tbuckley/cabot-search huggingface dataset:
Coronary Computed Tomography Angiography as the Investigation of Choice for Stable Chest Pain
Authors: James K. Min, David E. Newby
Journal: JAMA Cardiology (2019)

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 Cardiology 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 Cardiology journal
Abstract 1550: Bruteforcing immune oncology discovery with computational immuno-engineering
Authors: Sarah Ives, David Maurer, Christina Pettus, Raymond Newland, Valerie Chiou, Shahrad Daraeikia, Chelsea Jones, Kieran Hervold, Giles Day, Chris Smith, Ian D. Waddell, Sawsan Youssef, Jacob Glanville
Journal: Cancer Research (2019)

Abstract Recent Nobel awards in immune checkpoint inhibitor biology, phage display discovery and protein evolution highlight our current golden age of immune oncology research. While it took 15 years to bring anti-CTLA4 and anti-PD1 therapeutics from conception to global patient populations, new advances in synthetic and data driven immune engineering are enabling new therapeutics to be discovered and engineered in weeks rather than years. Here we review ten years of progress in computational optimization of antibody discovery libraries through the lens of high-throughput data collection technologies, with specific case studies of modern repertoire design principles applied to a panel of immune checkpoint targets. We emphasize the case study of PD1, where a computationally optimized library generated over 6500 unique anti-PD1 antibodies in two weeks, including picomolar binders, mouse/cyno/human triple cross-reactive epitopes, antagonists, agonists, and saturated epitope coverage of the target. Citation Format: Sarah Ives, David Maurer, Christina Pettus, Raymond Newland, Valerie Chiou, Shahrad Daraeikia, Chelsea Jones, Kieran Hervold, Giles Day, Chris Smith, Ian D. Waddell, Sawsan Youssef, Jacob Glanville. Bruteforcing immune oncology discovery with computational immuno-engineering [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1550.
High efficacy of resistance-guided retreatment of HCV patients failing NS5A inhibitors in the real world
Authors: Ana Belén Pérez, Natalia Chueca, Miguel García-Deltoro, Ana María Martínez-Sapiña, María Magdalena Lara-Pérez, Silvia García-Bujalance, Teresa Aldámiz-Echevarría, Francisco Jesús Vera-Méndez, Juan Antonio Pineda, Marta Casado, Juan Manuel Pascasio, Javier Salmerón, Juan Carlos Alados-Arboledas, Antonio Poyato, Francisco Téllez, Antonio Rivero-Juárez, Dolores Merino, María Jesús Vivancos-Gallego, José Miguel Rosales-Zábal, Federico García, María Dolores Ocete, Miguel Ángel Simón, Pilar Rincón, Sergi Reus, Alberto De la Iglesia, Isabel García-Arata, Miguel Jiménez, Fernando Jiménez, José Hernández-Quero, Carlos Galera, Mohamed Omar Balghata, Joaquín Primo, Mar Masiá, Nuria Espinosa, Marcial Delgado, Miguel Ángel von-Wichmann, Antonio Collado, Jesús Santos, Carlos Mínguez, Felícitas Díaz-Flores, Elisa Fernández, Enrique Bernal, José De Juan, José Joaquín Antón, Mónica Vélez, Antonio Aguilera, Daniel Navarro, Juan Ignacio Arenas, Clotilde Fernández, María Dolores Espinosa, María José Ríos, Roberto Alonso, Carmen Hidalgo, Rosario Hernández, María Jesús Téllez, Francisco Javier Rodríguez, Pedro Antequera, Cristina Delgado, Patricia Martín, Javier Crespo, Berta Becerril, Óscar Pérez, Antonio García-Herola, José Montero, Carolina Freyre, Concepción Grau
Journal: Journal of Hepatology (2019)
Abstract 148: Analysis of the tumor microenvironment in seven cancer types by single-cell RNA-seq
Authors: Michael Dean, Guibo Li, Jianhua Jin, Yong Hou, Kui Wu, Shida Zhu, Hanlin Zhou, Ruqian Lv, Feng Lin, Si Liu, Shichen Dong, Lei Wang, Cuijuan Zhang, Yi Zhao
Journal: Cancer Research (2019)

