors: Khurum Khan, Reyes González Expósito, David Cunningham, Dow-Mu Koh, Andrew Woolston, Kyriakos Kouvelakis, Monia Bali, James Mccall, Nasir Khan, Ian Chau, Nicola Valeri, Marco Gerlinger, Nicos Fotiadis
Journal: Annals of Oncology (2017)
Abstract 169: Angiotensin-Converting Enzyme 2: Species-Specific Features and Pharmacologic Characterization by RAS Fingerprinting
Authors: Marko Poglitsch, Oliver Domenig, Cornelia Schwager, Hans Loibner, Manfred Schuster
Journal: Circulation Research (2012)

The carboxypeptidase Angiotensin Converting Enzyme 2 (ACE2) is a crucial player of the Renin-Angiotensin-System (RAS) as it balances the ratio between vasoconstrictive and fibrotic Angiotensin II and vasodilative and anti-fibrotic Angiotensin 1-7. This balance is affected by ACE2 either by direct conversion of Angiotensin II to Angiotensin 1-7, or by cleavage of Angiotensin I to Angiotensin 1-9, which is further converted to Ang 1-7 by Angiotensin Converting Enzyme (ACE) or Neutral Endopeptidase (NEP). An increased activity of ACE2 leads to a shift of the RAS towards an Angiotensin 1-7 dominated pattern, which was shown to be protective in various models of cardiovascular and fibrotic diseases. We performed a comparative pharmacologic characterization of recombinant murine and human ACE2 using natural peptide substrates for the evaluation of the substrate specific ACE2 activity in whole blood. Furthermore, we investigated the impact of ACE2 activators and inhibitors on murine and human ACE2 in whole blood using an LC-MS/MS based approach allowing the simultaneous quantification of 10 different angiotensin peptides (RAS-Fingerprinting). The investigation of inhibitors and activators of ACE2 using our experimental setting revealed the presence of species-specific enzymatic features, which was indicated by differences between the human and murine enzyme regarding the susceptibility to pharmacologic manipulation and the specificity for different endogenous peptide substrates. Our studies demonstrate that sequence diversity observed between recombinant human and murine ACE2 significantly affects substrate specificity and pharmacologic enzyme properties. The utilization of Angiotensin I by ACE2 generates Angiotensin 1-7 via Angiotensin 1-9 and represents a pathway of alternative RAS activation, which might have been systematically underestimated in previous studies. The strongly reduced affinity of murine ACE2 for Angiotensin I results in a lack of production of Angiotensin 1-7 via this pathway, which might be of particular importance during anti-hypertensive treatments with ACE inhibitors, where the formation of Angiotensin II is prevented while increased levels of Angiotensin I are observed in circulation.
ILF2 Is a Regulator of RNA Splicing and DNA Damage Response in 1q21-Amplified Multiple Myeloma
Authors: Matteo Marchesini, Yamini Ogoti, Elena Fiorini, Anil Aktas Samur, Luigi Nezi, Marianna D'Anca, Paola Storti, Mehmet Kemal Samur, Irene Ganan-Gomez, Maria Teresa Fulciniti, Nipun Mistry, Shan Jiang, Naran Bao, Valentina Marchica, Antonino Neri, Carlos Bueso-Ramos, Chang-Jiun Wu, Li Zhang, Han Liang, Xinxin Peng, Nicola Giuliani, Giulio Draetta, Karen Clise-Dwyer, Hagop Kantarjian, Nikhil Munshi, Robert Orlowski, Guillermo Garcia-Manero, Ronald A. DePinho, Simona Colla
Journal: Cancer Cell (2017)
Limitations Concerning the Association of Physician Sex and Patient Outcomes
Authors: Filipe Prazeres
Journal: JAMA Internal Medicine (2017)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
Impact of Recurrence and Salvage Surgery on Survival After Multidisciplinary Treatment of Rectal Cancer
Authors: Naruhiko Ikoma, Y. Nancy You, Brian K. Bednarski, Miguel A. Rodriguez-Bigas, Cathy Eng, Prajnan Das, Scott Kopetz, Craig Messick, John M. Skibber, George J. Chang
Journal: Journal of Clinical Oncology (2017)

Purpose After preoperative chemoradiotherapy followed by total mesorectal excision for locally advanced rectal cancer, patients who experience local or systemic relapse of disease may be eligible for curative salvage surgery, but the benefit of this surgery has not been fully investigated. The purpose of this study was to characterize recurrence patterns and investigate the impact of salvage surgery on survival in patients with rectal cancer after receiving multidisciplinary treatment. Patients and Methods Patients with locally advanced (cT3-4 or cN+) rectal cancer who were treated with preoperative chemoradiotherapy followed by total mesorectal excision at our institution during 1993 to 2008 were identified. We examined patterns of recurrence location, time to recurrence, treatment factors, and survival. Results A total of 735 patients were included. Tumors were mostly midrectal to lower rectal cancer, with a median distance from the anal verge of 5.0 cm. The most common recurrence site was the lung followed by the liver. Median time to recurrence was shorter in liver-only recurrence (11.2 months) than in lung-only recurrence (18.2 months) or locoregional-only recurrence (24.7 months; P = .001). Salvage surgery was performed in 57% of patients with single-site recurrence and was associated with longer survival after recurrence in patients with lung-only and liver-only recurrence ( P < .001) but not in those with locoregional-only recurrence ( P = .353). Conclusion We found a predilection for lung recurrence in patients with rectal cancer after multidisciplinary treatment. Salvage surgery was associated with prolonged survival in patients with lung-only and liver-only recurrence, but not in those with locoregional recurrence, which demonstrates a need for careful consideration of the indications for resection.
Phase I trial of sorafenib in combination with interferon-alpha in Japanese patients with unresectable or metastatic renal cell carcinoma
Authors: Y. Sumiyoshi, K. Hashine, M. Niwakawa, R. Yamaguchi, H. Fujii, Y. Hamamoto, K. Fukino
Journal: Journal of Clinical Oncology (2009)

