bluuebunny/crossref_metadata_2025 huggingface dataset:
Abstract PO2-25-01: Tumor Derived Chitinase-3 like 1 Induces Neutrophil Extracellular Traps that Promote T cell Exclusion and Resistance to Immunotherapies in Breast Cancer
Authors: Taifour Tarek , Attalla Sherif Samer , Zuo Dongmei , Gu Yu , Sanguin-Gendreau Virginie , Dall-Proud Hailey , Solymoss Emilie , Bui Tung , Kuasne Hellen , Papavasiliou Vasilios , Lee Chun Geun , Kamle Suchitra , Siegel Peter , Elias Jack , Park Morag , Muller William
Published: May 2024

Breast cancer remains the most prevalent cancer and a major cause of mortality affecting women worldwide. Chemotherapy along with radiation and surgery have long been the standard of care for breast cancer patients. However, devastating side effects, resistance to treatments and relapse are major concerns for patients and physicians. With the rise of immunotherapies as a treatment option for various cancers, there is a critical need to understand the mechanisms through which cancers evade the immune system. Targeting such mechanisms holds the key to improve patient response to immunotherapy, especially in breast cancer where efficacy rates remain low.

In a subset of poor outcome Triple Negative Breast Cancers, cytotoxic T cells are excluded from the tumor nest and restricted to the surrounding stroma, a phenomenon known as stromal restriction. Our data from genetically engineered mouse models and human tumors identified that the secreted cytokine Chitinase-3 like 1 (Chi3l1) promotes stromal restriction of T cells in several tumor types including breast, lung and colon. Chi3l1 ablation in pre-clinical models of breast cancer results in increased T cell infiltration into the tumor nest which delayed mammary tumorigenesis and improved response to immunotherapy. We further demonstrate that Chi3l1 promotes T cell exclusion through the direct induction and deposition of neutrophil extracellular traps (NETs) which form a barrier that restricts T cell entry. Neutrophil depletion or pharmacological disruption of NET formation abrogates Chi3l1-induced T cell exclusion and histologically phenocopies Chi3l1 ablation.

Thus, our results indicate that Chi3l1 is a major immunosuppressive cytokine that promotes breast cancer progression by inducing NET formation and inhibiting T cell infiltration. Given the importance of T cell infiltration in immune elimination of nascent tumors, the future targeting of Chi3l1 should improve immunotherapy efficacy and outcomes in patients with tumors characterized by a T cell excluded microenvironment.

Citation Format: Tarek Taifour, Sherif Samer Attalla, Dongmei Zuo, Yu Gu, Virginie Sanguin-Gendreau, Hailey Dall-Proud, Emilie Solymoss, Tung Bui, Hellen Kuasne, Vasilios Papavasiliou, Chun Geun Lee, Suchitra Kamle, Peter Siegel, Jack Elias, Morag Park, William Muller. Tumor Derived Chitinase-3 like 1 Induces Neutrophil Extracellular Traps that Promote T cell Exclusion and Resistance to Immunotherapies in Breast Cancer [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO2-25-01.
Abstract PO2-27-02: Re-sensitizing the Refractory Breast Cancer Bone Metastasis to Endocrine Therapies
Authors: Das Anindita , Ernst Cheyenne
Published: May 2024

Approximately 90% of Breast Cancer (BrCa) related deaths are caused by metastasis and bone is the first and most frequent site of breast cancer metastatic expansion, which can lead to severe pain, immobility, fractures, and nerve damage, as well as the development of metastases in other organs, hence; a poor quality of life in patients. Currently, treatment options for these bone metastases (BoM) are limited because most patients with BoM shows reduced ER dependency which leads to resistance to standard endocrine or hormonal therapies for estrogen receptor-positive (ER+) BrCa. The long-term goal of the proposed research is to develop a strategy where metastatic cancer cells in bone can be dependent on ER signaling again thereby restoring their sensitivity to endocrine therapies. We observed a transient loss of ER expression in concert with enhanced activity of the transcriptional coactivators YAP/TAZ - the downstream effectors of the Hippo pathway (responsible for regulating cell proliferation and death) during bone colonization by BrCa cells. We hypothesize that the interaction between cancer cells and osteoblasts in the bone microenvironment leads to the activation of calcium signaling in cancer cells, resulting in the de-phosphorylation and nuclear localization of YAP/TAZ which subsequently suppresses the transcription of the estrogen receptor gene (ESR). Our research strategy is as presented below. First, we will employ a combination of 2D/3D co-culture models of BoM along with a mechanical loading system and determine the molecular mechanism driving the dynamical activation of YAP/TAZ in BrCa BoM. Using a unique ex vivo BM model called Bone In Culture Array (BICA) which replicates the in-vivo conditions, we will determine if verteporfin, a YAP/TAZ antagonist, can synergize and possibly enhance the effects of Fulvestrant, an ER antagonist in current use for certain types of BrCa in preventing BoM outgrowths and treating established BoM in mice. This research could ultimately lead to a favorable combination strategy to treat endocrine-resistant BoM in BrCa patients and prolong their survival.

