bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 4965: Detection of status of cancer in radiology notes using artificial intelligence
Authors: Arya Ankur , Niederhausern Andrew , Bahadur Nadia S. , Shah Neil J. , Nichols Chelsea , Chatterjee Avijit , Philip John 
Published: March 2024

Abstract
Introductory Statement: The goal is to use an AI model to replicate the human curator’s response on cancer status in radiology notes of ~20,000 cancer patients.
Introduction: MSKCC currently has ~100,000 patients with genomic testing (IMPACT) and continues to accrue more. Clinicians use this genomic data for research but lack clinical structured data to analyze alongside the genomic data. We use a vendor called VASTA Global to manually curate unstructured paragraph text. Depending on the data model, we found that a patient’s full cancer history can take up to 8 hours to curate. Therefore, we want to implement AI to automate the curation of this data to save time and cost.
We hope to achieve a faster curation process that allows us to accomplish more than 1 patient a day to catch up to the 100,000 MSK-IMPACT cohort. To decrease the average curation time per patient, we investigated the use of an NLP model to replicate manual curation of the PRISSMM™ ontology field for change in cancer status from radiology reports. Manual curation of radiology reports is time intensive due to curators understanding their cancer status and the volume of scans patients undergo.
Methods:A pre-trained Bidirectional Encoder Representations from Transformers (BERT) model is fine-tuned using training data using GPUs in IBM Cloud Pak for Data (CPD) platform. The hyperparameters were adjusted using accuracy and F1 metric of evaluation data. Using one vs. rest approach the model is evaluated on held out test data with results shown in table 1.Table 1 includes class 1-5: Progressing/worsening/enlarging, stable/no change, improving/responding, not stated/indeterminate or mixed.
Summary:The weighted AUCROC ~ 0.97, F1 ~ 0.85 and accuracy ~ 93%. These metric scores improve by choosing notes with higher class probabilities only.
Conclusion:Due to the above 0.9 calculated accuracy this NLP model is successful in replicating the curated results of cancer status and the next steps will be to run this model on a new cohort of patients not yet curated.
Cancer Status Metrics Class Prevalence Precision Recall F1 Score AUCROC Accuracy 1 38.9% 88.7% 87.0% 87.9% 96.5% 90.7% 2 24.7% 89.9% 88.2% 89.1% 98.3% 94.6% 3 15.9% 87.6% 90.7% 89.1% 98.7% 96.5% 4 15.7% 77.0% 72.6% 74.7% 94.4% 92.3% 5 4.8% 68.1% 74.4% 71.1% 97.9% 97.1% Weighted Average 85% 86% 85% 97% 93%
Citation Format: Ankur Arya, Andrew Niederhausern, Nadia S. Bahadur, Neil J. Shah, Chelsea Nichols, Avijit Chatterjee, John Philip. Detection of status of cancer in radiology notes using artificial intelligence [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 4965.
Abstract 497: Plant viruses against cancer
Authors: Steinmetz Nicole F. , Chung Young Hun , Moreno-Gonzalez Miguel , Zhao Zhongchao 
Published: March 2024

Abstract
Immunotherapy has significantly transformed the landscape of cancer treatment; however, concerns about safety, efficacy, and long-term outcomes across various tumor types persist. We have developed an intratumoral immunotherapy strategy with an engineered plant virus nanotechnology and demonstrated efficacy in tumor mouse models and canine cancer patients. This method is designed to elicit a systemic (abscopal effect), safe, and enduring anti-tumor immune response that is not limited by tumor type. The power of immunotherapy lies in synergistic combination treatments and toward this goal, we are engineering the next-generation plant virus nanotechnologies. We demonstrate synergistic combination with chemotherapy and immunization strategies the hone in on tumor-associated antigens and key players of inflammation. The combinatorial immunotherapy strategies prevent recurrence post-surgery in mice and canine patients. We will discuss the engineering design principles leading toward synergetic combination immunotherapies to treat and prevent cancer; efficacy studies and underlying mechanism is elucidated through immunomics studies.
Selected references: Steinmetz N.F. et al (2023) Viral nanoparticle vaccines against S100A9 reduce lung tumor seeding and metastasis. Proc. Natl. Acad. Sci. U.S.A. 120 (43) e2221859120. Wang C. and Steinmetz N.F. (2020) A Combination of Cowpea mosaic virus and Immune Checkpoint Therapy Synergistically Improves Therapeutic Efficacy in Three Tumor Models. Advanced Functional Materials, 2002299.
Citation Format: Nicole F. Steinmetz, Young Hun Chung, Miguel Moreno-Gonzalez, Zhongchao Zhao. Plant viruses against cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 497.
Abstract 4973: Impact of technology on quality of thoracic multidisciplinary cancer conferences
Authors: Ibekwe Opuruiche , Gaudioso Carmelo , Attwood Kristopher M. , Pokharel Saraswati , Roche Charles L. , Nwogu Chukwumere E. 
Published: March 2024

