Literatura científica selecionada sobre o tema "American Medical Association. Meeting 1876 : Philadelphia, Pa.)"

Abstract Background: Type2 diabetes mellitus(T2DM) is a risk factor for cancer. Recent studies have shown that DPP-4 inhibitor(DPP-4i) can either promote or suppress cancer progression. However, the detailed mechanisms remain unknown. Here, in this study, we investigated the effect of DPP-4i on tumor microenvironment and its effect on the prognosis of cancer patients. Method: We retrospectively examined the outcome of colorectal cancer (CRC) patients with T2DM who received curative surgery in Jichi Medical University Hospital and asked the impact of DPP-4i intake on their outcome. In addition, we performed immunohistochemistry to examine the phenotypes of TIL, TAM and epithelial-mesenchymal transition (EMT) of cancer cells in surgically removed CRC tissues in 40 CRC patients who had taken DPP-4i and propensity score-matched 40 patients who had not. Results: A total of 1696 patients underwent curative colectomy from April 2010 to March 2020. Among them, 260 patients had T2DM at the time of surgery, and 135 patients had been treated with drugs including DPP-4i. The postoperative disease-free survival rate (DFS) was significantly worse in the DPP-4i intake group compared with non-intake group (5 year DFS 18.5% vs 5.4%, HR=2.0, p<0.05). The number of Zeb1-positive tumor cells significantly increased in DPP-4i intake group. (Median(M)=29.0 (0-189)/mm2 vs 9.0 (0-71)/mm2, p<0.01). The number of CD3 (+) TIL in DPP-4i intake group was Median(M)=277.4(min 121.6-max 523.2)/mm2 which was significantly lower than those in non-intake group (M= 319.6, min 493.0-max 823.6/mm2). CD8(+) TIL in DPP-4i intake was reduced more significantly than in non-intake group (M=187.6, min 67.8-max 347.4/mm2 vs M=336.8, min 200.2-max 588.4/mm2, p<0.05) with less CD8/CD3 ratio (61.2% vs 67.1%, p<0.05). On the other hand, the density of CD68(+)CD163(+) TAM was significantly higher(M=202.6, min 122.8-max 257.0/mm2 vs M=126.6, min 94.8-max 247.6/mm2, p<0.05) in DPP-4i intake group. Conclusion: DPP-4i increases the number of M2-type TAM while decreases the number of effector TIL and promote EMT of cancer cells in tumor microenvironment, which might lead to the poor outcome of the patients with CRC. Citation Format: Akira Saito, Hideyuki Ohzawa, Yuki Kaneko, Kohei Tamura, Yurie Futoh, Kazuya Takahashi, Yuki Kimura, Mineyuki Tojo, Rie Kawashima, Hideyo Miyato, Naohiro Sata, Joji Kitayama. Dipeptidyl peptidase-4 inhibitor impairs the outcomes of patients with type 2 diabetes mellitus after curative resection for colorectal cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 6379.

