bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sarcoidosis in pregnancy
Authors: Odendaal Joshua , Mackie Fiona L , Tosounidou Sofia , Ghosh Swati , Knox Ellen 
Published: April 2024

Key content:

Sarcoidosis is an uncommon multi‐system disorder characterised by the presence of non‐caseating granulomas. It has a peak incidence between the ages of 20–40 years old.

The pathogenesis of sarcoidosis is uncertain; however, it is known to be associated with an exaggerated T helper 1 (TH1) immune response leading to systemic inflammation and granuloma formation.

Suppression in TH1 responses in pregnancy leads to disease remission in the majority of pregnancies. Nevertheless, the potential for decompensation in a subgroup remains, and consideration should be given to the pre‐pregnancy state.

Sarcoidosis is associated with increased risk of maternal‐fetal morbidity, including growth restriction and pre‐eclampsia. Clinical management should focus on medication optimisation and mitigation of this increased risk.

Learning objectives:

To understand the clinical features, pathogenesis and diagnosis of sarcoidosis.

To understand the effect of pregnancy on sarcoidosis.

To understand the effect of sarcoidosis on pregnancy and the related obstetric outcomes.

To understand the management of sarcoidosis in pregnancy.

Ethical issues:

There can be difficulties in appropriate management of medical disorders, such as sarcoidosis, with a limited obstetric evidence base.

There are challenges in decision‐making regarding continuation of pregnancy in severe disease with an uncertain evidence base.
Longitudinal evaluation of the cutaneous and rectal microbiota of German shepherd dogs with perianal fistulas undergoing therapy with ciclosporin and ketoconazole
Authors: Cain Christine L. , White Ellen , Citron Lindsey E. , Zheng Qi , Morris Daniel O. , Grice Elizabeth A. , Bradley Charles W. 
Published: April 2024

AbstractBackgroundPerianal fistulas are painful ulcers or sinus tracts that disproportionately affect German shepherd dogs and are proposed as a spontaneous animal model of fistulising Crohn's disease.ObjectivesTo characterise the rectal and cutaneous microbiota in German shepherd dogs with perianal fistulas and to investigate longitudinal shifts with lesion resolution during immunomodulatory therapy.AnimalsEleven German shepherd dogs with perianal fistulas and 15 healthy German shepherd dogs.Materials and MethodsAffected dogs were evaluated and swabbed at three visits, 30 days apart, while undergoing treatment with ciclosporin and ketoconazole. Healthy German shepherd dogs were contemporaneously sampled. Sites included the rectum, perianal skin and axilla. The microbiome was evaluated following sequencing of the V4 hypervariable region of the 16S ribosomal RNA (rRNA) gene.ResultsAlpha diversity was not significantly different between healthy and affected dogs at each of the three body sites (p > 0.5), yet rectal and perianal beta diversities from affected dogs differed significantly from those of healthy dogs at Day 0 (p = 0.004). Rectal and perianal relative abundance of Prevotella spp. increased and perianal Staphylococcus spp. relative abundance decreased in affected dogs over time, coincident with lesion resolution.Conclusions and Clinical RelevanceChanges in lesional cutaneous and rectal microbiota occur in German shepherd dogs with perianal fistulas and shift over time with lesion resolution during immunomodulatory therapy. Further investigations of the role of cutaneous and enteric microbiota in the pathogenesis of perianal fistulas, and whether manipulation of microbial populations may ameliorate disease, are needed.
Supplementary Figure S4 from Paclitaxel and Carboplatin in Combination with Low-intensity Pulsed Ultrasound for Glioblastoma
Authors: Habashy Karl J. , Dmello Crismita , Chen Li , Arrieta Victor A. , Kim Kwang-Soo , Gould Andrew , Youngblood Mark W. , Bouchoux Guillaume , Burdett Kirsten B. , Zhang Hui , Canney Michael , Stupp Roger , Sonabend Adam M. 
Published: April 2024