Abstract
Background: Complex cancer cases require discussion at Multidisciplinary Cancer Conferences (MCCs) to determine the best management. The study aim was to assess the impact of navify® tumor board solution (NTBS) technology on the quality of information presented, case discussions, and care plans at thoracic MCCs.
Methods: Between September 2020 and February 2022, using a before-after study design, we prospectively collected data through direct observation of thoracic MCCs at an academic cancer center. The NTBS technology was introduced in March of 2021. Additionally, we reviewed medical records to assess several factors including the rate of change in care plans as decided by the MCC, compliance of all care plans with national guidelines, and concordance of treatment received with MCC recommendations. Observational data was collected via a validated tool “Metric for the Observation of Decision-Making". We used SAS v9.4 (Cary, NC) for statistical analyses.
Results: We identified 151 and 166 thoracic cancer cases before and after implementation of NTBS, respectively. The overall quality of case presentation and discussion, represented by a mean composite score (the summation of individual variables scored on a 1-5 scale, poor to excellent), increased from 56.8 to 82.0 (p&lt;.001). This improvement was also observed across multiple sub-components of the composite score including case history (3.4 vs 4.6), reason for presentation (3.2 vs 4.6), comorbidities/performance status/psychosocial information (2.8 vs 4.2), patient views (1.2 vs 3.3), radiology and pathology presentations (3.5 vs 4.8 and 3.2 vs 4.4, respectively), and contribution from surgical, medical, and radiation oncologists (3.9 vs 4.3, 3.3 vs 3.8, and 3.5 vs 3.8, respectively), as well as the moderation by the MCC chair (4.9 vs 5.0). All these results were statistically significant with p&lt;.001. There was no statistically significant difference between the two cohorts in rate of change in care plans by the MCC, care plan compliance with national guidelines, and concordance of treatment received with MCC recommendations.
Conclusion: Technology improves the quality of information and discussion at tumor boards. However, this study did not demonstrate an impact on compliance with practice guidelines. Practitioners should explore the available tumor board technology platforms to optimize the conduct of MCCs in their respective institutions.
Citation Format: Opuruiche Ibekwe, Carmelo Gaudioso, Kristopher M. Attwood, Saraswati Pokharel, Charles L. Roche, Chukwumere E. Nwogu. Impact of technology on quality of thoracic multidisciplinary cancer conferences [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 4973.
Abstract 4978: Genomic characterization of metastatic pancreatic cancer according to tumor sample sites
Authors: Goksu Suleyman Y. , Ozer Muhammet , Goksu Busra Bacik , Sanford Nina N. , Jones Amy , Verma Nilesh , Kazmi Syed 
Published: March 2024

Abstract
Background: Our research aimed to evaluate and compare the genetic variations in the primary and metastatic sites of patients with metastatic pancreatic cancer.
Methods: In this study, we selected individuals with metastatic pancreatic cancer from the data provided by the American Association for Cancer Research Project GENIE (version 14.1). The comparison of genetic mutations between primary and metastatic tumor sites was conducted using the Fisher exact test, augmented with the Benjamini-Hochberg adjustment technique.
Results: In a study of 3,108 patients with metastatic pancreatic cancer, 38.9% had metastatic site tumor samples, while 61.1% had samples from the primary tumor. The most frequent mutations were KRAS (89.4%), TP53 (72.9%), SMAD4 (21.2%), and CDKN2A (17.4%). Metastatic samples showed higher rates of CDKN2A, CDKN2B, and MTAP mutations compared to primary site samples (40.1% vs. 29.1%; 20.3% vs. 10.4%; and 20.8% vs. 8.9%, respectively, all with p&lt;0.001 and q&lt;0.001). In patients with young-onset pancreatic cancer (younger than 50 years), there was no notable difference in gene mutations between the two sample groups.
Conclusion: Our findings corroborate the notion that identifying the precise genes that contribute to the development of metastatic pancreatic cancer is vital for gaining a more comprehensive understanding of the biological mechanisms. Moreover, genomic profiling could be a key in pinpointing potential biomarkers for diagnosis and therapy.
Citation Format: Suleyman Y. Goksu, Muhammet Ozer, Busra Bacik Goksu, Nina N. Sanford, Amy Jones, Nilesh Verma, Syed Kazmi. Genomic characterization of metastatic pancreatic cancer according to tumor sample sites [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 4978.
Abstract 4985: Pivotal roles for cancer cell-intrinsic mPGES-1 and autocrine EP4 signaling in suppressing anti-tumor immunity
Authors: Markosyan Nune , Kim Ilkyu , Arora Charu , Cheng Noah , Schechter Emma , Tobias John , Stanger Ben , Vonderheide Robert 
Published: March 2024