Citation Format: Anindita Das, Cheyenne Ernst. Re-sensitizing the Refractory Breast Cancer Bone Metastasis to Endocrine Therapies [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO2-27-02.
Abstract PO3-18-03: Preoperative single-dose camrelizumab and/or microwave ablation in women with early-stage breast cancer: A randomized window-of-opportunity trial
Authors: Zhou Wenbin , Xie Hui , Ding Qiang , Wang Shui
Published: May 2024

Immune checkpoint blockade (ICB) has shown low response rates for advanced breast cancer, and combinatorial strategies are needed to improve the effect of ICB. As an effective local therapy, microwave ablation (MWA) may be a trigger of antitumor immunity. This window-of-opportunity trial was conducted to determine the safety and feasibility of camrelizumab (anti-PD-1 antibody) combined with MWA in the treatment of early-stage breast cancer preoperatively. The peripheral immune response was also investigated. 60 participants were randomized to receive single-dose camrelizumab alone (n=20), microwave ablation (n=20), or both camrelizumab and microwave ablation (n=20), preoperatively. Camrelizumab and MWA were well tolerated alone and in combination. Different from that in single-dose camrelizumab or MWA group, participants showed stable quantity of blood cells after the combination therapy. After the combination therapy, peripheral CD8+T cells showed enhanced cytotoxic and effect-memory functions. Clonal expansional CD8+T cells showed different functions from emergent clones after the combination therapy, suggesting that the expansional clones may play a vital role in the enhanced biological functions of CD8+T cells. Enhanced interactions between clonal expansional CD8+T cells and monocytes was observed, suggesting monocytes contributed to enhanced functions of clonal expansional CD8+T cells. MHC I related pathways and interferon signaling pathways were activated in monocytes by the combination therapy. In conclusion, camrelizumab combined with MWA was feasible for the treatment of early-stage breast cancer. The peripheral CD8+T cells were activated after the combination therapy, dependent on monocytes with activated MHC I pathways.

Citation Format: Wenbin Zhou, Hui Xie, Qiang Ding, Shui Wang. Preoperative single-dose camrelizumab and/or microwave ablation in women with early-stage breast cancer: A randomized window-of-opportunity trial [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO3-18-03.
Abstract PO3-27-10: Financial Stress and Care Disruption in Breast Cancer: A Ten-Year National Health Interview Survey Analysis
Authors: Doyle Maya , Quinn Erina , Bell Sarah , Wekwerth Braelyn , Carlos Ruth
Published: May 2024

Background: Financial stress is an adverse event of BC. Increased availability of oral targeted therapy (OTT) is hypothesized to add to this burden. We assess financial stress at the population level as a function of availability of OTT. Design: We used 2013-2022 NHIS adult BC population data. Financial stress markers were care disruption, food insecurity and percent home ownership. Care disruption was defined as at least 1 event of skipping or taking less medication or delayed filling or unable to afford prescriptions. Available oral therapy Florida Blue July 2023 was cross-referenced with the NCI targeted therapy list for breast cancer as of July 2023. Initial FDA approval date for breast cancer for OTT determined the number of available OTT by survey year. We conducted a time-adjusted logistic regression to account of external effects such as COVID and adjusted for sociodemographics. Results: In a population of over 30 million respondents with BC, care disruption affected < 10%; food insecurity, < 1.3%, >83% reported home ownership. The number of available OTT did not affect outcomes. Survey year was associated with reduced care disruption (adjusted OR 0.82, 95% CI 0.68–0.99). Self-reported Black race affected home ownership (aOR 0.57, 95% CI 0.43-0.77) and any care disruption (a2.11, 95% CI 1.38-3.24). Non-White patients more likely reported food insecurity (aOR 5.56, 95% CI 2.58-12.01). Income < 200% of poverty level negatively affected outcomes. Stroke (aOR 1.97, 95% CI 1.09-3.55) and heart attack (aOR 2.10, 95% CI 1.11–4) history increased likelihood of care disruption. Conclusion: Available number of OTT did not influence financial stress in a BC population. Adverse sociodemographics and comorbidities correlated with care disruption. Our study was limited by absence of actual OTT use; further assessment at the individual level is needed.