Abstract Background: Programmed cell death ligand 1 (PD-L1) expression alone has limited predictive value for pembrolizumab plus 5-fluorouracil and platinum (PFP) therapy in recurrent or metastatic head and neck squamous cell carcinoma (HNSCC). An artificial intelligence (AI)-powered spatial tumor-infiltrating lymphocyte (TIL) analyzer may provide independent prognostic information. Methods: This study included 63 patients with locally incurable HNSCC who received first-line PFP at Samsung Medical Center. Patients were classified into inflamed phenotype (IP) or non-inflamed phenotype (NIP) based on the 5% proportion threshold of inflamed 1 mm2-sized grids over total grids within hematoxylin and eosin-stained whole-slide images (WSIs) analyzed using Lunit SCOPE IO. We evaluated the prognostic value of inflamed status and densities of intratumoral TILs (iTILs), stromal TILs (sTILs), and tumor microenvironment TILs (tTILs). Results: Patients were predominantly male (78%). The median age at PFP initiation was 57 years. The most common primary tumor site was oral cavity (49.2%), followed by oropharynx (16%) and hypopharynx (10%). Of the 37 patients with available PD-L1 combined positive score (CPS), 2 (5%), 23 (62%), and 12 (32%) had CPS values of <1, 1-19, and ≥20, respectively. The overall response rate was 54%, with 67% in the CPS ≥20 subgroup and 48% in the CPS <20 subgroup. The median progression-free survival (PFS) was 7.2 months, with 10.8 months for patients with CPS ≥20 and 5.5 months for patients with CPS <20. The median overall survival (OS) was 18.6 months. Among 62 patients with available WSIs, 47 (74%) and 15 (26%) patients were categorized as having an IP and NIP, respectively. Oral cavity cancer was enriched with IP (57.4% of all IP cases vs 26.7% of all NIP cases), while all four paranasal sinus tumors had NIP. The overall response rate was 57% in the IP group and 44% in the NIP group. Patients with IP had significantly longer PFS and OS than patients with NIP, both in unadjusted (hazard ratio [HR] for PFS, 0.4; 95% confidence interval [CI], 0.21-0.78; P = 0.007; HR for OS, 0.43; 95% CI, 0.2-0.95; P = 0.036) and PD-L1 CPS-adjusted analyses (HR for PFS, 0.41; 95% CI, 0.21-0.79; P = 0.008; HR for OS, 0.4; 95% CI, 0.18-0.89; P = 0.025). High densities (≥25th percentile) of iTILs, sTILs, and tTILs were all significantly associated with prolonged PFS after CPS adjustment (P = 0.001, 0.001, and 0.012). High density of iTILs was also significantly associated with improved OS (P = 0.001 after CPS adjustment), while there was no significant association between OS and high density of sTILs or tTILs (0.077 and 0.085, respectively, after CPS adjustment). Conclusion: An AI-driven spatial TIL analyzer might serve as a simple and independent prognostic biomarker in HNSCC patients receiving pembrolizumab plus chemotherapy. Citation Format: Sehhoon Park, Junghoon Shin, Chan-Young Ock, Chang Ho Ahn, Hyun Ae Jung, Se-Hoon Lee, Myung-Ju Ahn. Artificial intelligence-powered spatial analysis of tumor-infiltrating lymphocytes as a prognostic biomarker for pembrolizumab plus chemotherapy in recurrent or metastatic head and neck squamous cell carcinoma [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 7658.

Abstract Background: Programmed cell death protein 1 (PD-1) inhibitors are approved as second-line (2L) therapy for patients (pts) with ESCC. TMB is a predictive biomarker of response to immune checkpoint blockade in multiple cancers, but its role in ESCC is unclear. Here, we retrospectively investigated the association between TMB and clinical outcomes in the phase 3 RATIONALE-302 study of anti-PD-1 antibody tislelizumab (TIS) vs investigator-chosen chemotherapy (ICC) as 2L treatment for advanced unresectable/metastatic ESCC (NCT03430843). Methods: Genomic profiling was assessed on tumor tissues collected at baseline using BurningRock OncoScreen Plus 520 NGS panel to determine TMB status. Median progression-free survival (PFS) and overall survival (OS) were calculated using the Kaplan-Meier method. Objective response rate (ORR) was calculated using the binomial exact method. Cox model was applied to assess the effect of TMB on survival outcomes. Hazard ratio (HR) and 95% confidence interval (CI) for OS and PFS in TMB subgroups were estimated. Results: Of 512 pts enrolled, 209 had evaluable tumor samples (TIS, n=105; ICC, n=104). Using the widely used cutoff of 10 mutations per megabase (mut/Mb), numerically higher ORR and survival benefit with TIS over ICC were observed in the high TMB (TMB-H) vs the low TMB (TMB-L) subgroup (Table). The predictive effect of TMB on survival outcomes was not significant (interaction p-value = 0.0537 for PFS, 0.5374 for OS); however, the effect became significant using the increased cutoff of 12 mut/Mb (TMB-H prevalence = 16.7%; interaction p-value = 0.0267 for PFS, 0.0175 for OS). Conclusions: TMB status may play a role in predicting clinical outcomes in pts with advanced ESCC treated with TIS versus ICC, especially when a higher TMB cutoff is chosen. These findings need further prospective validation. Acknowledgments: This study was sponsored by BeiGene, Ltd. Medical writing support, under the direction of the authors, was provided by Sophie Cook, PhD, of Ashfield MedComms, an Inizio company, and was funded by BeiGene, Ltd. Table. Clinical outcomes by TMB status (cutoff 10 mut/Mb) TMB status TMB-H TMB-L Treatment TIS ICC TIS ICC n (% in TMB BEP, N=209) 27 (12.9) 31 (14.8) 78 (37.3) 73 (34.9) ORR, % (95% CI) 33.3 (16.5, 54.0) 6.5 (0.8, 21.4) 16.7 (9.2, 26.8) 17.8 (9.8, 28.5) Median PFS, months (95% CI) 2.4 (1.4, 5.5) 2.3 (1.3, 2.9) 1.4 (1.3, 2.7) 2.7 (1.5, 3.3) PFS HR (95% CI) 0.52 (0.28, 0.97) 1.06 (0.73, 1.53) Interaction p-value 0.0537 Median OS, months (95% CI) 6.1 (4.2, 18.6) 4.7 (3.4, 7.0) 8.6 (4.6, 11.8) 7.0 (4.6, 8.6) OS HR (95% CI) 0.58 (0.32, 1.04) 0.72 (0.50, 1.03) Interaction p-value 0.5374 TMB-adjusted OS HR (95% CI) 0.68 (0.5, 0.92) BEP, biomarker evaluable population; CI, confidence interval; HR, hazard ratio; ICC, investigator chosen chemotherapy; OS, overall survival; PFS, progression-free survival; ORR, objective response rate; TIS, tislelizumab; TMB-H, high tumor mutational burden; TMB-L, low tumor mutational burden; TMB-adjusted OS HR, overall HR adjusted for the impact of TMB on OS Citation Format: Lin Shen, Yongqian Shu, Kuaile Zhao, Taroh Satoh, Zhendong Chen, Eric Van Cutsem, Guohua Yu, Jun Wu, Chih-Hung Hsu, Sung Bae Kim, Wenting Du, Yang Shi, Ruiqi Huang, Qiao Li, Jingwen Shi, Yun Zhang, Kato Ken. Association of tumor mutational burden (TMB) and clinical outcomes with tislelizumab versus chemotherapy in esophageal cell carcinoma (ESCC) from RATIONALE-302 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 2 (Clinical Trials and Late-Breaking Research); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(8_Suppl):Abstract nr CT077.

Abstract Background: MTAP-loss is an emerging biomarker guiding druggable targets in cholangiocarcinoma and almost exclusively occurs in the setting of 9p21 loss, which has itself been associated with reduced IO responsiveness and poorer survival outcomes on a pan-cancer analysis. We sought to understand the clinical impact of MTAP status on treatment and survival outcomes, in a clinical cohort of molecularly characterized advanced cholangiocarcinoma patients. Methods: We analyzed advanced cholangiocarcinoma patients treated and evaluated at MD Anderson Cancer Center, tested for MTAP. Clinical information including genomic co-alterations, demographic information, treatment history and response to treatment were retrieved from retrospective medical record review. Comprehensive genomic profiling was performed with FDA-approved assays. Statistical analysis was performed with SPSS24 using Fisher's exact test, multivariate Cox regression and Kaplan-Meyer method for survival analysis. Results: 71 patients were identified (MTAP loss 31% (22/71); MTAP intact 69% (49/71)); 54,9% (39/71) were females. No