Abstract
Tumor cell-derived prostaglandin E2 (PGE2) is a tumor cell-intrinsic factor that supports immunosuppression in the tumor microenvironment (TME). Using a genetically engineered mouse model of pancreatic ductal adenocarcinoma, we demonstrate that deleting the terminal PGE2 synthesis enzyme or disrupting autocrine PGE2 signaling through cognate EP4 receptors on tumor cells reverses the T cell-low, myeloid cell-rich TME to activate T cell immunity and suppress tumor growth. Knockout (KO) of Ptges (the gene encoding PGE2 synthesis enzyme mPGES-1) or the EP4 receptor gene (Ptger4) in KPCY (KrasG12D/P53R172H/Yfp/CrePd) pancreatic tumor cells abolished growth of implanted tumors in a T cell-dependent manner (KO vs control p&lt;0.0001 for both). Blockade of the EP4 receptor in combination with immunotherapy, but not immunotherapy alone, induced complete tumor regressions and immunological memory. Mechanistically, Ptges and Ptger4 KO tumor cells exhibited altered T and myeloid cell attractant chemokines, became more susceptible to TNF-α killing, and exhibited reduced adenosine synthesis. In hosts treated with an adenosine deaminase inhibitor, Ptger4 KO tumor cells accumulated adenosine and gave rise to tumors. These studies reveal an unexpected role for autocrine mPGES1-PGE2-EP4 signaling axis in pancreatic cancer cells, nominating mPGES-1 inhibition and EP4 blockade as immune-sensitizing approaches in cancer therapy.
Citation Format: Nune Markosyan, Ilkyu Kim, Charu Arora, Noah Cheng, Emma Schechter, John Tobias, Ben Stanger, Robert Vonderheide. Pivotal roles for cancer cell-intrinsic mPGES-1 and autocrine EP4 signaling in suppressing anti-tumor immunity [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 4985.
Abstract 50: ALK inhibitors increase ALK expression and sensitize neuroblastoma cells to ALK.CAR-T cells
Authors: Bergaggio Elisa , Tai Wei-Tien , Aroldi Andrea , Mecca Carmen , Landoni Elisa , Nüesch Manuel , Mota Ines , Metovic Jasna , Molinaro Luca , Ma Leyuan , Alvarado Diego , Ambrogio Chiara , Voena Claudia , Blasco Rafael B. , Li Tongqing , Klein Daryl , Irvine Darrell J. , Papotti Mauro , Savolodo Barbara , Dotti Gianpietro , Chiarle Roberto 
Published: March 2024