Abstract The tumor microenvironment (TME) is composed of tumor cells, as well as immune and stromal cells. Cancer cells can interact with the tumor microenvironment to suppress anticancer immunity and host inflammatory cells can modulate that immune response to the lesion. To better understand the TME across cancer types we used single-cell RNA-seq analysis of 224,330 cells from 77 patients with breast, gastric, nasopharyngeal carcinoma (NPC), diffuse large B-cell lymphoma (DLBCL), pancreatic, colorectal and lung cancer. The tumor cells and immune cells from individual patients were analyzed simultaneously at the single-cell level to identify distinct cell clusters and subtypes. Comparison of the profile of T cells, macrophages, dendritic cells (DC), B cells, mast cells, granulocytes and cancer-associated fibroblasts (CAFs) identifies unique profiles by tumor type. Breast tumors have high numbers of macrophages, colorectal tumors are elevated for CD4+-T cells, DLBCLs are low in CAFs, gastric cancers have high levels of mast cells, lung tumors high levels of CD4+-T cells and natural killer (NK) T cells, NPC have elevated levels of B cells and DCs and pancreatic cancers high levels of CAFs and granulocytes and low levels of DC and CD8+-T cells. However, within a tumor type, there is also considerable heterogeneity. Understanding how the TME evolves and changes with therapy or predicts response to treatment and survival may provide insight into tumorigenesis and cancer progression. Note: This abstract was not presented at the meeting. Citation Format: Michael Dean, Guibo Li, Jianhua Jin, Yong Hou, Kui Wu, Shida Zhu, Hanlin Zhou, Ruqian Lv, Feng Lin, Si Liu, Shichen Dong, Lei Wang, Cuijuan Zhang, Yi Zhao. Analysis of the tumor microenvironment in seven cancer types by single-cell RNA-seq [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 148.
Abstract 5301: The role of ID4 in regulating SAT1 gene expression in prostate cancer phenotype
Authors: Majid Al-Zahrani
Journal: Cancer Research (2019)

Abstract Introduction: Inhibitor of DNA binding 4 (ID4), a bHLH protein and a transcriptional regulator, is a tumor suppressor gene in prostate cancer. ID4 is expressed in prostate cancer cells (LNCaP), which are androgen sensitive, but epigenetically silenced in a more aggressive DU145 cells. The epigenetic silencing of ID4 is associated with increasing tumor grade and castration resistant prostate cancer (CRPC). ID4 regulates the expression of some other genes such as SAT1, which is a rate limiting enzyme found in the X chromosome involved in the catabolic pathway of polyamine metabolism by catalyzing the N(1)-acetylation of spermidine and spermine. Recently, SAT1 was also shown to mediate histone H3 acetylation suggesting its role in regulating gene expression. Next generation sequencing (NGS) data showed a significant low expression of SAT1 when ID4 is up regulated and vise-versa, which led to a hypothesis that ID4 might regulate the expression of SAT1 gene in prostate cancer cells. Experimental procedures: The NGS (exon sequencing) was performed on prostate cancer cells either over-expressing ID4 (DU145(+)ID4) or cells in which ID4 was genetically silenced (LNCaP(-)ID4). Moreover, immunohistochemistry (IHC) analysis was performed on mice prostates tissues (WT and ID4-/- mice) and DU145(+)ID4 tumor xenografts tissues to analyze SAT1 protein expression in the presence and the absence of ID4. Results: The NGS and IHC data analysis suggested that Spermidine/spermine N(1)-acetyltransferase (SAT1) is up-regulated in cells lacking ID4 such as (LNCaP(-)ID4) but down-regulated in cells which express ID4 (DU145(+)ID4). These results prompted us to investigate the effect of silencing SAT1 on ID4 expression and on cancer phenotype. Conclusion: The expression of ID4 gene in prostate cancer cell lines LNCaP, and DU145(+)ID4 cells showed low expression of SAT1 gene compared with cells lacking ID4 gene as in LNCaP(-)ID4 and DU145 cells. Acknowledgment: These studies were supported by the NIH/NIMHD/P20 Grant #P20MD002285. Citation Format: Majid Al-Zahrani. The role of ID4 in regulating SAT1 gene expression in prostate cancer phenotype [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 5301.