significant difference in gender, age or ethnicity was seen between MTAP cohorts. We found that altered CDKN2A (p<0.01), CDKN2B (p<0.01), and IDH1 (p=0.048) were highly correlated with MTAP loss, while STK11 (p=0.095), a prognostic indicator of IO resistance, also showed a tendency to be a surrogate marker of MTAP loss status. Tumor mutational burden (TMB) was lower in MTAP loss group (2.18 vs. 4.88, p <0.01), but no difference was found in microsatellite instability (MSI) or PD-L1 status between groups. On multivariate analysis, patients harboring CDKN2A loss were noted to have worse OS compared to those without CDKN2A intact (18.6 vs 29.9 months, 95% CI, p=0.035). No statistically significant difference in OS was observed by MTAP status (25.9 vs. 29.2 months, 95% CI, p=0.168). Other genomic alterations with significant impact on OS were CCNE1 (p<0.01), FGF19 (p=0.04), and MYC (p=0.043). Treatment with chemotherapy regimens containing Gemcitabine in the first line setting of metastatic disease showed higher disease control rate in the MTAP intact cohort (91.4%) vs. MTAP loss cohort (38.5%) (p<0.01), but no statistically significant difference in response (PR/CR) (p=0.421). Few patients (14/71) received IO in this cohort; no significant difference in IO response was observed by MTAP status (p=0.152). Conclusions: MTAP loss cholangiocarcinoma has a distinct molecular profile compared with MTAP intact including key differences in co-altered tumor suppressor genes and TMB. To our knowledge, this is the first real-world data describing the clinical and genomic differences in advanced cholangiocarcinoma by MTAP status. Further prospective data are required to validate these findings. Citation Format: Cátia F. Gaspar, Natalie Y. Ngoi, Tin Tang, Jeffrey Ross, Dean Pavlick, Gregory Buchold, Shubham Pant, Milind Javle, Jordi Ahnert. Clinical impact of MTAP status in advanced cholangiocarcinoma: Genomic profile and response to treatment [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 963.

Abstract Subsets of tumor-produced proteins, referred to as Humoral Immuno-Oncology (HIO) factors, can bind to IgG1 antibodies and suppress their immune-effector activities. Antibody-drug conjugates (ADCs) targeting tumor cell surface antigens can internalize and kill target cells upon liberation of their cytotoxic payload. Binding of the antibody component of an ADC by a HIO factor may potentially hamper the efficacy of a bound ADC. To assess any suppression of ADC’s activity by HIO factors, we evaluated the efficacy of a HIO-refractory ADC, NAV-001, and a HIO-bound ADC, SS1, both targeting mesothelin. The HIO factor MUC16/CA125 protein, which binds to SS1 ADC, was shown to have a negative effect on its internalization and tumor cell killing. The MUC16/CA125 refractory NAV-001 ADC was shown to have robust killing of tumor cells regardless of MUC16/CA125 expression in vitro (EC50 ~20 pM) as well as in vivo at single, sub-mg/kg dosing. Moreover, NAV-001-PNU, which contains the PNU-159682 topoisomerase II inhibitor as a payload, demonstrated good stability in vitro and in vivo as well as robust bystander activity against tumor and stromal cells not expressing the target antigen mesothelin, while maintaining a tolerable safety profile in vivo. Single-dose NAV-001-PNU demonstrated robust tumor regression of a number of patient-derived xenograft models from different tumor types regardless of MUC16/CA125 expression. These findings suggest that identification of HIO-refractory antibodies to be used in ADC format may improve therapeutic efficacy as observed for NAV-001 and warrants NAV-001-PNU’s advancement to human clinical trials as a monotherapy to treat mesothelin-positive cancers. Citation Format: Luigi Grasso, J. Bradford Kline, Nicholas C. Nicolaides. NAV-001, a high-efficacy antibody-drug conjugate targeting mesothelin with improved delivery of potent payload by counteracting MUC16/CA125 effects [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 1876.