Table. Outcomes

Citation Format: Maya Doyle, Erina Quinn, Sarah Bell, Braelyn Wekwerth, Ruth Carlos. Financial Stress and Care Disruption in Breast Cancer: A Ten-Year National Health Interview Survey Analysis [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO3-27-10.
Abstract PO4-04-01: Antitumor activity and safety of sacibertinib (Hemay022) in combination with endocrine therapy in patients with ER and HER2 both positive metastatic breast cancer: A phase Ib study
Authors: Li Hui-Ping , Zhang Qingyuan , Zhang Ruyan , Liu Yaxin , Hu Xianjun
Published: May 2024

Abstract

PURPOSE Sacibertinib (Hemay022) is a novel irreversible tyrosine kinase inhibitor (TKI) blocking epidermal growth factor receptor and human epidermal growth factor receptor 2 (HER2). This study aimed to explore the safety and efficacy of sacibertinib plus endocrine therapy in patients with estrogen receptor-positive (

PATIENTS AND METHODS Using a phase 1b 3+3 dose escalation and expansion study design, patients with ER+/HER2+ MBC were treated with sacibertinib (200mg-500mg daily) plus endocrine therapy including exemestane, letrozole, fulvestrant. The safety, pharmacokinetic and clinical efficacy, including objective response rate (ORR), clinical benefit rate (CBR), disease control rate (DCR) and progression-free survival (PFS) were assessed.

RESULTS A total of 55 ER+/HER2+ MBC patients pretreated with chemotherapy and anti-HER2 therapy were enrolled in the study between March, 2018 and July, 2021. The incidence of ORR ranged from 17.6% to 42.9%, DCR ranged from 63.0% to 86.8%, CBR ranged from 42.3% to 69.7%, and the overall median PFS was 9.0 (95% CI, 5.5 ~ 11.00) months. In the 400 mg Sacibertinib plus exemestane cohort (N = 18), ORR was 38.9% (7/18), DCR was 72.2%(13/18), CBR was 66.7%(12/18), and median PFS was 8.9 months; In the 500 mg Sacibertinib plus exemestane cohort (N = 12), ORR was 25.0%(3/12), DCR was 100.0%(12/12), CBR was 50.0%(6/12), and median PFS was 9.0 months. The ORR, CBR, and DCR were better in the 400 mg and above dose cohorts than in the 200 mg and 300 mg cohorts. The DCR of the 500 mg combined with exemestane cohort was better than that of the other dose cohorts. Sacibertinib plus endocrine therapy was well-tolerated without dose-limiting toxicities. The most frequent grade 3 adverse events included diarrhoea (9.1%), leucopenia(5.5%), neutropenia (3.6%). One (1.8%) had grade 4 hydropericardium.

CONCLUSION Sacibertinib plus endocrine therapy had a favorable safety profile and antitumor activity in patients with ER+/HER2+ MBC, 400-500mg daily showed more efficacy, supporting further assessment in randomized studies.

This figure showed response of Sacibertinib plus endocrine therapy in ER+/HER2+ metastatic breast cancer.

Citation Format: Hui-Ping Li, Qingyuan Zhang, Ruyan Zhang, Yaxin Liu, Xianjun Hu. Antitumor activity and safety of sacibertinib (Hemay022) in combination with endocrine therapy in patients with ER and HER2 both positive metastatic breast cancer: A phase Ib study [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO4-04-01.
Abstract PO4-05-12: High expression of SLC9A2 is correlation with lymphatic metastasis and poor survival in breast cancer
Authors: Cong Binbin , Cao Xiaoshan , Jiang Wen , Ye Lin
Published: May 2024

Background: SLC9A2 encodes Na+/H+ exchanger 2 which is an essential solute carrier protein on the surface of multiple cells. The prediction potentials of SLC9A2 in lymphatic metastasis and survival were unknow but explored in this study of breast cancer.

