bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B076: Analyzing Hematological Parameters in Diabetes: Toward a Better Understanding of Pathophysiology
Authors: Rahman Nuran , Hira Israt Jahan , Fakruddin Md , Meheki Farha Rahman , Sharif Omar 
Published: February 2025

Abstract
Objectives: A person with diabetes is more prone to have dangerous diseases like cardiovascular disease, anemia, cancer, and COVID-19, which can be associated with modified levels of hematological markers. This research aims to find differences in hematological parameters and comorbidity factors in Bangladeshi diabetic patients. Methods: This 134-patient institutional cross-sectional comparison study included 62 patients with diabetes and 72 non-diabetic patients. Data on diabetes profile and hematological parameters has been collected from the study populations. Data were collected over a period from January 2023 to August 2023, with the analysis conducted subsequently. Statistical analysis was conducted using IBM SPSS Statistics version 29 software. P-value of (p&lt;0.05) was deemed statistically significant. We did a correlation matrix between variables using Python data visualization libraries. Results: This study showed patients with diabetes may experience changes in hematological parameters. An independent T-test showed that the mean and standard deviation of WBC, ESR, mean platelet volume, etc, are statistically significant (p&lt;0.05). Contrarily, other parameters like RBC, neutrophil, platelet, RDW-CV, etc, are shown to be statistically not significant (p&gt;0.05) in diabetic patients as compared to the control non-diabetic group. Acute diseases had the highest percentage of severity with a number of 39 (38.7%). We found hypertension highest in the case of disease, with a percentage of 31 (22.08%) in diabetic patients and 25 (18.05%) in nondiabetic control patients. In the correlation matrix between all the possible pairs of hematological correlation coefficient, where (1) was considered a strong relationship between variables and (-1) a not strong relationship, we found positive correlation and negative correlation. Conclusion: Our study shows diabetic patients may undergo significant alterations in hematological parameters, resulting in a decrease in hemoglobin to anemia and an increase in WBC for an asymptomatic infection. This undiagnosed stage can be an alliance for injurious comorbidity factors. Diabetic patients should prescreened for hematological parameters before other tests.
Citation Format: Nuran Rahman, Israt Jahan Hira, Md Fakruddin, Farha Rahman Meheki, Omar Sharif. Analyzing Hematological Parameters in Diabetes: Toward a Better Understanding of Pathophysiology [abstract]. In: Proceedings of the AACR IO Conference: Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2025 Feb 23-26; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2025;13(2 Suppl):Abstract nr B076.
Abstract B078: APMAP functions as a tumor-intrinsic target sensitizing cancer cells to macrophage-mediated phagocytosis
Authors: Davidson Rachel , Wang Ye , Ji Lei , Trombley Grace , Zhou Wenrong , Shen Binzhang , Choi Ashley , Stowe Hannah , Liu Shangtao , Meier Samuel R. , Doyon Brian , Whittington Douglas A. , Yu Yi , Teng Teng , Andersen Jannik N. , Huang Alan , Min Chengyin , Shaaban Salam , Gueroussov Serge 
Published: February 2025

Abstract
Macrophage-mediated phagocytosis plays a critical role in cancer cell elimination. Here, we developed an in vitro tumor-macrophage co-culture platform for unbiased identification of factors that impede macrophage phagocytosis using genome-wide CRISPR knockout. From the functional genomics screen, we identified APMAP as a tumor-intrinsic phagocytosis sensitizer. In vitro experiments validated that APMAP depletion in tumor cells enhances direct engulfment and selective killing of tumor cells by macrophages. In vivo experiments showed that APMAP depletion attenuates tumor growth and displays combinational effects with cetuximab in an MDA-MB-468 orthotopic model. To dissect the mechanism of action, we conducted a whole genome anchor screen using an APMAP-WT/KO isogenic pair and identified fatty acid biosynthesis pathway genes (including FASN, ACLY and ACC) that are required for APMAP deficiency-induced phenotypes; the metabolomics analysis suggests that sphingolipids are potential APMAP substrates. To inform drug discovery, we demonstrated that enzymatic activity is required for APMAP-enhanced phagocytosis. We further demonstrated that as a transmembrane protein, intracellularly localized APMAP was functional as a phagocytosis sensitizer, thereby suggesting that a small molecule inhibitor is preferred over a blocking antibody as a therapeutic strategy for disrupting APMAP activity.
Citation Format: Rachel Davidson, Ye Wang, Lei Ji, Grace Trombley, Wenrong Zhou, Binzhang Shen, Ashley Choi, Hannah Stowe, Shangtao Liu, Samuel R. Meier, Brian Doyon, Douglas A. Whittington, Yi Yu, Teng Teng, Jannik N. Andersen, Alan Huang, Chengyin Min, Salam Shaaban, Serge Gueroussov. APMAP functions as a tumor-intrinsic target sensitizing cancer cells to macrophage-mediated phagocytosis [abstract]. In: Proceedings of the AACR IO Conference: Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2025 Feb 23-26; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2025;13(2 Suppl):Abstract nr B078.
Abstract B081: Characterizing immune dysregulation and tertiary lymphoid structures in endometriosis: Pathogenic insights and therapeutic implications
Authors: Rahman Ariana F , Khazaie Khashayarsha , Javaheri Elika , Woldeamanuel Yohannes 
Published: February 2025