e16107 Background: Sorafenib (SOR) is a multi-kinase inhibitor, targeting Raf kinase and the receptor tyrosine kinases VEGFR-2 and PDGFR-β. Interferon-α (IFN) is most commonly used for metastatic renal cell carcinoma (RCC) in Japan. In this phase I study, we investigated the safety profile, pharmacokinetics (PK), and tumor response of SOR/(recombinant)IFN combination in Japanese patients (pts) with RCC. Methods: After 2 weeks of IFN-alone treatment, a total of 18 pts (6 in each cohort) with unresectable/metastatic RCC received 28-day cycles of continuous SOR 200 (Cohort 1 [C1]) or (Cohorts 2 and 3 [C2 and C3]) 400 mg bid combined with intramuscular IFN 6 (C1 and C2) or 9 (C3) MIU three times a week (tiw). Objectives were safety/tolerability and recommended dose of SOR/IFN as primary, and tumor response and PK as secondary. Results: Pt characteristics were: median 64.5 y.o.; ECOG-PS 0:1, 14:4; prior anticancer therapy in 13 pts. All pts completed Cycle 1 and entered Cycle 2 or later cycles. At data cut-off (September 30, 2008), dose-limiting toxicities were reported in all cohorts, including G3 fatigue, G3 anorexia, and G3 skin disorders. Common drug-related grade 3/4 adverse events (AEs) included fatigue (50%), lipase increased (44%) and neutropenia (39%), all of which were reversible and manageable. AEs resulting in treatment discontinuation in Cycle 2 or later cycles were seen in 5 pts in Cohort 3. One death was reported in C1 at Cycle 18 due to gastrointestinal and intraabdominal hemorrhage. It seemed attributable to DIC accompanied by RCC. Five PR (1 in C1 and 4 in C3) and 11 SD (4 in C1, 5 in C2, and 2 in C3) were achieved as the best response. IFN had no relevant impact on PK of SOR. Conclusions: SOR/IFN combination has promise for clinical benefit in RCC, and its recommended dose was continuous SOR 400 mg bid and IFN 6 MIU tiw. [Table: see text]
Prostate Cancer and Histamine 2 Antagonists
Authors: DAVID C. STOLINSKY
Journal: JNCI Journal of the National Cancer Institute (1991)

Journal Article Prostate Cancer and Histamine 2 Antagonists Get access DAVID C. STOLINSKY DAVID C. STOLINSKY Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 83, Issue 21, 6 November 1991, Page 1589, https://doi.org/10.1093/jnci/83.21.1589 Published: 06 November 1991
Informed Consent and the Disclosure of Clinical Results to Research Participants
Authors: Alessandro Blasimme, Celine Moret, Samia A. Hurst, Effy Vayena
Journal: The American Journal of Bioethics (2017)

The text of the Final Common Rule, promulgated on January 19, 2017, and due to become effective between 2018 and 2020, introduces a number of novelties regarding informed consent. For instance, it ...
Nuclear CD24 Drives Tumor Growth and Is Predictive of Poor Patient Prognosis
Authors: Jason E. Duex, Charles Owens, Ana Chauca-Diaz, Garrett M. Dancik, Lauren A. Vanderlinden, Debashis Ghosh, Mariah Z. Leivo, Donna E. Hansel, Dan Theodorescu
Journal: Cancer Research (2017)

Abstract Elevated tumor expression of the cell surface GPI-linked CD24 protein signals poor patient prognosis in many tumor types. However, some cancer cells selected to be negative for surface CD24 (surCD24−) still retain aggressive phenotypes in vitro and in vivo. Here, we resolve this apparent paradox with the discovery of biologically active, nuclear CD24 (nucCD24) and finding that its levels are unchanged in surCD24− cells. Using the complementary techniques of biochemical cellular fractionation and immunofluorescence, we demonstrate a signal for CD24 in the nucleus in cells from various histologic types of cancer. Nuclear-specific expression of CD24 (NLS-CD24) increased anchorage-independent growth in vitro and tumor formation in vivo. Immunohistochemistry of patient tumor samples revealed the presence of nucCD24, whose signal intensity correlated positively with the presence of metastatic disease. Analysis of gene expression between cells expressing CD24 and NLS-CD24 revealed a unique nucCD24 transcriptional signature. The median score derived from this signature was able to stratify overall survival in four patient datasets from bladder cancer and five patient datasets from colorectal cancer. Patients with high scores (more nucCD24-like) had reduced survival. These findings define a novel and functionally important intracellular location of CD24; they explain why surCD24− cells can remain aggressive, and they highlight the need to consider nucCD24 in both fundamental research and therapeutic development. Cancer Res; 77(18); 4858–67. ©2017 AACR.