Abstract
Neuroblastoma is the most common extracranial solid tumor of childhood, with limited success in treating refractory or relapsed cases using current therapies. Chimeric antigen receptor (CAR) T cell therapy targeting GD2 has shown promise in neuroblastoma treatment, but relapses are associated with loss of antigen expression. The selection of the best tumor antigen is critical for the therapeutic success of CAR-T cells in hematologic malignancies and solid tumors. The Anaplastic Lymphoma Kinase (ALK) receptor is expressed by most neuroblastomas while virtually absent in most normal tissues. ALK is an oncogenic driver in neuroblastoma and ALK inhibitors show promising clinical activity. All these features make ALK an attractive target for CAR-T cell therapy. We developed ALK.CAR-T cells that show potent efficacy in monotherapy against neuroblastoma with high ALK expression without toxicity. For neuroblastoma with low ALK expression, combination with ALK inhibitors specifically potentiates ALK.CAR-T cells but not GD2.CAR-T cells. In neuroblastoma cell lines and in a patient-derived xenograft (PDX), the combination of ALK inhibitors and ALK.CAR-T cells significantly reduced tumor growth and extended mice survival. Mechanistically, ALK inhibitors impair tumor growth and upregulate the expression of ALK, thereby facilitating the activity of ALK.CAR-T cells against neuroblastoma. Thus, while neither ALK inhibitors nor ALK.CAR-T cells will likely be sufficient as monotherapy in neuroblastoma with low ALK density, their combination specifically enhances therapeutic efficacy. These findings provide insights into the potential of ALK.CAR-T cells as a novel therapeutic strategy for neuroblastoma. A Phase I clinical trial to test ALK.CAR-T cells in combination with ALK TKIs in children with refractory/relapsed neuroblastoma is being implemented based on these results.
Citation Format: Elisa Bergaggio, Wei-Tien Tai, Andrea Aroldi, Carmen Mecca, Elisa Landoni, Manuel Nüesch, Ines Mota, Jasna Metovic, Luca Molinaro, Leyuan Ma, Diego Alvarado, Chiara Ambrogio, Claudia Voena, Rafael B. Blasco, Tongqing Li, Daryl Klein, Darrell J. Irvine, Mauro Papotti, Barbara Savolodo, Gianpietro Dotti, Roberto Chiarle. ALK inhibitors increase ALK expression and sensitize neuroblastoma cells to ALK.CAR-T cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 50.
Abstract 5053: Clinicopathologic and molecular genetic features of STAT3-mutated myeloid neoplasms
Authors: Ye Matthew T. , Zuo Zhuang , Calin Steliana , Ye Fengxi , He Hua , Kamata Wataru , You M. James 
Published: March 2024

Abstract
STAT3 is a key transcription factor that can mediate cancer progression through phosphorylation or gain-of-function mutations. STAT3 mutations have been mainly associated with large granular lymphocytic T-cell leukemia. Whereas STAT3 activation is common in myeloid neoplasms, it is primarily mediated through STAT3 phosphorylation. STAT3 mutation has only rarely been reported in myeloid neoplasms. We assessed the clinicopathologic and molecular genetic features of 32 STAT3-mutated myeloid neoplasms. Twenty (62.5%) cases were classified as acute myeloid leukemia (AML), 7 (21.9%) as myelodysplastic syndrome (MDS), and 5 (15.6%) as chronic myelomonocytic leukemia (CMML). It is of note that STAT3 mutation was not detected in myeloproliferative neoplasms (MPN). STAT3 mutations were detected at the initial diagnosis in 22 of 25 (88%) cases, suggesting STAT3 mutation is an early event in pathogenesis. However, STAT3 mutations represented the dominant clone in only 6 (18.8%) cases, all classified as AML. Most are missense mutations, located at the SH2 domain. The median variant allele frequencies were 6.8%, 4.6% and 3.1% for AML, MDS and CMML, respectively, and in a case of CMML, the VAF increased from 2.4% to 34.8% upon leukemic transformation. STAT3 mutation was accompanied by co-existing mutations in all cases, with SRSF2 (40.6%), TET2 (40.6%), ASXL1 (37.5%), and SETBP1 (34.4%) being most common. Cases with STAT3 mutations were usually associated with morphologic dysplasia and increased blasts. Monosomy 7/del7q was the most common cytogenetic abnormality, seen in 11 (34.4%) cases. With a median follow-up of 24.5 months, 21 patients died, 6 had persistent disease, and 5 achieved complete remission. We summarize that STAT3 mutation is present in a variety of myeloid neoplasms, but not seen in MPN. It is often an early events and always with concurrent mutations. It may play an important role in the pathogenesis and progression of myeloid neoplasms by activating JAK-STAT pathway, and may serve as a potential therapeutic target.
Citation Format: Matthew T. Ye, Zhuang Zuo, Steliana Calin, Fengxi Ye, Hua He, Wataru Kamata, M. James You. Clinicopathologic and molecular genetic features of STAT3-mutated myeloid neoplasms [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 5053.
Abstract 5098: Second-line treatment outcomes in Extensive Stage Small Cell Lung Cancer (ES-SCLC) patients after first-line immuno-chemotherapy
Authors: Wan Rui , Fan Linjie , Zhong Jia , Duan Jianchun , Wang Zhijie , Hao Xuezhi , Wang Jie 
Published: March 2024