Abstract
Endometriosis (EMS) is a prevalent systemic disorder impacting 10% of women of reproductive age, characterized by the growth of endometrial-like tissue outside the uterine cavity, chronic inflammation, and fibrosis, leading to pain, infertility, and organ dysfunction. Despite its widespread occurrence, the pathogenesis of EMS remains elusive, and current treatments are inadequate, with recurrence post-surgery being a significant issue. Notably, EMS displays features reminiscent of malignancy, including genetic mutations and clonal cell proliferation. The presence of tertiary lymphoid structures (TLSs) within lesions indicates a potential role of immune dysfunction in disease progression. This study aims to explore immune mechanisms underlying EMS through three specific aims: 1) Analyzing cellular, molecular, and spatial characteristics of T and B cell interactions; 2) Defining the functional phenotype of immune cells involved; and 3) Investigating the B cell antigen receptor repertoire and the specificity of locally produced antibodies. Techniques such as single-cell RNA sequencing, spatial transcriptomics, and multiplex immunofluorescence, are employed. The outcomes provide insights into immune contributions to EMS pathology and guide the development of novel diagnostic and therapeutic strategies.
Citation Format: Ariana F Rahman, Khashayarsha Khazaie, Elika Javaheri, Yohannes Woldeamanuel. Characterizing immune dysregulation and tertiary lymphoid structures in endometriosis: Pathogenic insights and therapeutic implications [abstract]. In: Proceedings of the AACR IO Conference: Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2025 Feb 23-26; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2025;13(2 Suppl):Abstract nr B081.
Abstract B087: Comparative Efficacy of Pomalidomide vs. Teclistamab in Preventing AL Amyloidosis Progression in Refractory Multiple Myeloma
Authors: Seylani Allen , Haile Yohannes , Sadighian Assal 
Published: February 2025

Abstract
Background: AL amyloidosis progression is a critical complication in patients with refractory multiple myeloma (MM), leading to poor outcomes. Pomalidomide, an immunomodulatory drug, and Teclistamab, a bispecific antibody targeting BCMA, are both used in the management of refractory MM. This study compares the efficacy of Pomalidomide versus Teclistamab in preventing the progression of AL amyloidosis in this patient population. Methods: We conducted a retrospective cohort study utilizing de-identified patient data from the TriNetX platform, which comprises electronic health records (EHRs) from 157 million patients across 128 healthcare systems in 18 countries. The study focused on 1,560 patients with relapsed/refractory multiple myeloma, comparing AL amyloidosis progression in those treated with Pomalidomide (n=779) versus Teclistamab (n=781). The primary outcome assessed was the risk of AL amyloidosis progression during treatment with Pomalidomide vs. Teclistamab. Propensity score matching was employed to balance baseline characteristics, including age, sex, ethnicity, and comorbidities, between the two cohorts. Results: In the Pomalidomide-treated group, 17 patients experienced AL amyloidosis progression, yielding a risk of 2.18%. In the Teclistamab-treated group, 12 patients had disease progression, with a risk of 1.38%. While Teclistamab demonstrated a lower risk compared to Pomalidomide, the difference was not statistically significant (p=0.1720). The calculated risk ratio (RR) was 1.704 (95% CI: 0.785, 3.699). Conclusion: Although Teclistamab showed a numerically lower risk of AL amyloidosis progression compared to Pomalidomide, the difference did not reach statistical significance. This preliminary result may be due to inadequate data available regarding Teclistamab use since Teclistamab is a new therapeutic approved by the FDA in October of 2022. Further prospective studies are warranted to evaluate the potential superior protective effect of Teclistamab against AL amyloidosis in refractory multiple myeloma, highlighting the necessity for additional research to optimize therapeutic strategies for this high-risk population.
Citation Format: Allen Seylani, Yohannes Haile, Assal Sadighian. Comparative Efficacy of Pomalidomide vs. Teclistamab in Preventing AL Amyloidosis Progression in Refractory Multiple Myeloma [abstract]. In: Proceedings of the AACR IO Conference: Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2025 Feb 23-26; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2025;13(2 Suppl):Abstract nr B087.
Abstract B101: Classification based on intratumoral microbiome confer the molecular characteristics and immune microenvironment in gastric cancer
Authors: Oh Han Na , Hur Hoon 
Published: February 2025