The application of radiotherapy to the pediatric preclinical testing program: Results of a pilot study.
Authors: Christopher E. Pelloski, Rita Kaplon, Mersiha Hadziahmetovic, Kathryn Bondra, Lanchun Lu, James Sommerfeld, Justin Leasure, Ning Li, Mamta Singh, Phuoung Nguyen, Christopher Chronowski, Raushan Kurmasheva, Kelsey McHugh, Nikhil Sebastian, Peter Houghton
Journal: Journal of Clinical Oncology (2012)

9544 Background: The Pediatric Preclinical Testing Program (PPTP) has been successfully utilized to determine the efficacy of novel agents by testing via its mouse-flank in vivo model. We report on the feasibility and biologic outcomes of a pilot study using rhabdomyosarcoma (RMS) xenograft lines treated with radiotherapy (RT) alone and concurrently with the mTOR tyrosine kinase inhibitor, AZD8055, using the PPTP model. Methods: We developed a mouse flank irradiation device for daily delivery of RT in clinically relevant doses (2 Gy per fraction up to 40 Gy).Two RMS xenograft lines of the PPTP, Rh30 (alveolar) and Rh18 (embryonal), were implanted into SCID mice, grown to appropriate volumes and were subjected to fractionated RT. In a second study, daily co-administration of AZD8055 (5-20 mg/Kg, gavage) with RT was performed. Cure rates (durable complete response &gt;12 weeks post-treatment) and RT dose densities (given dose / initial xenograft volume, Gy/cc) were compared between groups. Results: With RT alone at mean dose-densities of 59-60 Gy/cc, cure was achieved in only 4/18 (22%) of the Rh30-bearing mice and 9/12 (75%) of the Rh18-bearing mice (p=0.006). Profiling data revealed higher levels of Fanconi anemia pathway gene expression in Rh30 compared to the more sensitive Rh18. Since recent data showed conditional knockout of mTOR resulted in the loss of FANCD2 gene expression, we postulated that blockade of TORC1/TORC2 with AZD8055 would reduce FANCD2 and increase the RT-sensitivity of Rh30. The addition of AZD8055 to RT resulted in a selective sensitization of the Rh30 line. With a mean RT dose-density of 27 Gy/cc, the cure rate in Rh30-bearing mice improved to 11/15 (73%). For the Rh18 group, the cure rate was 7/15 (46%) at a mean dose density of 44 Gy/cc. Western blot analysis showed the co-administration of AZD8055 abrogated the brisk increase in mTOR signaling and FANCD2 expression after the first several 2 Gy fractions of RT; most strikingly in Rh30. Conclusions: This study demonstrates the feasibility of applying RT to the PPTP model. It recapitulated the expected clinical radiobiology and demonstrated its utility in preclinical testing and the discovery of novel mechanisms of RT resistance in pediatric tumors.
Final results from the phase Ib/II study (PX-171-006) of carfilzomib, lenalidomide, and low-dose dexamethasone (CRd) in patients with relapsed or progressive multiple myeloma.