<p>Supplementary Figure 4. Paclitaxel and carboplatin combination lead to cell cycle arrest in the S and G2/M phases.
Results of flow cytometric analysis of synchronized GBM6 and MES83 cells that received PTX, CBDCA, or a combination of both drugs for 24 or 48 hours. On the right, we show the proportion of cells arrested at each of the SubG1, G0/G1, S, and G2/M phases.</p>
Supplementary Figure 8 from CB307: A Dual Targeting Costimulatory Humabody V<sub>H</sub> Therapeutic for Treating PSMA-Positive Tumors
Authors: Archer Sophie , Brailey Phillip M. , Song Minjung , Bartlett Phillip D. , Figueiredo Ines , Gurel Bora , Guo Christina , Brucklacher-Waldert Verena , Thompson H. Lorraine , Akinwale Jude , Boyle Samantha E. , Rossant Christine , Birkett Neil R. , Pizzey Julia , Maginn Mark , Legg James , Williams Richard , Johnston Colette M. , Bland-Ward Philip , de Bono Johann S. , Pierce Andrew J. 
Published: April 2024

<p>Supplementary Figure 8: Spheroid end-of-study T=240h images</p>
Supplementary Figure 7 from CB307: A Dual Targeting Costimulatory Humabody V<sub>H</sub> Therapeutic for Treating PSMA-Positive Tumors
Authors: Archer Sophie , Brailey Phillip M. , Song Minjung , Bartlett Phillip D. , Figueiredo Ines , Gurel Bora , Guo Christina , Brucklacher-Waldert Verena , Thompson H. Lorraine , Akinwale Jude , Boyle Samantha E. , Rossant Christine , Birkett Neil R. , Pizzey Julia , Maginn Mark , Legg James , Williams Richard , Johnston Colette M. , Bland-Ward Philip , de Bono Johann S. , Pierce Andrew J. 
Published: April 2024

<p>Supplementary Figure 7: CRISPR-mediated PD-L1 gene knock-out in DU145-PSMA cells</p>
Supplementary Figure 6 from CB307: A Dual Targeting Costimulatory Humabody V<sub>H</sub> Therapeutic for Treating PSMA-Positive Tumors
Authors: Archer Sophie , Brailey Phillip M. , Song Minjung , Bartlett Phillip D. , Figueiredo Ines , Gurel Bora , Guo Christina , Brucklacher-Waldert Verena , Thompson H. Lorraine , Akinwale Jude , Boyle Samantha E. , Rossant Christine , Birkett Neil R. , Pizzey Julia , Maginn Mark , Legg James , Williams Richard , Johnston Colette M. , Bland-Ward Philip , de Bono Johann S. , Pierce Andrew J. 
Published: April 2024

<p>Supplementary Figure 6: Synergy quantitation for CB307 / pembrolizumab combination</p>
Supplementary Figure 11 from CB307: A Dual Targeting Costimulatory Humabody V<sub>H</sub> Therapeutic for Treating PSMA-Positive Tumors
Authors: Archer Sophie , Brailey Phillip M. , Song Minjung , Bartlett Phillip D. , Figueiredo Ines , Gurel Bora , Guo Christina , Brucklacher-Waldert Verena , Thompson H. Lorraine , Akinwale Jude , Boyle Samantha E. , Rossant Christine , Birkett Neil R. , Pizzey Julia , Maginn Mark , Legg James , Williams Richard , Johnston Colette M. , Bland-Ward Philip , de Bono Johann S. , Pierce Andrew J. 
Published: April 2024

<p>Supplementary Figure 11: Vipivotide tetraxetan does not interfere with CB307 activity</p>
Abstract P07: Extracellular Vesicles Secreted from Daratumumab Resistant Cells Promote Resistance and Proliferation of Daratumumab Sensitive cells, possibly Through the Transfer of miRNA Cargo
Authors: Azaman Muhamad Irfan Bin , Chng Wee Joo , de Mel Sanjay , Mustafa Nurulhuda 
Published: April 2024

