bluuebunny/crossref_metadata_2025 huggingface dataset:
Abstract 6798: CD8α+ dendritic cells potentiate the antitumor and immune activities against murine ovarian cancers
Authors: Lee Shin-Wha , Oh Dasol , Lee Hyunah , Lee Kyung-Won , Kim Min-Je , Kang Sung Wan , Lee Young-Jae , Kim HyunSoo , Kim Yong-Man
Published: April 2023

Objectives: Dendritic cell (DC) based immunotherapies have been shown to be a potential treatment option for various cancers; however, the exact strategies in ovarian cancer remain unknown. This study aimed to evaluate the effectiveness of mouse CD8α+ dendritic cells (DCs), corresponding to human CD141+ DCs, derived from bone marrow (BM) hematopoietic stem cells (HSCs) in a syngeneic and orthotopic mouse ovarian cancer model.

Methods: Stem-DCs from HSCs and Mono-DCs from monocytes were generated from the bone marrow mononuclear cells (BM-MNCs) of C57BL/6 mice in condition of pulsing with ID8 tumor cell lysates. C57BL/6 mice were intraperitoneally injected with 5 × 106 ID8 cells. They were treated with vehicle, low/medium/high dose pulsed Stem-DCs, Mono-DCs, and unpulsed Stem-DCs. At 8 to 9 weeks, the treated mice were sacrificed, and tumor responses and immune responses, such as lymphocyte proliferation and cytokine secretion, were analyzed.

Results: Mono-DCs and Stem-DCs were characterized by CD11c+CD80+CD86+ and CD8α+Clec9a+ expression, respectively. They were confirmed by the secretion of immunostimulatory cytokines, such as interleukin (IL)-12 and interferon (IFN)-γ, and T cell proliferation was observed after maturation. Despite a lower dose compared with Mono-DCs, mice treated with pulsed Stem-DCs showed a reduced amount of ascitic fluid and lower body weights compared with those of vehicle treated mice (P = 0.0021 and P = 0.0092, respectively). These mice treated with pulsed Stem-DCs appeared to have fewer tumor implants which were usually confined in the epithelium of ovaries, diaphragm and peritoneum. All mice injected with DCs demonstrated longer survival than the vehicle group (P = 0.0187), especially the medium/high dose pulsed Stem-DC treatment groups. Moreover, these favorable tumor responses were associated with a low proportion of myeloid-derived suppressor cells (MDSCs) and regulatory T cells, high IL-12 and IFN-γ levels, and accumulation of several tumor-infiltrating lymphocytes.

Conclusions: We demonstrated that mouse CD8α+ DCs derived from BM HSCs could decrease tumor progression and enhance antitumor immune responses against murine ovarian cancer. Further studies are necessary to develop potent DC vaccines using human CD141+ DCs.

Citation Format: Shin-Wha Lee, Dasol Oh, Hyunah Lee, Kyung-Won Lee, Min-Je Kim, Sung Wan Kang, Young-Jae Lee, HyunSoo Kim, Yong-Man Kim. CD8α+ dendritic cells potentiate the antitumor and immune activities against murine ovarian cancers. [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 6798.
Abstract 6800: Unique autologous cancer vaccine comprised of irradiated whole tumor cells and MBTA (rWTC-MBTA) triggers antitumor immune response to prevent metastasis
Authors: Ye Juan , Wang Herui , Sun Mitchell , Uher Ondrej , Gilbert Mark R. , Pacak Karel , Zhuang Zhengping , Medina Rogelio , Chakraborty Samik , Zenka Jan
Published: April 2023

Despite the advances made in cancer treatment over the past decades, one statistic has remained unchanged: metastatic cancer accounts for 90 percent of annual cancer deaths in the United States. Our group previously demonstrated that an autologous whole tumor cell vaccine (rWTC-MBTA: irradiated autologous whole tumor cells pulsed with Mannan-BAM, TLR ligands, and anti-CD40 antibody) had a potent anti-tumor immune response and prolonged survival in a mouse colon carcinoma model. To investigate whether rWTC-MBTA would work in “cold” tumor models, we evaluated the vaccine’s effect on preventing and treating tumor metastasis in 4T1 breast tumors. Our data showed that vaccinated mice could significantly prevent lung metastasis in both intravenous injection and mammary pad subcutaneous implantation animal models. Further, we used another metastasis model that more closely mimics clinical practice by resecting the primary tumor after metastasis development. The data showed that vaccinated mice could prevent tumor recurrence, increase T-cell infiltration in the metastatic tumor, and prolong the survival curve. The mechanistic investigation by immunophenotyping revealed that rWTC-MBTA vaccination induced both effector memory (CD44+CD62L−) and center memory (CD44+CD62L+) T cells as well as increased overall CD4+ and CD8+ T-cell count while depletion experiments demonstrated that CD8+ T cells were required for vaccine efficacy. Isolated splenocytes co-cultured with 4T1 cells showed rWTC-MBTA significantly increased T-cell mediated cytotoxicity through TNF-a and IFN-γ in CD107a+CD4+ T cells and Granzyme B and IFN-γ in CD107a+CD8+ T cells. In all experiments, vaccination exerted negligible systemic toxicity. Collectively, our study demonstrates that the rWTC-MBTA vaccine is a safe and promising therapeutic option to prevent and treat tumor metastasis by triggering an antitumor immune response.