Abstract Background: Upregulated glucose metabolism is one of the strategies cancer cells use to fuel their abnormal cell growth and division. Targeting the cancer-specific glucose transporter GLUT-1 is a promising approach to restrict glucose uptake and challenge the metabolic needs of tumor cells. Antibodies, as opposed to small molecule inhibitors, are an attractive modality to therapeutically target complex muti-pass membrane transporters. Here we report the development of antibodies that very specifically block the function of only GLUT-1. Methods: Monoclonal antibodies against GLUT-1 were generated using virus-like particles. For immunization, chickens were used as they are evolutionarily distant from mammals and can produce antibodies with prolonged CDR3-s in VH, which could facilitate their binding to the limited extracellular region of GLUT-1. Antibody discovery was performed with HybriFree B cell cloning technology followed by functional screens with 2-deoxyglucose uptake interference or cell proliferation measurements. Results: The discovered antibodies specifically bind to GLUT-1 with low nanomolar EC50 values and do not target other glucose transporters. The lead candidate, ICO-33, inhibits glucose uptake and rewires the metabolism of GLUT-1-dependent cancer cells to rely on oxidative phosphorylation. This results in a significantly synergistic cancer proliferation inhibition with ICO-33 and OXPHOS inhibitor combinations in doses that do not inhibit proliferation as single agents. ICO-33 and OXPHOS inhibitor treatment is well-tolerated and demonstrates a drastic tumor growth inhibition in in vivo colorectal and pancreatic cancer models. Conclusions: We describe the discovery of highly specific monoclonal antibodies targeting GLUT-1. We further demonstrate that the restriction of the much-needed glucose uptake by ICO-33 makes cancer cells highly susceptible to OXPHOS inhibitor co-therapy both in vitro and in vivo, validating the antibody as a promising candidate for clinical development. Citation Format: Siret Tahk, Kai Virumae, Korneelia Anton, Paule Hermet, Robin Pau, Mario Plaas, Maiken Abel, Denis Belitškin, Luciano Galdieri, Steven Garner, Jillian Krings, Kaleb Collver, Emily Schultz, Kaitlyne Powers, Alastair King, Francisca Neethling, Anu Planken, Mart Ustav, Joan Terya, Andres Mannik, Mart Ustav. Development of therapeutic antibodies targeting the GLUT-1 transporter to restrict cancer cell growth [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 1876.

Abstract The use of adjuvant therapy in stage II-III colon cancer (CC) has been controversial for decades. No markers or models now is satisfactory enough to be adopted widely by the medical community. Here, we analyzed the proteomics of paraffin-embedded tissue (FFPE) biopsy samples from 230 CC patients (stages II-III) with up to 10 years of survival by using pressure cycling technology (PCT) and data-independent acquisition (DIA) mass spectrometry. Using machine learning, we established a novel and practical protein-based clinical classification system for CC prognosis which was further verified in an independent validation cohort. Using the nine protein-based clinical model, we improved the area under the curve (AUC) value to 0.926 in the training cohort and 0.872 in the validation cohort. Our promising model will be a potential approach to prognostication to aid in rational follow-up schedule-making and risk-adaptive individualized therapies. Citation Format: Kailun Xu, Xiaoyang Yin, Tiannan Guo, Shu Zheng, Yingkuan Shao. Prediction of overall survival in stage II and III colon cancer through machine learning of rapidly-acquired proteomics [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 7093.

Abstract Prescribing a combination of medications is a common strategy to enhance the effectiveness of disease treatment. While this approach aims to improve therapeutic outcomes, it may lead to unintended adverse drug reactions (ADRs) due to interactions between prescribed drugs and individual factors. Recognizing the importance of ADRs, various machine learning models have been developed. However, these models face limitations, particularly in predicting reactions induced by three or more drugs and in accounting for individual patient factors, such as age and medical history. To address these limitations, we propose a systematic framework that leverages medical data for predicting ADR signals. In the framework, the MIMIC-IV database was systematically preprocessed, and a series of machine learning models were developed that predict the ADR signals. The model predictions were validated using the eICU collaborative research database. The machine learning models process multiple inputs, including information on administered drugs, age, gender, ethnicity, and underlying medical conditions to predict ADR signals. The ADR signals are determined by classifying abnormalities in 20 specific laboratory test values, such as hematocrit, creatinine, and hemoglobin. The machine learning models developed in this study hold promise as a valuable tool for assessing potential risks, such as ADRs, associated with the concurrent use of multiple drugs. Citation Format: Junhyeok Jeon, Eujin Hong, Hyun Uk Kim. A systematic framework for predicting adverse drug reaction signals using medical data [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 4923.