Abstract
Background: First-line immune checkpoint inhibitors (ICIs) has significantly improved overall survival (OS) of ES-SCLC. However, second-line treatment options are still controversial with limited overall survival. This study aims to evaluate the efficacy of different second-line regimens for relapsed ES-SCLC after first-line immuno-chemotherapy.
Patients and Methods: We retrospectively reviewed 96 ES-SCLC patients receiving first-line immuno-chemotherapy in Cancer Hospital Chinese Academy of Medical Sciences, from Jan 2019 to Dec 2022. Clinical data were collected from electronic medical records. The clinical outcomes, including objective response rate (ORR), progression-free survival (PFS) and overall survival (OS) were assessed by Kaplan-Meier method and standard log-rank test.
Results: From January 4, 2019 to December 18, 2022, a total of 96 ES-SCLC patients received first-line immuno-chemotherapy and 49 of them went through second-line treatment in our center. Patient characteristics were listed as follows : median age 63 (31-79), male 76 (79.2%) , heavy smoker 59 (61.5%), liver metastasis 40 (41.7%), brain metastasis 33 (34.4%) and refractory recurrence 58 (60.4%). Second-line treatments included immunotherapy crossover and combination with chemotherapy (n=40), anlotinib with or without chemotherapy (n=5), chemotherapy alone (n=4). ORR of the whole group in the second-line setting was 22.4%. Median PFS was 3.23 months (95% CI 1.96-4.50). Cross-line immunotherapy failed to improved survival for relapsed ES-SCLC compared with those without ICIs ( mPFS 3.23 vs 3.13m, p=0.829). Anlotinib based treatment showed numerically superior PFS for relapsed SCLC compared with those without anlotinib therapy (mPFS 6.00 vs 3.13m, p=0.089).
Conclusion: This retrospective study indicated cross-line ICIs failure to improve clinical outcome for relapsed ES-SCLC, and implied the potential benefits of anlotinib in second-line setting.
Citation Format: Rui Wan, Linjie Fan, Jia Zhong, Jianchun Duan, Zhijie Wang, Xuezhi Hao, Jie Wang. Second-line treatment outcomes in Extensive Stage Small Cell Lung Cancer (ES-SCLC) patients after first-line immuno-chemotherapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 5098.
Abstract 5160: Evaluation of circulating microRNAs as predictive and prognostic biomarkers for advanced melanoma patients
Authors: Durante Giorgio , Comito Francesca , Naddeo Maria , De Matteis Serena , Bonafè Massimiliano , Dika Emi , Ardizzoni Andrea , Ferracin Manuela 
Published: March 2024

Abstract
Introduction Metastatic melanoma is the deadliest form of skin cancer whose incidence has been rising dramatically over the last few decades. The advent of Immune checkpoint inhibitors (ICIs) has strongly improved the survival of melanoma patients. However, a high fraction of patients shows primary resistance or will develop secondary resistance during therapy. For these reasons, it is of utmost importance to develop biomarkers that could predict response or resistance to therapies. Among the most promising biomarkers analyzed in peripheral blood there are circulating microRNAs (miRNAs). The aim of this study is to identify a miRNA signature able to predict prognosis and clinical relapse in advanced melanoma patients treated with ICIs.
Methodology We collected longitudinal blood draws from metastatic melanoma patients treated with ICIs at Bologna University-Hospital (Italy). We separated plasma from whole blood, extracted RNA and determined the absolute levels of miR-155-5p, miR-424-5p and miR-320a using EvaGreen-based droplet digital PCR. Moreover, in the subset of first-line anti-PD-1 treated patients, we performed cytofluorimetric leukocyte analysis.
Results and discussion We found that patients with pre-therapy (baseline) high expression of circulating miR-155-5p, miR-320a and mir-424-5p had longer progression-free survival (PFS), and overall-survival (OS). In patients treated with anti PD-1 as first-line treatment, we found that baseline miR-155-5p levels were significantly higher in patients who responded to therapy, and therefore miR-155-5p could have a predictive value. Moreover, using a flow cytometric approach, we noted that baseline miR-155-5p levels correlated with CD4+Naïve (r:-0.91, p:0.027) and CD4+PD1+ T-cells (r:0.94, p:0.015) in patients treated with first-line anti-PD-1 treatment.
Conclusion These preliminary findings propose baseline circulating miRNAs as potential predictive and prognostic biomarkers in the setting of advanced melanoma patients treated with immunotherapy.
Citation Format: Giorgio Durante, Francesca Comito, Maria Naddeo, Serena De Matteis, Massimiliano Bonafè, Emi Dika, Andrea Ardizzoni, Manuela Ferracin. Evaluation of circulating microRNAs as predictive and prognostic biomarkers for advanced melanoma patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 5160.