Citation Format: Juan Ye, Herui Wang, Mitchell Sun, Ondrej Uher, Mark R. Gilbert, Karel Pacak, Zhengping Zhuang, Rogelio Medina, Samik Chakraborty, Jan Zenka. Unique autologous cancer vaccine comprised of irradiated whole tumor cells and MBTA (rWTC-MBTA) triggers antitumor immune response to prevent metastasis. [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 6800.
Abstract 691: Irradiated whole tumor cells pulsed with mannan-BAM, TLR ligands and anti-CD40 antibody serve as a potent tumor cell vaccine against glioblastoma
Authors: Wang Herui , Medina Rogelio , Ye Juan , Chakraborty Samik , Uher Ondrej , Sun Mitchell , Zenka Jan , Gilbert Mark R. , Pacak Karel , Zhuang Zhengping
Published: April 2023

Despite numerous therapeutic advances in cancers, the treatment of glioblastoma multiforme (GBM) remains a challenge. Boosting T-lymphocyte mediated responses against GBM offers a promising approach towards solving this problem. Herein, we present a therapeutic vaccination strategy that promotes the phagocytosis of tumor cells, enhances tumor antigen presentation, and induces a tumor-specific adaptive immune response with subsequent tumor eradication. This strategy consists of subcutaneous injection of irradiated whole tumor cells (rWTC) pulsed with phagocytic agonists (Mannan-BAM), TLR ligands (LTA, Poly (I:C), and R-848), and anti-CD40 agonistic antibody (collectively abbreviated as rWTC-MBTA). We evaluated the therapeutic efficacy of rWTC-MBTA strategy in mouse syngeneic GBM tumor models with GL261 and SB28 cells. In GL261 GBM model, complete regression (CR) of intracranial tumors was achieved in 70% (7/10) of rWTC-MBTA treated animals while none survived in the control group. Of note, the therapeutic efficacy of rWTC-MBTA was abolished in CD4-T and/or CD8-T lymphocyte depleted mice. Immunophenotyping analyses of peripheral lymph nodes and brain tumors of rWTC-MBTA treated mice demonstrated increased antigen presenting cells (dendritic cells and MHC II+ monocytes) and increased cytotoxic IFNγ, TNFα, and granzyme B-secreting CD4-T and CD8-T cells. All three CR mice that were rechallenged with GL261 cells intracranially 14 months after their last rWTC-MBTA treatment resisted tumor development, confirming the establishment of long-term immunological memory. In SB28 GBM model, 80% (8/10) rWTC-MBTA treated mice survived past 95 days after tumor cell implantation without any GBM-related symptoms, with median survival being only 35 days in control groups. In summary, our study demonstrated that rWTC-MBTA strategy can induce potent adaptive immune response against GBM in pre-clinical models.

Citation Format: Herui Wang, Rogelio Medina, Juan Ye, Samik Chakraborty, Ondrej Uher, Mitchell Sun, Jan Zenka, Mark R. Gilbert, Karel Pacak, Zhengping Zhuang. Irradiated whole tumor cells pulsed with mannan-BAM, TLR ligands and anti-CD40 antibody serve as a potent tumor cell vaccine against glioblastoma [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 691.
Abstract 724: Leaving cancer patients behind for greener pastures: The clinical oncology workforce in Nigeria
Authors: Chidebe Runcie C.W.
Published: April 2023

Background: For a population of over 201 million, Nigeria has only 4 doctors per 10,000 patients and 16.1 nurses, midwives per 10,000 patients, and less than 100 clinical oncologists for over 100,000 cancer patients. While Nigeria has one of the worst cancer burdens in the world and workforce shortage; 9 in 10 Nigerian physicians are seeking for opportunities to leave for the USA, UK and Canada. To improve oncology care in Nigeria, it may be important to understand the push and pull factors contributing to migration of clinical oncology (CO) workforce. Mathew (2018), Vanderpuye, et al., (2019), Balogun, et al., (2017), and Adebayo, (2016) have done research on CO; however, their studies were vastly focused on the African continent and not country-specific nor focused on the CO workforce in Nigeria.

Aim: The aim of this study is to explore the push and pull factors to stay or leave clinical oncology workforce in Nigeria.

Method: Using a mixed-method research approach, 80 participants completed the questionnaire and 9 participants responded to semi-structured interview. Multiple linear regression and Grounded theory was used for the data analysis.

Results: The results show that CO workload and satisfaction were significantly related to turnover intention. The qualitative results showed that CO as a new area of specialization, mentorship, career growth and attractiveness of radiation science are pull factors. While, high CO workload, poor healthcare system, poor remuneration, corruption in the public sector, and few other themes are push factors. Empathy for patients, patriotism and sense of fulfilment unexpectedly emerged as retention factors in the study.

Conclusion: Nigeria can improve patient’s treatment outcome by the reduction of CO workload through the employment of more CO. More CO can be available for employment when they are attracted, and their training is optimized. Those employed can be retained by improving working conditions and the introduction of work benefits. Our

recommendations are that health leaders should create more CO training and awareness of CO in Nigeria.

Citation Format: Runcie C.W. Chidebe. Leaving cancer patients behind for greener pastures: The clinical oncology workforce in Nigeria [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 724.
Abstract 93: An endogenous molecular brake preventing APOBEC-driven tumor mutational burden, heterogeneity and therapy resistance
Authors: Mu Ping , Li Xiaoling , Wang Yunguan , Wang Tao , Deng Su
Published: April 2023

Tumor mutational burden and heterogeneity fuel resistance to many targeted therapies, which inevitably limits the clinical outcome of patients. The cytosine deaminase APOBEC proteins are major drivers of mutagenesis in human cancer, with over 70% of tumors exhibiting a mutational signature that is impacted by APOBEC activity. Nevertheless, the mechanisms through which tumor cells hijack the powerful APOBEC mutagenesis machinery to promote heterogeneity and therapy resistance remain largely unknown. Through a multi-disciplinary approach integrating bulk and single cell RNA-Seq (scRNA-Seq), whole-genome exome-sequencing (WES), and CRISPR library screening, we identified a long sought-after cell-intrinsic mechanism that prevents APOBEC-driven mutagenesis in non-malignant cells. The loss of this “molecular brake”, unleashes APOBEC3B-driven mutagenesis in malignant cells, which then becomes a key mutator and represents the long sought-after molecular source of driver mutations in some frequently mutated genes in cancers, including FOXA1, EP300, and AR. Functional screening identified eight crucial drivers for Androgen Receptor (AR)-targeted therapy resistance in prostate cancer that are mutated by APOBEC3B: BRD7, CBX8, EP300, FOXA1, HDAC5, HSF4, STAT3 and AR. Finally, contrary to conventional understanding, our study reveals that driver mutations in FOXA1 induced by APOBEC3B, not mutations in AR, evolutionarily outcompete other driver mutations and eventually dominate the resistant tumors. Collectively, these results uncover a cell-intrinsic mechanism that unleashes APOBEC-driven mutagenesis, which plays a significant role in conferring targeted therapy resistance and could be the potential therapeutic targets to overcome resistance.