Methods: Expression of SLC9A2 was determined in breast cancers (n=127) using real time quantitative polymerase chain reaction. Transcript levels of this gene was analysed in the breast cancers for the implication in lymph node involvement and survival using Mann-Whitney test with SPSS (Version 27). The relation of prognosis was also analysed by Kaplan Meier plotter in breast cancer.

Results: In lymph node positive breast cancer, the expression of SLC9A2 shown an increase trend than no metastasis (n=43, median=25.9, interquartile range [IQR] [0.9-215.4] vs. n=44, median=4.9, IQR [0.2-31.8], p=0.1213). SLC9A2 expression in TNM stage Ⅱ was significantly higher than stage Ⅰ (n=31, median=42, IQR [0-195] vs. n=47, median=3.3, IQR [0.2- 31.6], p=0.0267) and also showed in the pathological type of invasive ductal carcinoma (n=27, median=42, IQR [3- 550] vs. n=35, median=3.3, IQR [0.2-31.8], p=0.0223). Kaplan Meier plotter showed over survival of SLC9A2 high expression was significantly worse than SLC9A2 low expression (66 months vs. 123.6 months, Hazard Ratio [HR]=1.57 [1.3-1.9], p=0.000), also found in estrogen receptor (ER) positive (63.8 months vs. 173.7 months, HR=2.19 [1.6-3.01], p=0.000). In patients with tamoxifen therapy, SLC9A2 high expression also had poor survival comparing to low expression (HR=2.86 [1.4-5.86], p=0.0026).

Conclusions: High expression of SLC9A2 is correlation with lymph node metastasis and poor survival in breast cancer. SLC9A2 could be as a predictor for lymphatic involvement and survival and might be an indicator for detection of resistance to endocrine therapy.

Citation Format: Binbin Cong, Xiaoshan Cao, Wen Jiang, Lin Ye. High expression of SLC9A2 is correlation with lymphatic metastasis and poor survival in breast cancer [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO4-05-12.
Abstract PO4-22-09: Impact of time to surgery after neoadjuvant chemotherapy on pCR rate in locally-advanced breast cancer
Authors: Petrovskiy Alexander , Amosova Viktory , Trofimova Oxana , Frolova Mona , Soloshenko Anastasya , Rumyantsev Alexey
Published: May 2024

Objective: Neoadjuvant chemotherapy along with surgical treatment are the important parts of treatment for locally advanced breast cancer. Extending the interval between the end of neoadjuvant chemotherapy and surgery may decrease tumor response in patients with locally advanced breast cancer. However, data if timing of surgery after neoadjuvant therapy affect the Pathologic complete response (pCR) rate is controversial.

Materials and methods: We performed a retrospective analysis of 874 consecutive patients with IIIA-IIIC breast cancer that received neoadjuvant chemotherapy and surgery between 2000 and 2020 in N.N. Blokhin National Cancer Research Center. The median interval between the last injection of chemotherapy and surgery was 30 days (range 10 to 95 days). The variables were compared using log-rank statistics and Cox regression model.

Results. Pathologic complete response (pCR) was registered in 250 (31,4%) patients. Univariate analysis showed that extending the interval between the end of neoadjuvant chemotherapy and surgery for each day were associated with decrease of probability of pCR (OR 0,982; p = 0,009). Patients with triple-negative and ER-/HER2+ achieved higher rates of pCR compared to luminal A subtype (p< 0,0001). Tumor grade, tumor size, Ki67 were independent predictive factors for tumor pCR (p < 0,001). Multivariate analysis also showed an independent negative effect of the time interval before surgery on the achieving pCR. Then the patients were stratified into three cohorts according to the time of surgery after neoadjuvant chemotherapy: < 22 days, 22-42 days, or >42 days. The odds ratio (OR) for pCR was 1 for < 22 days (reference), 0,833 for 22-42 days (p=0,332) and 0,576 for ≥43 days (p=0,033). Cox regression model demonstrated that the interval between the end of neoadjuvant chemotherapy and surgery (more than 42 days), tumor size, triple-negative and ER-/HER2+ were the significant predictive factors for pCR. Tumor grade, tumor size and age of patients were not independent predictive factors for in-breast pCR.

Conclusion: Our study showed improved pCR if surgery was performed within 6 weeks after the end of neoadjuvant chemotherapy in locally advanced breast cancer.