Abstract
Daratumumab (dara) is an anti-CD38 monoclonal antibody used for Multiple Myeloma (MM) treatment, but responses are heterogeneous, and resistance is inevitable.
We established three dara resistant (dara R) cell lines in Natural Killer T-cell Lymphoma (NKTL), T-cell acute lymphoblastic leukaemia (T-ALL) and MM via long-term exposure to increasing concentrations of dara. We have previously demonstrated that the exosome biogenesis pathway plays a significant role in the survival of dara R cell lines.
Coculture of dara sensitive (dara S) cell lines with dara R cell lines separated by a cell-impermeable transwell insert promoted cell proliferation and reduced response to dara treatment in dara S cell lines thereby suggesting a potential role for extracellular vesicles (EVs) in mediating these responses. To assess the specific role of EVs, we isolated dara R EVs and added it to the culture of dara S cells. We observed that uptake of dara R EVs directly promote proliferation and reduced cytotoxic response to dara treatment in dara S cells.
In this study, we seek to investigate the role of EVs secreted by dara R cells, in particular, that of EV-derived miRNAs.
Exosomal miRNAs are known to play a role in regulating cellular pathways driving cancer cell resistance and survival. To evaluate the potential role of EV-derived miRNA cargo, we performed miRNA sequencing of EVs isolated from the plasma fraction of bone marrow samples obtained from MM patients. We found that the EVs from patients with a progression free survival (PFS) of less than 2 years after dara based therapy had an enrichment of mir-155 and mir-181a as compared to those with a PFS longer than 2 years. These data align with our findings in the cell lines and suggest that these miRNAs may be utilised as potential biomarkers for daratumumab resistance.
Citation Format: Muhamad Irfan Bin Azaman, Wee Joo Chng, Sanjay de Mel, Nurulhuda Mustafa. Extracellular Vesicles Secreted from Daratumumab Resistant Cells Promote Resistance and Proliferation of Daratumumab Sensitive cells, possibly Through the Transfer of miRNA Cargo [abstract]. In: Proceedings of Frontiers in Cancer Science; 2023 Nov 6-8; Singapore. Philadelphia (PA): AACR; Cancer Res 2024;84(8_Suppl):Abstract nr P07.
Abstract P18: RHBDL2 PROMOTES NON-SMALL CELL LUNG CANCER METASTASIS AND OSIMERTINIB RESISTANCE BY ACTIVATING RAS/MEK/ERK SIGNALING PATHWAY THROUGH INTERACTION WITH FGFR
Authors: Deng Jun , Qin Jia-jia , Lin Neng-ming 
Published: April 2024

Abstract
Non-small cell lung cancer (NSCLC) is a highly malignant form of cancer, distinguished by prompt metastasis, restricted response to chemotherapy, and unfavorable prognosis. As a result, there is an imperative requirement to investigate novel therapeutic approaches for NSCLC. Rhomboid-like protein 2 (RHBDL2) is overexpressed in various tumor cells and is associated with poor prognosis. However, the relevance of RHBDL2 to NSCLC remains unclear. This study aims to investigate the potential role of RHBDL2 as a diagnostic and prognostic biomarker for NSCLC, as well as its biological functions and molecular mechanisms in NSCLC.
We found that RHBDL2 was highly expressed in human NSCLC cells and tissues, and was significantly correlated with distant metastasis and poor survival of NSCLC patients. Gain- and loss-of-function assays showed that RHBDL2 could accelerate NSCLC metastasis in vitro and in vivo. KEGG/GO enrichment analysis identified that the function of RHBDL2 was significantly associated with the activity of RAS signaling pathway. RNA-Seq results also suggested that RHBDL2 might be involved in the activation of the RAS/MEK/ERK signaling pathway. ERK1/2 inhibitor Ravoxertinib could partially restore the metastatic ability of NSCLC cells mediated by RHBDL2. CO-IP/MS results suggested that RHBDL2 interacted with FGFR. GST-pulldown assay confirmed the above findings. RHBDL2 could directly interact with FGFR and affect its phosphorylation, and promote NSCLC cell migration by activating the downstream RAS/MEK/ERK signaling pathway. In addition, we also found that RHBDL2 was involved in osimertinib resistance through FGFR/RAS pathway.
Our study results indicate that RHBDL2 promotes NSCLC cell migration and osimertinib resistance by interacting with FGFR and thereby activating the RAS/MEK/ERK signaling pathway. Moreover, it can serve as a novel diagnostic and prognostic biomarker for NSCLC patients.
Citation Format: Jun Deng, Jia-jia Qin, Neng-ming Lin. RHBDL2 PROMOTES NON-SMALL CELL LUNG CANCER METASTASIS AND OSIMERTINIB RESISTANCE BY ACTIVATING RAS/MEK/ERK SIGNALING PATHWAY THROUGH INTERACTION WITH FGFR [abstract]. In: Proceedings of Frontiers in Cancer Science; 2023 Nov 6-8; Singapore. Philadelphia (PA): AACR; Cancer Res 2024;84(8_Suppl):Abstract nr P18.
Abstract P22: C16orf72/HAPSTR1/TAPR1 Interacts with BRCA1 and Senataxin to Regulate R-loops at Stalled Replication Forks and Confer Resistance to PARP Disruption
Authors: Sharma Abhishek Bharadwaj , Ramlee Muhammad Khairul , Kosmin Joel , Higgs Martin R. , Wolstenholme Amy , Ronson George E. , Jones Dylan , Ebner Daniel , Shamkhi Noor , Sims David , Wijnhoven Paul W. G. , Forment Josep , Gibbs-Seymour Ian , Lakin Nicholas D. 
Published: April 2024