Abstract Background: Although Black Americans have 2-3 times multiple myeloma (MM) incidence and mortality as compared to Whites, increasingly research is demonstrating that many may have genetic characteristics that have better survival outcomes. Yet delayed diagnoses and inappropriate first lines of therapy often wipe out whatever “advantages” they may have had, keeping mortality statistics higher than would be expected (PMID: 25469920). For underserved populations, a number of commonly accepted disparities exist in myeloma, and more broadly, cancer care. Patients who receive treatment by a high-volume provider (myeloma specialist) is a factor that can help patients with MM to have a longer life expectancy (PMID: 31487686). Therefore, we analyzed whether there is a disparity between race and receiving care from a myeloma specialist which may contribute to the differences in survival that is being seen. Methods: Validated real-world (RW) MM patient data was collected through HealthTree Cure Hub for Multiple Myeloma (healthtree.org). We examined the patient’s race which was either Caucasian American or Black American and whether or not they were being treated by a myeloma specialist. The association between race and specialist was examined by a chi-squared (X2) test. Results: In this retrospective analysis of 2,871 MM patients, we compared Caucasian Americans (n= 2716) and Black Americans (n=155). Our analysis revealed a significant association between the two races and whether or not they had a myeloma specialist, X2(1, N = 2,871) = 5.85, p = 0.015. Black Americans were less likely to be treated by a myeloma specialist. Conclusion: The findings of this RW analysis identify a glaring disparity in Black American MM patients and receiving care from a myeloma specialist. Addressing the underlying cause of the findings could extinguish other MM-related issues, such as delays in getting a correct diagnosis, lack of access to myeloma specialists, and many other non-medical issues leading to less-than-optimal outcomes from the majority of these Black American patients. Citation Format: Christian S. Cheung, Nathan W. Sweeney, Zena M. Tiu, Cynthia Chmielewski, Jennifer M. Ahlstrom. Comparison of multiple myeloma provider for Black Americans and Caucasian Americans [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 6287.

Abstract Colorectal cancer (CRC) disproportionately affects African American (AA) patients who experience a higher incidence and mortality than any other demographic groups in the United States. Yet molecular profiling in this population is scarce. Here, we performed whole-exome sequencing (WES) of 342 immediately snap-frozen tissues comprising AA CRC and matched, distant normal colon and identified distinct genomic drivers, DNA signatures, and, surprisingly, mosaic pathogenic mutations that are not present in the patient-matched CRC. We inferred T cell infiltration and tissue-resident microbiome (TR-M) directly from WES, enabling integrative analyses. Compared to normal colon, T cell infiltration is strongly decreased in tumours with microsatellite stability (MSS), while microsatellite unstable (MSI) and Polymerase Epsilon (POLE) mutant tumours had similar levels, suggesting immune evasion in MSS rather than increased T cell infiltration in MSI/POLE-mutants. Analyses of matched normal and tumour tissues revealed the evolving TR-M at unprecedented granularity and identified distinct niches of interactions with genomic and tumour-microenvironmental features. Together, this study represents the largest comprehensive genomic analysis of CRC in AA and provides a framework for performing a multi-layered analysis from a single analyte, thus, affording a cost-effective approach to expedite medical discoveries in underrepresented ancestries. Citation Format: Carino Gurjao, Edmond Chan, Michael J. Lee, Sho Hangai, Raul Rabadan, Tal Korem, Hanina Hibshoosh, Benjamin Izar. Single analyte profiling of the mutational, immune and microbiome landscape in african american colon cancer 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 994.