Citation Format: Ping Mu, Xiaoling Li, Yunguan Wang, Tao Wang, Su Deng. An endogenous molecular brake preventing APOBEC-driven tumor mutational burden, heterogeneity and therapy resistance [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 93.
Abstract 936: Clinicogenomic predictors for the pattern of failure in high-grade glioma
Authors: Lee Joo Ho , Kang Byung-Hee , Lee Seungbok
Published: April 2023

Background: High-grade gliomas, the most common primary brain tumors, are highly lethal, and treatment options remain limited. Despite advances in genomic technologies, there are few molecular biomarkers to guide precision medicine for high-grade glioma. Here, we aimed to identify the clinicogenomic features associated with its prognosis and recurrence patterns.

Materials/Methods: Our single-institution retrospective analysis included 223 patients diagnosed with high-grade gliomas who underwent next-generation sequencing targeting 82 brain tumor-relevant genes. We categorized them according to the 2021 WHO classification, and their clinicopathological statuses, treatment characteristics, survival, and genomic profiles were analyzed.

Results: The most common genomic variants were TERT promoter (51%), TP53 (39%), IDH1/2 (18%), NF1 (13%), ATRX (12%), PTEN (11%), PIK3CA (9%), SETD2 (7%), and H3F3A (6%) mutation. Regarding copy number variants, amplification of EGFR (21%), PDGFRA (11%), CDK4 (9%) and loss of CDKN2A/2B (55%), PTEN (29%), 19q (17%), NF2 (14%), and RB1 (10%) were the most common copy number aberrations. At a median follow-up of 18 months (range, 2-54 months), 174 patients (78%) had progression or recurrences. A total of 15.2% of our patients were re-classified under the 2021 WHO classification, and there was a clear separation of overall survival(OS) and progression-free survival(PFS) curves between grade 3 and 4 groups using the revised grading system. On multivariate cox regression analysis, MYCN amplification (HR 6.08, p = 0.002) and SETD2 mutation (HR 0.19, p =0.06) were independent predictors of OS and PFS.

Conclusion: The assessment of genomic characteristics in conjunction with the pattern of failure for high-grade glioma aids in identifying patients who are likely to benefit from personalized medicine. The 2021 WHO grading system explains survival differences between grade 3 and 4 tumors better than the 2016 WHO classification dose. We identified SETD2 mutation and MYCN as prognostic biomarkers with potential therapeutic implications in patients with high-grade glioma.

Citation Format: Joo Ho Lee, Byung-Hee Kang, Seungbok Lee. Clinicogenomic predictors for the pattern of failure in high-grade glioma [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 936.
Abstract 973: Uncovering gene signatures of Ewings sarcoma drug sensitivity during the evolution of resistance
Authors: Lin-Rahardja Kristi , Scarborough Jessica , Hitomi Masahiro , Scott Jacob G.
Published: April 2023

The evolution of chemotherapeutic resistance can cause treatment failure in patients with metastatic Ewings sarcoma (EWS), a rare pediatric bone cancer. As resistance to the first-line therapy evolves, there is potential for the tumor to develop sensitivities to other chemotherapeutic agents besides the active treatment. This concept is known as collateral sensitivity, and it presents an opportunity for medical providers to plan more effective treatment regimens. However, it can be difficult to predict due to the stochastic nature of evolution. By analyzing gene expression patterns among independent populations of an EWS cell line that have repeatedly evolved collateral responses, we aim to extract a collection of gene signatures, or sets of genes, that will predict states of collateral sensitivity against various existing chemotherapies.

To accomplish this, we will treat independently evolving replicates of an EWS cell line (A673) with the standard-of-care therapy to evolve resistance. Throughout this treatment regimen, we will regularly screen for collateral sensitivity against 100 FDA-approved cancer drugs and perform bulk RNA-sequencing. When collateral sensitivity against a drug is observed, we will utilize the RNA-sequencing data to extract gene signatures using differential expression analysis. The signatures will then be validated using patient-derived xenografts collected in our lab as well as from collaborators.

When completed, the sizable archive of sensitivity signatures we expect to assemble could greatly streamline the process of treatment planning for EWS patients, especially those with advanced disease. When a patient's response to primary therapy begins to decline, RNA- sequencing can be performed on a tumor biopsy, gene expression patterns can be compared with the validated signature library, and the most appropriate drug for the individual patient can be determined and used for subsequent treatment. Using this method, a patient's sensitivity profile can be reassessed at any point. This proposed method of treatment planning mitigates the need for excessive treatment regimens that are not guaranteed to be effective for every patient, thereby expanding the reach of precision medicine and potentially improving outcomes for EWS patients.

Citation Format: Kristi Lin-Rahardja, Jessica Scarborough, Masahiro Hitomi, Jacob G. Scott. Uncovering gene signatures of Ewings sarcoma drug sensitivity during the evolution of resistance [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 973.
Abstract 998: A blood-based extracellular vesicles DNA methylation signature for colorectal cancer screening
Authors: Zhang Sheng , Wang Faming , Chen Mingxi , Kim Jeongyun , Lu Mengrou , He Hongzhang , Zheng Siyang
Published: April 2023