Results of multivariate logistic regression analysis to assess the probability of achieving complete pathomorphological regression

Results of multivariate logistic regression analysis to assess the probability of achieving complete pathomorphological regression

Citation Format: Alexander Petrovskiy, Viktory Amosova, Oxana Trofimova, Mona Frolova, Anastasya Soloshenko, Alexey Rumyantsev. Impact of time to surgery after neoadjuvant chemotherapy on pCR rate in locally-advanced breast cancer [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO4-22-09.
Abstract PO5-06-12: Genetic screen identifies epigenetic drivers of breast cancer brain metastasis
Authors: Chen Jocelyn , Cai Wesley , Xu Peng , Nguyen Don , Yan Qin
Published: May 2024

Metastatic breast cancer remains a major cause of cancer-related deaths in women, and there are few effective therapies against this advanced disease. Brain metastases, found in 15~35% of patients with breast cancer, are often incurable. Accumulating evidence suggests that key steps of tumor progression and metastasis are controlled by reversible epigenetic mechanisms. To systematically identify the druggable epigenetic regulators essential for breast cancer brain metastasis, we conducted an in vivo shRNA screen and identified multiple epigenetic regulators, including RNA acetyltransferase NAT10 as drivers of breast cancer brain metastasis. Knockdown of NAT10 significantly restrains breast cancer cell proliferation and migration in vitro and brain metastases in vivo. NAT10 promotes breast cancer cell growth through its RNA helicase activity but not its acetyltransferase activity. Integrative analyses of transcriptomics, proteomics, and NAT10 eCLIP-Seq data identify NAT10 downstream targets critical for breast cancer progression and metastasis. Thus, these results reveal novel therapeutic strategies to treat metastatic breast cancer.

Citation Format: Jocelyn Chen, Wesley Cai, Peng Xu, Don Nguyen, Qin Yan. Genetic screen identifies epigenetic drivers of breast cancer brain metastasis [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO5-06-12.
Abstract PO5-14-06: Transcriptomics-based drug screening in 3D ex vivo patient-derived breast cancer model and patient biopsy for personalized therapy
Authors: Zhang Yueyun , Ronchi Carlos Henrique Venturi , Ambrosini Giovanna , Liu Yuanlong , Aouad Patrick , Matvienko Daria , Merten Christoph , Brisken Cathrin
Published: May 2024

Breast cancer is a leading cause of cancer-related mortality for women worldwide. Hormone receptor-positive (HR+) breast tumors, which represent 70% of all breast cancer cases, are treated with endocrine therapy. However, not all patients benefit from this treatment regimen because of patient-to-patient variation. Therefore, high throughput drug screening system is warranted to enable personalized medicine. Patient-derived organoids, which serve as a screening platform, lose their hormone receptors and response upon ex vivo culturing, and may not be adequate models for HR+ breast tumors. Moreover, unidentified biological components in the widely-used basement membrane matrix, Matrigel, result in high batch-to-batch variations and poor reproducibility in organoid cultures. Here, we propose a hydrogel-based 3D ex vivo model with defined structural and chemical properties to test hormone and drug sensitivity of HR+ breast tumors from patient-derived xenografts (PDXs) and patient tumor biopsies using microfluidics. Our data demonstrate the feasibility of this model to preserve cell proliferation and hormone receptor expression over 7 days. We also demonstrate that responses to hormones and FDA-approved drugs are faithfully maintained in this model. Finally, to establish a high throughput hormone and drug testing workflow with transcriptomic readout, we multiplexed barcoded- and drug-treated tumor samples in a single experiment with bulk RNA-sequencing. Our preliminary data demonstrate patient-specific responses to hormones and drugs that correspond to patient genetic mutation profiles, treatment history, disease stages and subtypes. This platform also enables testing of drugs in clinical trials that shows promising therapeutic outcomes for breast cancer, such as CDK4/6i, AKTi, PARPi, mTORi and their combination with endocrine therapy, thanks to the high throughput of the screening system and the low consumption of patient-derived or patient tissue. Given the capability of combining this physiologically-relevant 3D ex vivo model with RNA-seq for HR+ breast tumors, this platform holds potential for high throughput compound testing and transcriptomic profiling of patient biopsies for personalized medicine.