Authors: Michael Wang, Thomas Martin, William Bensinger, Melissa Alsina, David Samuel DiCapua Siegel, Edward Kavalerchik, Ruben Niesvizky
Journal: Journal of Clinical Oncology (2013)

8529 Background: Carfilzomib (CFZ) is approved in the US as single-agent treatment for patients with multiple myeloma (MM) who have progressed after bortezomib (BTZ) and an IMiD and are refractory to last line of treatment. We previously reported interim data from PX-171-006 (NCT00603447), a Ph 1b/2 study of CRd in relapsed or progressive MM (Wang et al. ASCO 2011). Herein we report final results. Methods: Patients (1–3 prior treatments) received CRd in 28-day (D) cycles—CFZ IV on D1, 2, 8, 9, 15, 16, lenalidomide (LEN) PO D1–21, and dexamethasone (dex) wkly. In phase 1, CFZ (15–27 mg/m 2 ) and LEN (10–25 mg) doses were escalated to determine the maximum tolerated dose (MTD) with a maximum planned dose (MPD) of CFZ 20 mg/m 2 D1, 2 of Cycle 1 and 27 mg/m 2 thereafter, LEN 25 mg/d, and dex 40 mg/wk, followed by phase 2 expansion at MTD/MPD. Endpoints included IMWG overall response rate (ORR), duration of response (DOR), progression-free survival (PFS), and safety. Results: A total of 84 patients were enrolled since June 2008. Overall, prior treatment included BTZ (77%/18% refractory) and LEN (70%/35% refractory); 20% had high-risk cytogenetics/FISH. MTD was not reached in Ph 1, supporting expansion at the MPD (n=52, 23% BTZ refractory and 42% LEN refractory). As of Nov 2012 (median follow-up 24.4 mo): ORR was 69% overall and 76.9% at MPD with very good partial response in 36.9% and 38.5% and stringent complete response in 3.6% and 3.8%, respectively; median DOR was 18.8 (95% CI 9.7–41.5) and 22.1 mo (95% CI 9.5–NE) respectively; median PFS was 11.8 (95% CI 7.6–20.7) and 15.4 mo (95% CI 7.9–NE), respectively. Seven responders at MPD pursued other therapy and were censored for PFS.A median of 8.5 (range 1−46) CFZ cycles were started; 4% required CFZ dose reductions; 15% discontinued CFZ due to adverse events (AEs). Grade 3/4 AEs were generally consistent with earlier studies in advanced MM that used similar doses of single-agent CFZ; grade 3/4 peripheral neuropathy was 1%. Conclusions: CRd was well tolerated, providing robust and durable responses in this pt population where 35% were LEN refractory. This combination is being further evaluated in several ongoing phase 2/3 trials. Clinical trial information: NCT00603447.
ΔNp73 and Δ133p53 in liquid biopsy as early diagnostic markers for colorectal cancer
Authors: J. Rodriguez-Cobos, D. Viñal, C. Poves, M. Fernández-Aceñero, J. Santos-Lopez, P. Carnicero, A. Amor, H. Peinado, R. Barderas, N. Rodríguez-Salas, G. Domínguez
Journal: Annals of Oncology (2019)
Recognizing Risk Factors Associated With Unplanned 30-Day Readmissions in Hematopoietic Cell Transplantation
Authors: Mohamed A. Kharfan-Dabaja, Joseph C. Alvarnas
Journal: JAMA Network Open (2019)

Binod Dhakal, MD, MS; Smith Giri, MD; Adam Levin, MD; Lisa Rein, MS; Timothy S. Fenske, MD; Saurabh Chhabra, MD; Nirav N. Shah, MD; Aniko Szabo, PhD; Anita D’Souza, MD, MS; Marcelo Pasquini, MD, MS; Parameswaran Hari, MD, MS; Mehdi Hamadani, MD
Abstract 3915: YH25248, a selective PI3K delta inhibitor, shows synergistic effect with an anti-PD-L1 antibody