Colorectal cancer (CRC) is the third most common cancer worldwide and the fourth leading cause of cancer related deaths, accounting for an estimated 1.8 million new cancer diagnoses and over 880,000 deaths in 2018. Furthermore, CRC patients who are diagnosed at the most advanced (metastatic) stage is estimated to have the 5-year survival rate of 14%. Dramatically, studies shows that if it can be detected at an early stage when surgical removal is feasible, the 5-year survival rate significantly increases to 90%. Therefore, early detection for CRC with curative treatment intent is crucially important to significantly reduce the mortality and morbidity and even cure CRC. Extracellular vesicles (EVs) are lipid-bilayer-enclosed vesicles of sub-micrometer size that are secreted by virtually all cell types. They contain hundreds of different proteins, thousands of intact RNA species, and double-stranded DNA (dsDNA) fragments that sample the entire human genome. Recent findings further corroborate the potential role of EVs in early cancer screening, cancer diagnosis, treatment selection and monitoring. In this study, we used lipid nanoprobe (LNP) for EV isolation and methylation-specific qPCR assay for detecting SEPT9 methylation to develop a minimal invasive CRC screening test. Firstly, we have successfully detected promoter methylation of cancer specific genes SEPT9 in EVs derived from both genomic DNA and EV DNA of the CRC cell line. Secondly, we isolated EV using LNP from plasma samples in a cohort of 19 CRC patients and 9 healthy donor controls. In parallel, we isolated circulating free DNA (cfDNA) from the same cohort of the plasma samples using commercially cfDNA isolation Kit. Then, SEPT9 methylation signature was analyzed by our quantitative real-time PCR assay in these 28 EV DNA samples and 28 cfDNA samples, respectively. In the 19 CRC samples, we identified 10 SEPT9 gene methylation samples from LNP-isolated EV DNA and cfDNA, respectively. In 9 healthy control samples, no SEPT9 methylation was detection in the EV-DNA samples, while one false-positive was detected with cfDNA. Thus, the sensitivity and specificity of EV-DNA in the detection of SEPT9 gene methylation from CRC were determined to be 53% and 100% respectively. In comparison, the sensitivity and specificity of cfDNA are 53% and 89%, respectively from this preliminary pilot study. This indicated that EV-DNA might be superior to cfDNA in detecting SEPT9 gene methylation for CRC screening.

Citation Format: Sheng Zhang, Faming Wang, Mingxi Chen, Jeongyun Kim, Mengrou Lu, Hongzhang He, Siyang Zheng. A blood-based extracellular vesicles DNA methylation signature for colorectal cancer screening [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 998.
Abstract 999: Colocalization of MAGE-A3 and MAGE-A4 in bladder cancer
Authors: Gilmore Bailey , Gonzalez Rachel , Su Aubrey , Kong Dehe , Zewdu Eden , Yom Jina , Qu Tianli , Guo Zhaoying , Hu Xiaomin , Ren Qi , Zhang Ranran , Christenson Eric , Ma Yan , Yin Dezhong , Yin Patrick , Fu Wei , Liu Xuan , Allampallam Krishnan
Published: April 2023

The treatment of bladder cancers has improved with new immunotherapy such as PD-L1. However, not all bladder cancers respond to PD-L1 immunotherapy which is why new targets are being assessed. Melanoma-associated antigen gene A (MAGE-A) family proteins are expressed in a variety of tumors, with each MAGE-A protein having unique roles in cancer pathogenesis. One advantage of targeting MAGE-A family members is the lack of expression in normal tissues which makes them well-suited for targeted cancer immunotherapy. The challenge with screening the MAGE-A family is to find a specific antibody since the 12-member family has over 60% sequence in homology. In this study, we evaluate multiple MAGE-A3 and MAGE-A4 antibodies using CytoSections, a reproducible alternative to control tissue with an expression of target biomarkers. A series of antibodies specific to each MAGE-A3 and MAGE-A4 protein were discovered and used to screen twenty-five bladder cancer tissues. The results showed that MAGE-A3 was present in 9 of the 25 bladder cancers, while MAGE-A4 was present in 10 of the 25 bladder cancers evaluated; in the meantime, 7 bladder cancers were positive for both targets after double immunofluorescence staining with MAGE-A3 or A4 specific antibodies. The data presented here could be an important development in treatment protocols for pre-screening patients who are at risk. Our findings show that MAGE-A3 and MAGE-A4 can be both present in bladder cancer, suggesting that targeting both genes may be necessary for the success of immunotherapy treatment.

Citation Format: Bailey Gilmore, Rachel Gonzalez, Aubrey Su, Dehe Kong, Eden Zewdu, Jina Yom, Tianli Qu, Zhaoying Guo, Xiaomin Hu, Qi Ren, Ranran Zhang, Eric Christenson, Yan Ma, Dezhong Yin, Patrick Yin, Wei Fu, Xuan Liu, Krishnan Allampallam. Colocalization of MAGE-A3 and MAGE-A4 in bladder cancer [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 999.
Abstract SY15-01: Tumor agnostic dendritic cell vaccines
Authors: De Palma Michele
Published: April 2023

Dendritic cells (DCs) are specialized myeloid cells with the ability to uptake, process, and present antigens to T lymphocytes; they also generate cytokine and chemokine gradients that regulate immune cell trafficking, activation, and function. DCs pulsed with tumor antigens have been used as a platform for therapeutic vaccination in cancer. In a broadly tested clinical application called a DC vaccine, autologous monocyte-derived DCs (moDCs) are isolated from a patient with cancer, exposed to tumor antigens ex vivo (antigen loading), and matured before reinfusion to the patient. However, in spite of significant development and testing, DC vaccines based on antigen-loaded moDCs have delivered mixed clinical results. The suboptimal performance of DC vaccines may be due to the use of moDCs - a heterogenous population of non-professional antigen-presenting cells - and the artificial nature of the procedure used to "load" selected tumor antigens on moDCs ex vivo. To address both issues, we developed a DC vaccine that uses a population of mouse or human DC progenitors (DCPs) engineered to produce immunostimulatory cytokines. While not involving antigen loading, the new DC platform outperformed antigen-loaded moDCs in mouse models of cancer. Engineered DCPs produced professional cDC1 and cCD2 in mice, reprogrammed the tumor microenvironment to a form characterized by broad IFNg signaling, and inhibited tumors, including autochthonous models, in an antigen-agnostic fashion. In one application, engineered DCPs synergized with antigen-specific CAR-T cells to eradicate gliomas in mice.