Citation Format: Yueyun Zhang, Carlos Henrique Venturi Ronchi, Giovanna Ambrosini, Yuanlong Liu, Patrick Aouad, Daria Matvienko, Christoph Merten, Cathrin Brisken. Transcriptomics-based drug screening in 3D ex vivo patient-derived breast cancer model and patient biopsy for personalized therapy [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO5-14-06.
Abstract PO5-21-01: Carcinoma en cuirasse- a rare, but striking, cutaneous manifestation of metastatic breast cancer
Authors: Godbole Manasi , Wani Kashmira , Zia Shereen , Dabak Vrushali
Published: May 2024

Introduction:

Carcinoma en cuirasse is a rare cutaneous metastatic presentation most commonly arising from primary breast cancers, typically after mastectomy. It appears like cellulitis and later develops into thickened rough patches of skin and even nodules. Carcinoma en cuirasse holds a poor prognosis, and treatment is difficult. Chemotherapeutic agents are unable to reach the tumor cells necessary, and radiation is ineffective because of skin curvature.

Case Presentation:

We report a female in her 70s with prior history of left breast ductal carcinoma in situ status post-radiation and lumpectomy, who presented with skin thickening of the left breast and solid masses in bilateral breasts 10 years later. Biopsy showed invasive ductal carcinoma of left breast (estrogen receptor [ER]/progesterone receptor positive [PR], human epidermal growth factor receptor-2 [HER2] negative) and ductal carcinoma in situ of right breast (ER/PR positive). She underwent right breast lumpectomy; however, the left breast mastectomy was aborted due to worsening of her skin findings on preoperative examination. An excisional skin biopsy revealed poorly differentiated invasive ductal carcinoma involving the dermis, deep dermis and focally involving the epidermis. Her diagnosis changed to stage 4 breast cancer, specifically carcinoma en cuirasse. Systemic treatment was initiated with palbociclib and letrozole and subsequently, she underwent left breast mastectomy given an excellent response to initial therapy. Surgical biopsy interestingly was HER2 positive and therefore her regimen was changed to taxotere, trastuzumab and pertuzumab. She completed adjuvant treatment and has been on maintenance trastuzumab along with letrozole currently and is doing well 5 years later with negative PET scans.

Discussion:

Our case is unique due to diagnosis of carcinoma en cuirasse before mastectomy, change in HER2 receptor status during treatment and excellent response to therapy with ongoing response to date. We think that an early diagnosis as well as targeted treatment could be the possible reasons for prolonged survival of more than 5 years.

Conclusion:

Any unexplained skin findings in breast cancer patients should prompt consideration of carcinoma en cuirasse. With ongoing treatment advances, many newer therapy options are available for metastatic breast cancer. Based on our case, we think that patients with this disease can have better outcomes.

Citation Format: Manasi Godbole, Kashmira Wani, Shereen Zia, Vrushali Dabak. Carcinoma en cuirasse- a rare, but striking, cutaneous manifestation of metastatic breast cancer [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO5-21-01.
Abstract PO5-27-07: A novel ROR1 inhibitor CPD86 suppresses Triple-Negative Breast Cancer cells via regulation of AKT/GSK3β pathway
Authors: Ta Tram , Reed Victoria , Chandra Nikhil , Dwyer Nick , Fultang Norman , Gupta Shradheya , Singh Indrakant , Peethambaran Bela
Published: May 2024

Breast cancer is the second most commonly diagnosed cancer in women in the United States. The most aggressive subtype is triple negative breast cancer (TNBC), which accounts for 15-20% of new cases on average each year. Histologically, it is characterized by the absence of estrogen receptors (ER), progesterone receptors (PR) and human epidermal growth factor receptor 2 (HER2), which are typically targeted by hormone therapies such as tamoxifen, fulvestrant, or letrozole. Standard of care for TNBC includes traditional chemotherapy and radiation, which are detrimental to both cancerous and normal cells. Therefore, the lack of all hormone receptors in TNBC calls for the investigation of novel anti-cancer compounds that specifically target TNBC with minimal damage to non-cancerous tissues. Receptor orphan tyrosine kinase-like receptor 1 (ROR1) is an oncoprotein that is overexpressed in several human malignancies such as lung, breast, prostate and pancreatic cancers, but not in normal tissues. Inhibition of ROR1 signaling has shown to repress proliferation and induce apoptosis of cancer cells. Through in-silico docking and isothermal titration calorimetry, we identified a novel compound CPD86 that interacts with and inhibits ROR1. We hypothesize that CPD86 selectively targets TNBC cells by reducing the phosphorylation of AKT/GSK3β via the inhibition of ROR1. Our in vitro results suggest that CPD86 inhibits cell viability and induces intrinsic apoptosis of TNBC cells at a half-maximal inhibitory concentration of 2-5 µM, but not in normal breast epithelial cells with minimal ROR1 expression. CPD86 also represses TNBC cell migration and invasion while leaving non-malignant cells unharmed. This study highlights that ROR1 inhibitors could be developed as a potential therapeutic for TNBC and the data would serve as proof-of-concept justification for evaluation in other ROR1-upregulated cancers.