Abstract
Gastric cancer (GC) with the immuno-activating tumor microenvironment (TME) significantly correlated with better oncologic outcomes or response to immunotherapy. Increasing evidence suggests that intratumoral microbiome promote carcinogenesis or tumor progression by genetic instability and remodeling of the immune landscape and oncogenic signals. However, the correlation between intratumoral microbiome and genetic or immune profiling has not been clearly disclosed in GC. To capture the complexity of bacterial composition within GC and its TME, we analyzed The Cancer Microbiome Atlas (TCMA)-public data from 100 GC patients, including bacterial abundance profiles, bulk RNA sequencing, CIBERSORT, and DNA mutation in this study. Using partitioning around medoids (PAM) clustering, we classified GC microbiome structures into four distinct types based on dominant bacterial genera: Lactobacillus, Helicobacter, Prevotella, and Streptococcus. By using rcorr-based Pearson’s correlation analysis and Redundancy Analysis (RDA), we found that association of intratumor microbiome with immune cell proportion and cancer gene mutation. The Lactobacillus-dominant type exhibited both bacteria-immune cell and bacteria-bacteria interactions with upregulation of bacterial invasion of epithelial cells, and the Streptococcus-dominant type showed downregulation of gastric acid secretion pathways. While, the Prevotella-dominant type was characterized by higher abundance of activated memory CD4 T cells, CD8 T cells, M1 macrophages than other types, especially Streptococcus-dominant type, and also associated with KRAS mutations. It implies that intratumoral Prevotella-dominant type play a role of immune activation in the TME. This study demonstrated that a specific intratumoral microbiome cluster, Prevotella-dominant type, may promote immune activation of TME in patients with GC. Overall, this study provides insights into the potential impact of specialized intratumoral microbiomes on the TME in GC patients.
Citation Format: Han Na Oh, Hoon Hur. Classification based on intratumoral microbiome confer the molecular characteristics and immune microenvironment in gastric cancer [abstract]. In: Proceedings of the AACR IO Conference: Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2025 Feb 23-26; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2025;13(2 Suppl):Abstract nr B101.
Abstract B104: Comparative Efficacy of Pomalidomide vs. Teclistamab in Preventing AL Amyloidosis Progression in Refractory Multiple Myeloma
Authors: Seylani Allen , Haile Yohannes , Sadighian Assal 
Published: February 2025