Abstract
Poly (ADP-ribose) polymerase (PARP) proteins play a crucial role in DNA repair, and their inhibition is toxic in cells with defects in homologous recombination (HR). Whilst this interaction is well-established, other synthetic lethal interactions with PARP1/PARP2 disruption are poorly explored. Hence, we performed a genome-wide CRISPR screen to identify genes which are synthetic lethal with PARP1/PARP2 disruption. We discovered that the uncharacterized C16orf72/HAPSTR1/TAPR1 gene is essential for the survival of PARP1/PARP2 double knock-out cells but not the parental wildtype cells. We further show that C16orf72 is a novel modulator of R-loop and is crucial in facilitating replication fork restart and suppressing DNA damage in response to replication stress. We show that C16orf72 functions in a parallel pathway to PARP1/PARP2 to suppress DNA:RNA hybrids that accumulate at stalled replication forks, and it does this by interacting with BRCA1 and the DNA/RNA helicase Senataxin.
Citation Format: Abhishek Bharadwaj Sharma, Muhammad Khairul Ramlee, Joel Kosmin, Martin R. Higgs, Amy Wolstenholme, George E. Ronson, Dylan Jones, Daniel Ebner, Noor Shamkhi, David Sims, Paul W. G. Wijnhoven, Josep Forment, Ian Gibbs-Seymour, Nicholas D. Lakin. C16orf72/HAPSTR1/TAPR1 Interacts with BRCA1 and Senataxin to Regulate R-loops at Stalled Replication Forks and Confer Resistance to PARP Disruption [abstract]. In: Proceedings of Frontiers in Cancer Science; 2023 Nov 6-8; Singapore. Philadelphia (PA): AACR; Cancer Res 2024;84(8_Suppl):Abstract nr P22.
Abstract P24: Elucidating the Mechanism of Action of Lenvatinib in Estrogen Receptor-Positive (ER+) Breast Cancer
Authors: Gandasasmita Natasha , Vaidya Gauri , Datta Arpita , Marvalim Charlie , Lim Joline Si Jing , Lee Soo Chin 
Published: April 2024

Abstract
Background: ER+ breast cancer is the most common subtype of breast cancer. Although most patients respond initially to endocrine therapy (ET), endocrine resistance inevitably develops, leading to disease progression. Lenvatinib, a multi-kinase inhibitor, demonstrated clinical benefit in the treatment of patients with advanced ER+ breast cancer who have progressed on ET in a phase Ib/II clinical trial from our group. Our study aims to elucidate the molecular mechanism of action of lenvatinib in ER+ breast cancer.
Methods: A cell viability assay was performed to assess the sensitivity of four ER+ cell lines to lenvatinib. Western blot was used to elucidate its effect on downstream pathway signalling, and cell cycle arrest investigated through flow cytometry. A series of functional assays, including BrdU, colony formation and wound-healing assays assessed proliferative, clonogenic and migratory activity respectively. The effect of lenvatinib on epithelial-mesenchymal transition (EMT) was analysed using RT-qPCR, and compared with siRNA knockdown (KD) of Fgfr1 and Fgfr2.
Results: ER+ cell lines demonstrated sensitivity to lenvatinib in the micromolar range. Western blot showed downregulation of FGFR1, FGFR2, pERK and pAKT expression post-treatment. Lenvatinib was found to induce a G1 phase arrest, suppressed cell proliferation in a dose-dependent manner, and diminished both the clonogenic ability and migratory activity of ER+ cells. Lenvatinib treatment reduced expression of Fgfr1, Fgfr2 and the mesenchymal markers N-cad and Fibronectin, while increasing the expression of the epithelial markers E-cad and Claudin-1, indicating potential inhibition of EMT. A similar change in EMT marker expression was observed in Fgfr1 KD but not Fgfr2 KD cells.
Conclusion: Lenvatinib demonstrated potent anti-cancer activity and induction of G1 phase arrest, leading to decreased cell proliferation, reduction of clonogenic ability and cell migration. EMT inhibition was also observed, possibly through the FGFR1 signalling pathway.
Citation Format: Natasha Gandasasmita, Gauri Vaidya, Arpita Datta, Charlie Marvalim, Joline Si Jing Lim, Soo Chin Lee. Elucidating the Mechanism of Action of Lenvatinib in Estrogen Receptor-Positive (ER+) Breast Cancer [abstract]. In: Proceedings of Frontiers in Cancer Science; 2023 Nov 6-8; Singapore. Philadelphia (PA): AACR; Cancer Res 2024;84(8_Suppl):Abstract nr P24.
Abstract P32: Cell Type-specific Genetic Therapy of Cancer, Virus Infection and Mitochondrial Disease
Authors: Loh (Rachel) Pei She , Poddar Sushmita , Chatterjee Kaustav , Wen Chiu Jing , Liang Derrick Wee Zan , Lai Fritz , Qingfeng Chen , Patzel Volker 
Published: April 2024