Citation Format: Michele De Palma. Tumor agnostic dendritic cell vaccines. [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 SY15-01.
Abstract SY23-02: Mechanistic insights of brain tumor relapse
Authors: Rodriguez-Blanco Jezabel
Published: April 2023

Pediatric brain tumors are the number one cause of cancer-related death in children, with medulloblastoma (MB) being the most common type. Genomic-based classification has enabled the stratification of MB into four distinct molecular subgroups: WNT, Sonic Hedgehog, Group 3, and Group 4. Such classification allows a better understanding of these malignancies, which has resulted in a significant improvement in the stratification of clinical trials. Despite substantial progress made in the field, still, 30% of children with MB will relapse. Recurrent disease in MB is commonly metastatic and virtually none of these patients will live beyond the 1-year hallmark. These sobering statistics underscore the largely unmet need for brain tumor therapies aimed at treating or preventing the emergence of relapsed disease. In this session, we will review recent advances in the identification of treatment-resistant pools of brain tumor cells, giving special emphasis to the signaling mechanisms that allow these cell populations to evade therapeutics and expand.

Citation Format: Jezabel Rodriguez-Blanco. Mechanistic insights of brain tumor relapse. [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 SY23-02.
Abstract SY29-01: Integrating evolutionary dynamics into cancer therapy
Authors: Gatenby Robert A.
Published: April 2023

Evolution of resistance remains a barrier to successful therapy in most metastatic cancers despite the increasing number of treatment options. A major driver of the evolutionary capacity of cancer populations is the dynamic interactions of spatial and temporal variations in environmental conditions with malignant cells that can access a vast number of phenotypic properties encoded in the human genome. The research paradigm in cancer treatment remains focused on finding “magic bullets” that can kill all cancer cells while leaving normal cells unharmed - the cure for cancer. Current standard of care principles for metastatic cancers applies one or more drugs as though they were the cure for cancer - continuously at Maximum Tolerated Dose (MTD) until unambiguous evidence of tumor progression. However, because of the phenotypic diversity in most large metastatic cancers, this approach is usually unsuccessful because continuous MTD therapy will eventually kill the population of drug-sensitive cells and leave behind a population of resistant cancer cells that can proliferate unopposed by competition with other populations. I will discuss integration of evolutionary dynamics into cancer therapy. Arguably, this is already widespread because the search for magic bullets and the MTD treatment strategy is built upon an implicit assumption that cancer cure requires a one-cause, one-event extinction similar to the KT impact that eradicated non-avian dinosaurs. However, investigations of recent actual (e.g., Passenger pigeons) and attempted (e.g., pest management) species extinctions in the Anthropocene era have demonstrate more complex dynamics. In fact, most species extinctions are caused by a sequence of perturbations none of which, by itself, could eradicate the population. These dynamics can be integrated into evolution-based treatment approaches to control and perhaps cure currently fatal metastatic cancers with currently available (i.e., non-magic bullet) drugs.

Citation Format: Robert A. Gatenby. Integrating evolutionary dynamics into cancer therapy. [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 SY29-01.
Supplementary Data from High-Density Lipoprotein Induces Proliferation and Migration of Human Prostate Androgen–Independent Cancer Cells by an ABCA1-Dependent Mechanism
Authors: Sekine Yoshitaka , Demosky Steve J. , Stonik John A. , Furuya Yosuke , Koike Hidekazu , Suzuki Kazuhiro , Remaley Alan T.
Published: April 2023

Supplementary Data from High-Density Lipoprotein Induces Proliferation and Migration of Human Prostate Androgen–Independent Cancer Cells by an ABCA1-Dependent Mechanism
Supplementary Data from Transcription Factor Egr-1 Is Essential for Maximal Matrix Metalloproteinase-9 Transcription by Tumor Necrosis Factor α
Authors: Shin Soon Young , Kim Ji Ho , Baker Andrew , Lim Yoongho , Lee Young Han
Published: April 2023

Supplementary Data from Transcription Factor Egr-1 Is Essential for Maximal Matrix Metalloproteinase-9 Transcription by Tumor Necrosis Factor α
Supplementary Data from Cyclooxygenase-Deficient Pancreatic Cancer Cells Use Exogenous Sources of Prostaglandins
Authors: Omura Noriyuki , Griffith Margaret , Vincent Audrey , Li Ang , Hong Seung-Mo , Walter Kimberly , Borges Michael , Goggins Michael
Published: April 2023

Supplementary Figures S1-S3 and Supplementary Tables S1-S2.
Supplementary Figure 8 from Inhibition of DNA-Dependent Protein Kinase Induces Accelerated Senescence in Irradiated Human Cancer Cells
Authors: Azad Arun , Jackson Susan , Cullinane Carleen , Natoli Anthony , Neilsen Paul M. , Callen David F. , Maira Sauveur-Michel , Hackl Wolfgang , McArthur Grant A. , Solomon Benjamin
Published: April 2023

PDF file - 4.8MB, Representative immunofluorescence images of phospho-DNA-PKcs (Thr2609) foci in H460 cells at 30 minutes after 10 Gy radiation (x 60 magnification). Green, phospho-DNA-PKcs foci. Blue, DAPI staining.
Supplementary Figures 1-7 from Extracellular Matrix–Bound FGF2 Mediates Estrogen Receptor Signaling and Therapeutic Response in Breast Cancer
Authors: DiGiacomo Josh W. , Godet Inês , Trautmann-Rodriguez Michael , Gilkes Daniele M.
Published: April 2023

Figure S1. RNA sequencing of MCF7 cells cultured in ECM scaffolds indicate activation of estrogen response signatures. Figure S2. ER+ cell lines cultured in ECM scaffolds activate estrogen-responsive genes. Figure S3. ER+ cell lines cultured in ECM scaffolds enhance Erk phosphorylation. Figure S4. FGF2 activates the estrogen-like response of ER+ cells cultured in ECM scaffolds. Figure S5. Heatmap visualization on gene expression of Hallmark estrogen response early genes from biopsies of extratumoral regions of breast cancer patients with annotation of high or low mammographic breast density (<25% vs >=25%). Figure S6. Culturing of ER+ breast cancer cells in ECM scaffolds reduces sensitivity to endocrine therapies through ECM-FGF2. Figure S7. Proliferation and cell cycle analyses of MCF7 cells cultured in ECM scaffolds indicates reduction of arrest caused by endocrine therapy.
Figure S4 from Epstein-Barr Virus Induces Lymphangiogenesis and Lympth Node Metastasis via Upregulation of VEGF-C in Nasopharyngeal Carcinoma
Authors: Li Deng-Ke , Chen Xing-Rui , Wang Li-Na , Wang Jia-Hong , Wen Yue-Ting , Zhou Zi-Ying , Li Ji-Ke , Liu Jing-Xian , Cai Lin-Bo , Zhong Shui-Sheng , Lyu Xiao-Ming , Damola Faleti Oluwasijibomi , Li Min-Ying , Zhang Jing-Jing , Zeng Yu-Mei , Wang Qian-Li , Zhang Qian-Bing , Lyu Hao , Fu Xiao-Yan , Wang Wei , Li Xin , Huang Zhong-Xi , Yao Kai-Tai
Published: April 2023