Abstract
Background: AL amyloidosis progression is a critical complication in patients with refractory multiple myeloma (MM), leading to poor outcomes. Pomalidomide, an immunomodulatory drug, and Teclistamab, a bispecific antibody targeting BCMA, are both used in the management of refractory MM. This study compares the efficacy of Pomalidomide versus Teclistamab in preventing the progression of AL amyloidosis in this patient population. Methods: We conducted a retrospective cohort study utilizing de-identified patient data from the TriNetX platform, which comprises electronic health records (EHRs) from 152 million patients across 128 healthcare systems in 18 countries. The study focused on 1,560 patients with relapsed/refractory multiple myeloma, comparing AL amyloidosis progression in those treated with Pomalidomide (n=779) versus Teclistamab (n=781). The primary outcome assessed was the risk of AL amyloidosis progression during treatment with Pomalidomide vs. Teclistamab. Propensity score matching was employed to balance baseline characteristics, including age, sex, ethnicity, and comorbidities, between the two cohorts. Results: In the Pomalidomide-treated group, 17 patients experienced AL amyloidosis progression, yielding a risk of 2.18%. In the Teclistamab-treated group, 12 patients had disease progression, with a risk of 1.38%. While Teclistamab demonstrated a lower risk compared to Pomalidomide, the difference was not statistically significant (p=0.1720). The calculated risk ratio (RR) was 1.704 (95% CI: 0.785, 3.699). Conclusion: Although Teclistamab showed a numerically lower risk of AL amyloidosis progression compared to Pomalidomide, the difference did not reach statistical significance. Further prospective studies are warranted to determine whether Teclistamab offers a superior protective effect against AL amyloidosis in refractory multiple myeloma. These findings highlight the need for additional research to optimize therapeutic strategies for this high-risk population.
Citation Format: Allen Seylani, Yohannes Haile, Assal Sadighian. Comparative Efficacy of Pomalidomide vs. Teclistamab in Preventing AL Amyloidosis Progression in Refractory Multiple Myeloma [abstract]. In: Proceedings of the AACR IO Conference: Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2025 Feb 23-26; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2025;13(2 Suppl):Abstract nr B104.
Abstract B115: Epithelial stromal interaction 1 protein (ESPTI1) expression in breast cancers with known estrogen receptor, progesterone receptor and human epidermal growth receptors-2 immunoreactivity: Any prognostic indication?
Authors: Ogenyi Samuel Ifedioranma , Ezenwa Bruno Onochie , Onu June Amara , Ike Amalachukwu Okwukwe , Okoye Jude Ogechukwu , Ogenyi Samuel Ifedioranma 
Published: February 2025

Abstract
Background: The heterogeneous nature of breast cancers has shifted the focus from pathogenesis, and clinicopathological correlations to prognostication; with increased attention being paid to identifying morphological features and biomarkers of prognostic significance. Objective: This study evaluated the expression pattern of EPSTI1protein biomarker in breast cancers with known Estrogen, Progesterone, and Human epidermal receptors (Her-2-neu) immunoreactivity. Methods: One hundred archived formalin fixed-paraffin embedded (FFPE) diagnosed breast cancer samples involving sixty-two triple-negative breast cancers (TNBC) and thirty-eight other breast cancer groups comprising mono negatives, bi negatives and triple positives were retrieved from the archives of the Department of Histopathology, Nnamdi Azikiwe University Teaching Hospital, Nnewi, Nigeria. Real-time polymerase chain reaction (RT-PCR) of EPSTI1 was performed to determine EPSTI1 expression levels while immunohistochemistry was employed to determine ER, PR and Her-2 reactivity. Results: An increasing expression pattern of EPSTI1 in an ascending order ranging from triple-positive to triple-negative breast cancers was revealed. There was a significant increase in EPSTI1 levels in mono-negative cancers compared to mono-negative cancers. Similarly, a strong negative association between triple positive and triple negative cancers and mono positive and mono negative lesions were noted. Conclusion: The study revealed an inverse relationship between EPST1 and hormonal receptor expressions. EPST1 expression characterization of breast cancers may be explored further as a formidable prognostic and therapeutic biomarker for the more aggressive triple-negative breast cancers.
Citation Format: Samuel Ifedioranma Ogenyi, Bruno Onochie Ezenwa, June Amara Onu, Amalachukwu Okwukwe Ike, Jude Ogechukwu Okoye, Samuel Ifedioranma Ogenyi. Epithelial stromal interaction 1 protein (ESPTI1) expression in breast cancers with known estrogen receptor, progesterone receptor and human epidermal growth receptors-2 immunoreactivity: Any prognostic indication? [abstract]. In: Proceedings of the AACR IO Conference: Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2025 Feb 23-26; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2025;13(2 Suppl):Abstract nr B115.
Abstract B124: Molecular mimicry of SARS-COV-2 antigens with tumor associated antigens
Authors: Ragone Concetta , Mauriello Angela , Cavalluzzo Beatrice , Cavalcanti Ernesta , Russo Luigi , Mangano Simona , Cembrola Biancamaria , Tagliamonte Maria , Buonaguro Luigi 
Published: February 2025