Abstract
Cell type-specific gene delivery which restricts gene transfer to therapy-relevant cells, hence reducing unwanted side effects caused by the ectopic expression of transgenes, remains one of the biggest challenges. To mitigate potential off-target effects, we developed a programmable cell type-specific gene therapy using an RNA trans-splicing-based approach for gene replacement therapy or suicide gene therapy that can selectively express therapeutic proteins or suicide signals based on the cell’s endogenous pre-mRNA expression profile.
Using the liver as a medical target organ, we developed a hepatocellular carcinoma (HCC)-specific trans-splicing based Herpes simplex virus thymidine kinase (HSVtk)/ganciclovir (GCV) suicide gene therapy approach. We rationally designed suicide RNAs that can target multiple HCC-related pre-mRNA biomarkers thereby increasing the overall concentration of targetable pre-mRNA.
For delivery, non-viral redosable dumbbell-shaped DNA vectors were designed, manufactured, and tested in tissue culture cells, in 3D patient-derived xenograft spheroids and in mouse model. For cell-type specific delivery, the conjugation of dumbbell vectors with GalNAc3 residues enabled targeted delivery into hepatoblastoma-derived human tissue culture cells.
To deliver nucleic acids into the mitochondria of human cells, we studied the long non-coding β2.7 RNA of the human cytomegalovirus which was previously reported to colocalise with mitochondrial complex I. Using thermodynamic profiling, we identified four thermodynamically conserved structural subdomains within the β2.7 RNA that are responsible for its mitochondrial targeting activity. A vector comprising eight mitochondrial targeting domains exhibited a three times higher mitochondrial targeting activity as compared with the parental β2.7 RNA. The amalgamation of mitochondrial targeting RNA and trans-splicing allows cell type-specific transcription of mRNA which can be delivered into mitochondria for mitochondrial gene therapy.
Trans-splicing based gene therapy represent a technology that is highly translational offering promising perspectives towards suicide gene therapy of any cancer types or incurable infections with integrating viruses and may enable cell type-specific mitochondrial gene therapy.
Citation Format: Pei She Loh (Rachel), Sushmita Poddar, Kaustav Chatterjee, Chiu Jing Wen, Derrick Wee Zan Liang, Fritz Lai, Chen Qingfeng, Volker Patzel. Cell Type-specific Genetic Therapy of Cancer, Virus Infection and Mitochondrial Disease [abstract]. In: Proceedings of Frontiers in Cancer Science; 2023 Nov 6-8; Singapore. Philadelphia (PA): AACR; Cancer Res 2024;84(8_Suppl):Abstract nr P32.
Abstract P33: Novel Reporter Cell Models for Efficient Interrogation of Helicase Activity in Cancer-associated DDX3X Mutations
Authors: Poh Zhi Sheng , Wei James Tan Chia , Wong Brandon Han Siang , Amuthavalli Kottaiswamy , Tan Suat Hoon , Grigoropoulos Nicholas Francis , Verma Navin Kumar 
Published: April 2024