BART15 and PHLPP1 are associated with NPC LN stage
Supplementary S3 from Combined Targeting of PARG and Wee1 Causes Decreased Cell Survival and DNA Damage in an S-Phase–Dependent Manner
Authors: Agostini Lebaron C. , Jain Aditi , Shupp Alison , Nevler Avinoam , McCarthy Grace , Bussard Karen M. , Yeo Charles J. , Brody Jonathan R.
Published: April 2023

Figure S3 shows IHC staining and quantification of Ki67 and phospho-h2ax
Supplementary Figure 1 from Radiomics Biomarkers Correlate with CD8 Expression and Predict Immune Signatures in Melanoma Patients
Authors: Aoude Lauren G. , Wong Bernadette Z.Y. , Bonazzi Vanessa F. , Brosda Sandra , Walters Shaun B. , Koufariotis Lambros T. , Naeini Marjan M. , Pearson John V. , Oey Harald , Patel Kalpana , Bradford Julia J. , Bloxham Conor J. , Atkinson Victoria , Law Phillip , Strutton Geoffrey , Bayley Gerard , Yang Samuel , Smithers B. Mark , Waddell Nicola , Miles Kenneth , Barbour Andrew P.
Published: April 2023

Kaplan-Meier (log-rank) analysis of MPP4 and SD3 showing the PFS and OS for stage III patients only. a. PFS for MPP4, **p=0.0017, b. OS for MPP4, *p=0.0117, c. PFS for SD3, ***p=0.0003 and d. OS for SD3, **p=0.0094.
Movie 5 from HER2 Isoforms Uniquely Program Intratumor Heterogeneity and Predetermine Breast Cancer Trajectories During the Occult Tumorigenic Phase
Authors: Ginzel Joshua D. , Acharya Chaitanya R. , Lubkov Veronica , Mori Hidetoshi , Boone Peter G. , Rochelle Lauren K. , Roberts Wendy L. , Everitt Jeffrey I. , Hartman Zachary C. , Crosby Erika J. , Barak Lawrence S. , Caron Marc G. , Chen Jane Q. , Hubbard Neil E. , Cardiff Robert D. , Borowsky Alexander D. , Lyerly H. Kim , Snyder Joshua C.
Published: April 2023

d16HER2 mammary intraepithelial neoplasm. d16HER2 shown in magenta. Krt14 antibody staining shown in green.
Supplementary Figure 5 from NP-ALT, a Liposomal:Peptide Drug, Blocks p27Kip1 Phosphorylation to Induce Oxidative Stress, Necroptosis, and Regression in Therapy-Resistant Breast Cancer Cells
Authors: Jilishitz Irina , Quiñones Jason Luis , Patel Priyank , Chen Grace , Pasetsky Jared , VanInwegen Allison , Schoninger Scott , Jogalekar Manasi P. , Tsiperson Vladislav , Yan Lingyue , Wu Yun , Gottesman Susan R.S. , Somma Jonathan , Blain Stacy W.
Published: April 2023

NP-ALT inhibits palbociclib-resistant cells, but still requires estrogen to induce ROS and necroptosis.
Supplementary Figure Legends from Dasatinib Stimulates Its Own Mechanism of Resistance by Activating a CRTC3/MITF/Bcl-2 Pathway in Melanoma with Mutant or Amplified c-Kit
Authors: Sabbah Malak , Krayem Mohammad , Najem Ahmad , Sales François , Miller Wilson , del Rincon Sonia , Awada Ahmad , Ghanem Ghanem E. , Journe Fabrice
Published: April 2023

Supplementary Figure Legends 1-4
Supplemental Information from Cytidine Deaminase APOBEC3A Regulates PD-L1 Expression in Cancer Cells in a JNK/c-JUN-Dependent Manner
Authors: Zhao Kailiang , Zhang Qiang , Flanagan Sheryl A. , Lang Xueting , Jiang Long , Parsels Leslie A. , Parsels Joshua D. , Zou Weiping , Lawrence Theodore S. , Buisson Rémi , Green Michael D. , Morgan Meredith A.
Published: April 2023

Supplemental Information
Supplementary Table 2 from The PI3K/mTOR Inhibitor Ompalisib Suppresses Nonhomologous End Joining and Sensitizes Cancer Cells to Radio- and Chemotherapy
Authors: Du Jie , Chen Fuqiang , Yu Jiahua , Jiang Lijun , Zhou Meijuan
Published: April 2023

Table S2. Full table of the screening results.
Supplementary Table S3 from SHOC2 Is a Critical Modulator of Sensitivity to EGFR–TKIs in Non–Small Cell Lung Cancer Cells
Authors: Terai Hideki , Hamamoto Junko , Emoto Katsura , Masuda Takeshi , Manabe Tadashi , Kuronuma Satoshi , Kobayashi Keigo , Masuzawa Keita , Ikemura Shinnosuke , Nakayama Sohei , Kawada Ichiro , Suzuki Yusuke , Takeuchi Osamu , Suzuki Yukio , Ohtsuki Sumio , Yasuda Hiroyuki , Soejima Kenzo , Fukunaga Koichi
Published: April 2023