Authors: Jinhwi Park, Ho-Woong Kang, Hyun-Mo Koo, Jongsuk Park, Tae-Wang Kim, Se-Woong Oh, Soongyu Choi
Journal: Cancer Research (2019)

Abstract Phosphatidylinositol 3-kinase (PI3K) plays critical roles in numerous intracellular processes. Of the four known subtypes, PI3Kδ subtype is primarily expressed in immune cells and has been reported to promote B cell differentiation and regulatory T (Treg) cell activation. Treg cell-mediated immunosuppression is thought to be a major resistance mechanism for immune checkpoint inhibitors. We therefore hypothesized that an effective PI3Kδ inhibitor could enhance anti-cancer immunity when combined with immune checkpoint inhibitors. Through recent efforts, we have discovered YH25248, an oral PI3Kδ-specific inhibitor. YH25248 effectively inhibits PI3Kδ (IC50 = 10nM) showing more than 100-fold selectivity over α, β, and γ subtypes, and exhibited favorable kinase selectivity in 463 kinase panels. In cellular experiments, phospho-AKT was effectively blocked (IC50 = 7 nM), with basophil activation, a known PI3Kδ specific signal, was also inhibited. YH25248 reduced the activity of Treg cells (CD4+/CD25+) isolated from the splenocytes of CT26 tumor-bearing mice, while sparing conventional T cells (CD4+/CD25-). When YH25248 was orally administered (10 mg/kg) to mice, drug exposure in plasma was reasonable, with a half-life of 4.3 hours, while once-daily oral administration of YH25248 (10 ~ 60 mg/kg) significantly inhibited tumor growth of CT26 colon carcinomas in mouse. When the immune cells of tumors were analyzed by flow cytometry, the number of Treg cells was reduced, CD8 + T cells increased. In this model, YH25248 (30 mg/kg, QD) showed synergistic efficacy when combined with an anti-PD-L1 antibody (200 μg/mice, 10F.9G2 clone). In other syngeneic models using 4T1 or MC38 cells, YH25248 (30 mg/kg, QD) also exhibited similar synergistic efficacy in combination with the anti-PD-L1 antibody. In conclusion, YH25248 is a potent, selective, oral inhibitor of PI3Kδ that reduces tumor growth in syngeneic mouse tumor models by increasing the ratio of CD8+ to Treg cells. The combination of YH25248 and anti-PD-L1 antibody resulted in substantially greater tumor growth inhibition in several syngeneic models. These data support the promising potential of YH25248 for combination therapy with immune checkpoint inhibitors to increase therapeutic response rates. Citation Format: Jinhwi Park, Ho-Woong Kang, Hyun-Mo Koo, Jongsuk Park, Tae-Wang Kim, Se-Woong Oh, Soongyu Choi. YH25248, a selective PI3K delta inhibitor, shows synergistic effect with an anti-PD-L1 antibody [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 3915.
Management of Chronic Myeloid Leukemia (CML) during Pregnancy Among Patients (pts) Treated with a Tyrosine Kinase Inhibitor (TKI): A Single-Center Experience
Authors: Rita Assi, Hagop M. Kantarjian, Michael J. Keating, Naveen Pemmaraju, Srdan Verstovsek, Guillermo Garcia-Manero, Farhad Ravandi, Gautam Borthakur, Jenny Dahl, Elias J. Jabbour, Jorge E. Cortes
Journal: Blood (2017)
Hypothesis: does adrenalitis caused by immune checkpoint-inhibitors put melanoma patients at an elevated risk for recurrence?