Abstract
The entire SARS-CoV-2 proteome was scanned to predict potential T cell antigens linked to HLA-A*02:01 and homology to TAAs (tumor-associated antigens) was searched by BLAST. Viral epitopes with high affinity (&lt;100nM) to the HLA-A*02:01 allele were predicted. Shared and variant-specific epitopes were identified. Significant homologies in amino acidic sequence have been found between SARS-CoV-2 peptides and multiple TAAs, mainly associated with breast, liver, melanoma and colon cancers. The molecular mimicry of the viral epitopes and the TAAs was found in all viral proteins, mostly the Orf 1ab and the Spike, which is included in the BNT162b2 vaccine. Predicted structural similarities confirmed the sequence homology and comparable patterns of contact with both HLA and TCR α and β chains were observed. CD8+ T cell clones cross-reactive with the paired peptides have been found by MHC class l-dextramer staining. Our results show for the first time that several SARS-COV-2 antigens are highly homologous to TAAs and cross-reactive T cells are identified in infected and BNT162b2 preventive vaccinated individuals. The implication would be that the SARS-Cov-2 pandemic could represent a natural preventive immunization for breast, liver, melanoma and colon cancers. In the coming years, real-world evidences will provide the final proof for such immunological experimental evidence. Moreover, such SARS-CoV-2 epitopes can be used to develop “multi-cancer” off-the-shelf preventive/therapeutic vaccine formulations, with higher antigenicity and immunogenicity than over-expressed tumor self-antigens, for the potential valuable benefit of thousands of cancer patients around the World. Ragone et al., Front. Immunol. 15:1398002
Citation Format: Concetta Ragone, Angela Mauriello, Beatrice Cavalluzzo, Ernesta Cavalcanti, Luigi Russo, Simona Mangano, Biancamaria Cembrola, Maria Tagliamonte, Luigi Buonaguro. Molecular mimicry of SARS-COV-2 antigens with tumor associated antigens [abstract]. In: Proceedings of the AACR IO Conference: Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2025 Feb 23-26; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2025;13(2 Suppl):Abstract nr B124.
Abstract B125: SARS-CoV-2 mRNA vaccines sensitize tumors to immune checkpoint blockade
Authors: Grippin Adam , Marconi Christiano , Copling Sage , Mendez-Gomez Hector , Wargo Jennifer , Heymach John , Jiang Wen , Sayour Elias , Lin Steven H 
Published: February 2025

Abstract
Although immune checkpoint inhibitors (ICI) have substantially extended survival in a subset of patients with cancer, they remain ineffective in most patients. Personalized mRNA vaccines sensitize tumors to ICIs in part by unleashing a cytokine/chemokine cascade that broadly activates immune cells. Since this cascade is not dependent on mRNA species, we hypothesized that mRNA vaccines encoding non-tumor-specific antigens might also be used to reset immunotolerance and sensitize response to ICIs. Here, we show that mRNA vaccines targeting SARS-CoV-2 spike protein dramatically augment responses to ICIs. In two cohorts of patients with non-small cell lung cancer and metastatic melanoma, receipt of a COVID mRNA vaccine within 100 days of ICI initiation was associated with near doubling of overall survival after controlling for over 38 covariates with Cox Proportional Hazards Regression. Preclinical models confirmed that mRNA vaccines targeting SARS-COV-2 sensitize response to ICIs. By inducing a surge in interferon-α and Th1 chemokines, spike mRNA vaccines mediate antigen presenting cell co-localization with T cells in lymphoid organs for induction of anti-tumor immunity. Due to increases in PD-L1 on tumor cells, concomitant ICI treatment elicits increased PD-1+ T cells and epitope spreading against cancer associated antigens. Similar correlates of response were seen in both patients and healthy volunteers. Together, these results demonstrate that clinically available mRNA vaccines targeting non-tumor antigens are potent immune modulators capable of sensitizing tumors to ICIs.
Citation Format: Adam Grippin, Christiano Marconi, Sage Copling, Hector Mendez-Gomez, Jennifer Wargo, John Heymach, Wen Jiang, Elias Sayour, Steven H Lin. SARS-CoV-2 mRNA vaccines sensitize tumors to immune checkpoint blockade [abstract]. In: Proceedings of the AACR IO Conference: Discovery and Innovation in Cancer Immunology: Revolutionizing Treatment through Immunotherapy; 2025 Feb 23-26; Los Angeles, CA. Philadelphia (PA): AACR; Cancer Immunol Res 2025;13(2 Suppl):Abstract nr B125.