Abstract
DDX3X is an ATP-dependent RNA helicase involved in diverse cellular processes. Somatic mutations in the DDX3X gene exhibit oncogenic or tumor suppressive activities depending on cancer types. However, helicase modulating roles of specific DDX3X mutations remain elusive mainly due to lack of an appropriate cell culture model system. Here, we report our development of novel transgenic cell lines capable of interrogating DDX3X helicase activity. To evaluate the helicase activity of the DDX3X mutations in question, we designed a reporter plasmid that measures the luciferase signal corresponding to the helicase activity. Using 8 different point mutations in the DDX3X that we identified earlier in relapsed/refractory patients with diffuse large B cell lymphoma (DLBCL), we show that these DDX3X mutants displayed defective helicase activity. DDX3X mutant knock-in DLBCL cells also displayed abolished helicase unwinding capabilities, validating our reporter cell models. We were able to extend the application of our reporter cells to interrogate Y chromosome-linked male paralog DDX3Y. In male lymphoma patients, ectopic DDX3Y expression can compensate for DDX3X loss to restore global protein synthesis. We narrowed down DDX3Y helicase and ATPase domains to be critical for cellular translation, ruling out DDX3Y involvement in ribosomal elongation. Unexpectedly, DDX3Y helicase is less efficient in RNA unwinding as compared to DDX3X revealing subtle differences despite having a high level of homology. The developed DDX3X reporter cells can be applied widely to evaluate the effects of DDX3X mutations in diseases as well as study the biology of DDX3X and DDX3Y.
Citation Format: Zhi Sheng Poh, James Tan Chia Wei, Brandon Han Siang Wong, Kottaiswamy Amuthavalli, Suat Hoon Tan, Nicholas Francis Grigoropoulos, Navin Kumar Verma. Novel Reporter Cell Models for Efficient Interrogation of Helicase Activity in Cancer-associated DDX3X Mutations [abstract]. In: Proceedings of Frontiers in Cancer Science; 2023 Nov 6-8; Singapore. Philadelphia (PA): AACR; Cancer Res 2024;84(8_Suppl):Abstract nr P33.
Abstract P37: Establishment of Gastric Organoids Biobank and Its Usage
Authors: Hagihara Takeshi , Huang Kie Kyon , Sundar Raghav , Uchihara Tomoyuki , Ng Clara Shi Ya , Tay Su Ting , Tan Angie Lay Keng , So Jimmy Bok Yan , Tan Patrick 
Published: April 2024

Abstract
Gastric cancer is highly heterogeneous. To analyze their biology, patient-derived organoids (PDOs) are useful because they maintain intra-tumor heterogeneity (ITH) as well as inter-patient heterogeneity. Recently, four groups reported the establishment of gastric PDOs. However, it is still not easy because of the need to overcome a common problem: “contamination” of the culture with “non-cancer cell”-derived organoids from the specimen. These non-cancer organoids often overgrow and became dominant. Furthermore, PDOs have another limitation. They contain only epithelial cells and no other types of cells, making it difficult to study the tumor microenvironment (TME).
Since October 2021, we have been working on establishing our own gastric PDO biobank. 63 gastric PDOs have been successfully established from 24 patients. Cancer organoids are enriched by manual selection under a microscopy. Our biobank contains 35 gastric cancer PDOs, 16 of which were confirmed as cancer using WES and WTS. Profiling for the remaining PDOs is ongoing.
12 fibroblasts and 26 cancer associated fibroblasts (CAFs) have also been successfully established. To overcome the difficulties of TME research with PDOs, co-culture platform for PDOs and fibroblasts has been established. This co-culture platform can provide new insights into the functions of CAFs, one of the major components of TME.
In this poster, I will describe the progress of our gastric PDO biobank establishment and the prospects for my projects using it.
Citation Format: Takeshi Hagihara, Kie Kyon Huang, Raghav Sundar, Tomoyuki Uchihara, Clara Shi Ya Ng, Su Ting Tay, Angie Lay Keng Tan, Jimmy Bok Yan So, Patrick Tan. Establishment of Gastric Organoids Biobank and Its Usage [abstract]. In: Proceedings of Frontiers in Cancer Science; 2023 Nov 6-8; Singapore. Philadelphia (PA): AACR; Cancer Res 2024;84(8_Suppl):Abstract nr P37.