Authors: Igor Alexander Harsch
Journal: Journal for ImmunoTherapy of Cancer (2019)

Primary adrenal failure (Addison's disease) is a rare complication of immune checkpoint inhibitor (ICI) therapy. Untreated – and also sometimes under adequate hydrocortisone replacement therapy – the levels of ACTH (Adrenocorticotropic hormone) and MSH (Melanocyte stimulating hormone) are elevated. This may be a reason for concern in patients with malignant melanoma (MM): Melanocortin receptors bind to ACTH and the different isoforms of MSH. For example, the melanocortin 1 receptor (MC1R) is overexpressed in many human melanoma cells. Since it is also involved in the proliferation of melanoma cells, the elevated levels of ACTH and its proteolytic cleavage product α-MSH typical for primary failure may lead to an activation of the receptor and, thus, put MM patients that suffered from primary adrenal failure after ICI therapy at an elevated risk for recurrence or an unfavorable course of the disease. Novel dual-release hydrocortisone therapy results in lower ACTH (and most probably lower α-MSH) levels due to the more physiological mode of hydrocortisone release. Given that the concern raised in this hypothesis is confirmed in future investigations, patients who suffer from primary adrenal failure after ICI therapy may benefit from a dual-release hydrocortisone replacement regimen.
Negative Minimal Residual Disease Associated with Extended Response to Moxetumomab Pasudotox in Patients with Relapsed/Refractory Hairy Cell Leukemia: Long-Term Follow-up of Bone Marrow Immunohistochemistry Analyses from a Phase 1 Study
Authors: Robert Kreitman, Martin S. Tallman, Tadeusz Robak, Steven Coutre, Shannon Marshall, Jie Yang, Ira Pastan, Nai Shun (Nancy) Yao
Journal: Blood (2017)
Abstract 4390: Dietary soy isoflavone equol promotes breast cancer progression via regulation of protein synthesis initiation
Authors: Ailed M. Cruz-Collazo, Columba De la Parra, Robert Schneider, Suranganie Dharmawardhane
Journal: Cancer Research (2019)

Abstract We previously reported that dietary daidzein, a soy isoflavone, increased breast cancer progression in a nude mouse model of breast cancer metastasis. Further studies indicated that equol, a metabolite of the soy isoflavone daidzein is responsible for the cancer promoting effects of soy isoflavones in breast cancer cells in vitro. We reported that equol increases the expression of the eukaryotic protein synthesis initiation factor eIF4G1, and the transcription factor c-Myc. Increased eIF4G in response to equol resulted in the non-canonical protein synthesis of pro-cancer molecules such as Cyclin D, Bcl-XL, p120, matrix metalloproteinases, etc., as confirmed by ribosome profiling and eIF4G1 knockdown studies. This study tested the hypothesis that equol promoted breast cancer progression via eIF4G1 upregulation. Immunocompromised nude mice were used to establish mammary fatpad tumors from human metastatic breast cancer cells expressing eIF4G1 knockdowns via a Tetracycline-inducible promoter. Oral gavage of 50 mg/kg BW Doxycycline 3X a week for 4 weeks was enough to knockdown eIF4G1 expression by ~80%. Therefore, one week following tumor establishment, the mice were treated with vehicle (90% corn oil, 10% ethanol), equol, Doxycycline or, equol and Doxycycline. Data show that as expected, equol treatment increased tumor growth relative to vehicle treatment. Moreover, eIF4G1 knockdown abolished the effect of equol on tumor growth. Interestingly, the effect of eIF4G1 knockdown on mammary tumor growth was not evident until 55 days of doxycycline treatment. Therefore, we tested the cell and tumor lysates for potential expression of the eIF4G1 isoform Dap5 when eIF4G1 is knocked out. Dap5 protein was expressed in eIF4G1 knockdown cells and was increased by equol treatment, indicating that Dap5 may compensate for eIF4G1 knockdown by inducing alternative cap-mediated protein synthesis. In conclusion, the cancer promoting effect of equol is abolished in breast tumors where eIF4G1 expression was stably knocked down, thus, validating our hypothesis that equol increases breast cancer progression via upregulation of eIF4G1 dependent protein synthesis initiation. Citation Format: Ailed M. Cruz-Collazo, Columba De la Parra, Robert Schneider, Suranganie Dharmawardhane. Dietary soy isoflavone equol promotes breast cancer progression via regulation of protein synthesis initiation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4390.