The combination of osimertinib and celastrol demonstrated a synergistic anti-proliferative effect in PC9 cells and H1975 cells.
Supplementary Table S1 from SHOC2 Is a Critical Modulator of Sensitivity to EGFR–TKIs in Non–Small Cell Lung Cancer Cells
Authors: Terai Hideki , Hamamoto Junko , Emoto Katsura , Masuda Takeshi , Manabe Tadashi , Kuronuma Satoshi , Kobayashi Keigo , Masuzawa Keita , Ikemura Shinnosuke , Nakayama Sohei , Kawada Ichiro , Suzuki Yusuke , Takeuchi Osamu , Suzuki Yukio , Ohtsuki Sumio , Yasuda Hiroyuki , Soejima Kenzo , Fukunaga Koichi
Published: April 2023

A list of sgRNAs in a small-scale custom library
Figure S7 from Mastermind Like Transcriptional Coactivator 3 (MAML3) Drives Neuroendocrine Tumor Progression
Authors: Alzofon Nathaniel , Koc Katrina , Panwell Kristin , Pozdeyev Nikita , Marshall Carrie B. , Albuja-Cruz Maria , Raeburn Christopher D. , Nathanson Katherine L. , Cohen Debbie L. , Wierman Margaret E. , Kiseljak-Vassiliades Katja , Fishbein Lauren
Published: April 2023

C6 Oncogenic pathway analysis. GSEA of MAML3 dEx1 and FL transfected cells compared to control showed dysregulation of WNT and SHH signaling pathways. Filled circles represent an adjusted p value of less than 0.05, whereas empty circles represent an adjusted p value of less than 0.10. (NES- Normalized Enrichment Score)
Figure S4 from Mastermind Like Transcriptional Coactivator 3 (MAML3) Drives Neuroendocrine Tumor Progression
Authors: Alzofon Nathaniel , Koc Katrina , Panwell Kristin , Pozdeyev Nikita , Marshall Carrie B. , Albuja-Cruz Maria , Raeburn Christopher D. , Nathanson Katherine L. , Cohen Debbie L. , Wierman Margaret E. , Kiseljak-Vassiliades Katja , Fishbein Lauren
Published: April 2023

β-catenin and FL or dEx1 MAML3 colocalize in the nucleus. Cell lines (A. SK-N-SH, B. QGP-1, C. BON-1) were co-transfected with either FL or dEx1 MAML3 and Î²-catenin or control plasmid. Cells overexpressing FL or dEx1 MAML3 alone showed some faint nuclear accumulation of Î²-catenin, as denoted by the arrows. When FL or dEx1 MAML3 was co-transfected Î²-catenin to increase overall levels of Î²-catenin in the cell, the nuclear accumulation and colocalization with MAML3 was even more apparent. (scale bar represents 10 Î¼m)
Supplementary Figure 2 from SOX9 Defines Distinct Populations of Cells in SHH Medulloblastoma but Is Not Required for Math1-Driven Tumor Formation
Authors: Adolphe Christelle , Millar Amanda , Kojic Marija , Barkauskas Deborah S. , Sundström Anders , Swartling Fredrik J. , Hediyeh-zadeh Soroor , Tan Chin Wee , Davis Melissa J. , Genovesi Laura A. , Wainwright Brandon J.
Published: April 2023

S2. Math1CrePtchlox/Ptchlox;Math1 GFP mice display GFP expression in the majority of tumour cells
Table S1 from Epigenetic Silencing of BMP6 by the SIN3A–HDAC1/2 Repressor Complex Drives Melanoma Metastasis via FAM83G/PAWS1
Authors: Min Dongkook , Byun Jaemin , Lee Eun-Joon , Khan Abdul A. , Liu Christina , Loudig Oliver , Hu Wei , Zhao Yong , Herlyn Meenhard , Tycko Benjamin , Cole Phillip A. , Ryu Byungwoo
Published: April 2023

Supplementary Table S1 showing pathological and demographic information of patient samples
Supplementary Figure from The Role of ARID1A in the Nonestrogenic Modulation of IGF-1 Signaling
Authors: Jdeed Sham , Erdős Edina , Bálint Bálint L. , Uray Iván P.
Published: April 2023

Supplementary Figure from The Role of ARID1A in the Nonestrogenic Modulation of IGF-1 Signaling
Supplementary Appendix: Epidemiologic Questionnaire from Incremental Value of Pulmonary Function and Sputum DNA Image Cytometry in Lung Cancer Risk Prediction
Authors: Tammemagi Martin C. , Lam Stephen C. , McWilliams Annette M. , Sin Don D.
Published: April 2023

PDF file - 235K
Supplementary Fig 1C from Single Nucleotide Polymorphism–Based Genome-Wide Chromosome Copy Change, Loss of Heterozygosity, and Aneuploidy in Barrett's Esophagus Neoplastic Progression
Authors: Li Xiaohong , Galipeau Patricia C. , Sanchez Carissa A. , Blount Patricia L. , Maley Carlo C. , Arnaudo Jessica , Peiffer Daniel A. , Pokholok Dmitry , Gunderson Kevin L. , Reid Brian J.
Published: April 2023

Supplementary Fig 1C from Single Nucleotide Polymorphism–Based Genome-Wide Chromosome Copy Change, Loss of Heterozygosity, and Aneuploidy in Barrett's Esophagus Neoplastic Progression
Supplementary Fig 1A from Single Nucleotide Polymorphism–Based Genome-Wide Chromosome Copy Change, Loss of Heterozygosity, and Aneuploidy in Barrett's Esophagus Neoplastic Progression
Authors: Li Xiaohong , Galipeau Patricia C. , Sanchez Carissa A. , Blount Patricia L. , Maley Carlo C. , Arnaudo Jessica , Peiffer Daniel A. , Pokholok Dmitry , Gunderson Kevin L. , Reid Brian J.
Published: April 2023

Supplementary Fig 1A from Single Nucleotide Polymorphism–Based Genome-Wide Chromosome Copy Change, Loss of Heterozygosity, and Aneuploidy in Barrett's Esophagus Neoplastic Progression
Perspective from A Prediction Model for Lung Cancer Diagnosis that Integrates Genomic and Clinical Features
Authors: Beane Jennifer , Sebastiani Paola , Whitfield Theodore H. , Steiling Katrina , Dumas Yves-Martine , Lenburg Marc E. , Spira Avrum
Published: April 2023

Perspective from A Prediction Model for Lung Cancer Diagnosis that Integrates Genomic and Clinical Features
Supplementary Figure 2 from Aerosolized 3-Bromopyruvate Inhibits Lung Tumorigenesis without Causing Liver Toxicity
Authors: Zhang Qi , Pan Jing , North Paula E. , Yang Shoua , Lubet Ronald A. , Wang Yian , You Ming
Published: April 2023

PDF file - 205K
Supplementary Figure 2 from American Ginseng Suppresses Colitis through p53-Mediated Apoptosis of Inflammatory Cells
Authors: Jin Yu , Hofseth Anne B. , Cui Xiangli , Windust Anthony J. , Poudyal Deepak , Chumanevich Alex A. , Matesic Lydia E. , Singh Narendra P. , Nagarkatti Mitzi , Nagarkatti Prakash S. , Hofseth Lorne J.
Published: April 2023

Supplementary Figure 2 from American Ginseng Suppresses Colitis through p53-Mediated Apoptosis of Inflammatory Cells
Supplementary Figure 1 from Methyl-Selenium Compounds Inhibit Prostate Carcinogenesis in the Transgenic Adenocarcinoma of Mouse Prostate Model with Survival Benefit
Authors: Wang Lei , Bonorden Melissa J.L. , Li Guang-xun , Lee Hyo-Jeong , Hu Hongbo , Zhang Yong , Liao Joshua D. , Cleary Margot P. , Lü Junxuan
Published: April 2023

Supplementary Figure 1 from Methyl-Selenium Compounds Inhibit Prostate Carcinogenesis in the Transgenic Adenocarcinoma of Mouse Prostate Model with Survival Benefit
Supplementary Materials 4 from Bowman Birk Inhibitor Concentrate and Oral Leukoplakia: A Randomized Phase IIb Trial
Authors: Armstrong William B. , Taylor Thomas H. , Kennedy Ann R. , Melrose Raymond J. , Messadi Diana V. , Gu Mai , Le Anh D. , Perloff Marjorie , Civantos Francisco , Goodwin William Jarrard , Wirth Lori J. , Kerr Alexander Ross , Meyskens Frank L.
Published: April 2023

PDF - 140K, Characteristics of Placebo. In this section, estimates are given for the molar concentrations of certain compounds in BBIC and the Masa Harina placebo in the mouth and in the body of the oral leukoplakia patients.
Supplementary Materials 2 from Bowman Birk Inhibitor Concentrate and Oral Leukoplakia: A Randomized Phase IIb Trial
Authors: Armstrong William B. , Taylor Thomas H. , Kennedy Ann R. , Melrose Raymond J. , Messadi Diana V. , Gu Mai , Le Anh D. , Perloff Marjorie , Civantos Francisco , Goodwin William Jarrard , Wirth Lori J. , Kerr Alexander Ross , Meyskens Frank L.
Published: April 2023

PDF - 59K, Summary of Adverse Events. There were 322 case-report forms on adverse events from the 132 randomized patients. Of these 322, 147 were blank or listed only "None," "Not Applicable," "No Complaints" and the like. These were set aside, as were a further 37 reports dated before the subject was randomized. The number of adverse-event reports from the 132 randomized subjects dated on or after randomization was 138.
Supplementary Materials 1 from Bowman Birk Inhibitor Concentrate and Oral Leukoplakia: A Randomized Phase IIb Trial
Authors: Armstrong William B. , Taylor Thomas H. , Kennedy Ann R. , Melrose Raymond J. , Messadi Diana V. , Gu Mai , Le Anh D. , Perloff Marjorie , Civantos Francisco , Goodwin William Jarrard , Wirth Lori J. , Kerr Alexander Ross , Meyskens Frank L.
Published: April 2023

PDF - 53K, Clinical Impression from Photographs. Across study arms, 91 participants had evaluable photo pairs: 45 in the drug arm and 46 in the placebo arm
Supplementary Table 1 from β-Cryptoxanthin Restores Nicotine-Reduced Lung SIRT1 to Normal Levels and Inhibits Nicotine-Promoted Lung Tumorigenesis and Emphysema in A/J Mice
Authors: Iskandar Anita R. , Liu Chun , Smith Donald E. , Hu Kang-Quan , Choi Sang-Woon , Ausman Lynne M. , Wang Xiang-Dong
Published: April 2023

PDF file - 78K, Means body weight of mice
Related Article from Breaking the NF-κB and STAT3 Alliance Inhibits Inflammation and Pancreatic Tumorigenesis
Authors: Surh Young-Joon , Bode Ann M. , Dong Zigang
Published: April 2023

Related Article from Breaking the NF-κB and STAT3 Alliance Inhibits Inflammation and Pancreatic Tumorigenesis
Supplementary Table 2 from Caffeic Acid Phenethyl Ester Suppresses the Proliferation of Human Prostate Cancer Cells through Inhibition of p70S6K and Akt Signaling Networks
Authors: Chuu Chih-Pin , Lin Hui-Ping , Ciaccio Mark F. , Kokontis John M. , Hause Ronald J. , Hiipakka Richard A. , Liao Shutsung , Jones Richard Baker
Published: April 2023

XLS file - 14K, This file contains data from the micro-western array protein analysis
Supplementary Figures 1-3 from An EMILIN1-Negative Microenvironment Promotes Tumor Cell Proliferation and Lymph Node Invasion
Authors: Danussi Carla , Petrucco Alessandra , Wassermann Bruna , Modica Teresa Maria Elisa , Pivetta Eliana , Belluz Lisa Del Bel , Colombatti Alfonso , Spessotto Paola
Published: April 2023

PDF file - 274K, Additional information for Figure 3 and 6 and full length blots for Figure 2K and Figure 4C
Related Article from Oral Cancer Prevention Advances with a Translational Trial of Green Tea
Authors: Shin Dong M.
Published: April 2023

Related Article from Oral Cancer Prevention Advances with a Translational Trial of Green Tea