Citation Format: Tram Ta, Victoria Reed, Nikhil Chandra, Nick Dwyer, Norman Fultang, Shradheya Gupta, Indrakant Singh, Bela Peethambaran. A novel ROR1 inhibitor CPD86 suppresses Triple-Negative Breast Cancer cells via regulation of AKT/GSK3β pathway [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO5-27-07.
Abstract SoA1-03: Current overview of immunotherapy in breast cancer
Authors: Loi S.
Published: May 2024

T cell checkpoint inhibitors are now standard of care for patients with triple negative breast cancer. Currently these agents are combined with combination cytotoxic chemotherapy. In this talk we will cover the composition of the immune infiltrate, rationale for T cell therapies, more or less chemotherapy and biomarkers of response and resistance.

Citation Format: S. Loi. Current overview of immunotherapy in breast cancer [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr SoA1-03.
Abstract SS03-06: Screening for Health Related Social Needs, and now what?
Authors: Segarra-Vazquez B.
Published: May 2024

Screening cancer patients for health related social needs (HRSN) presents benefits and challenges for the patients as well as for the health care facilities. Who gets screened? How often? What are the results used for? What services can be provided? These are some of the issues that institutions face. At the same time patients can feel singled out, afraid to be honest thinking they would receive sub-optimal treatment, and have wrong expectations, among others. In this session we will address the importance of screening for HRSN such as transportation, housing, food security, and financial strain. Strategies to approach the patient and possible ways to address the needs will also be discussed.

Citation Format: B. Segarra-Vazquez. Screening for Health Related Social Needs, and now what? [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr SS03-06.
Supplementary Table 2 from SCUBE3 Exerts a Tumor-Promoting Effect in Tongue Squamous Cell Carcinoma by Promoting CEBPA Binding to the CCL2 Promoter
Authors: Zhu Minhui , Ma Yi , Wang Wei , Li Meng , Chen Shicai , Liu Fei , Shi Xiaoqiong , Bi Hongsen , Zhang Chen , Nie Fangfei , Zheng Hongliang , Zhang Caiyun
Published: May 2024

Table S2. Primers used in qPCR.
Supplementary Table 3 from Unraveling the Global Proteome and Phosphoproteome of Prostate Cancer Patient-Derived Xenografts
Authors: Sychev Zoi E. , Day Abderrahman , Bergom Hannah E. , Larson Gabrianne , Ali Atef , Ludwig Megan , Boytim Ella , Coleman Ilsa , Corey Eva , Plymate Stephen R. , Nelson Peter S. , Hwang Justin H. , Drake Justin M.
Published: May 2024

Supplementary Table 3. LuCaP Proteome VSN Normalized
Supplementary Table 27 from Unraveling the Global Proteome and Phosphoproteome of Prostate Cancer Patient-Derived Xenografts
Authors: Sychev Zoi E. , Day Abderrahman , Bergom Hannah E. , Larson Gabrianne , Ali Atef , Ludwig Megan , Boytim Ella , Coleman Ilsa , Corey Eva , Plymate Stephen R. , Nelson Peter S. , Hwang Justin H. , Drake Justin M.
Published: May 2024

Supplementary Table 27. LuCaP Proteome VSN Normalized z-scores
Supplementary Table 26 from Unraveling the Global Proteome and Phosphoproteome of Prostate Cancer Patient-Derived Xenografts
Authors: Sychev Zoi E. , Day Abderrahman , Bergom Hannah E. , Larson Gabrianne , Ali Atef , Ludwig Megan , Boytim Ella , Coleman Ilsa , Corey Eva , Plymate Stephen R. , Nelson Peter S. , Hwang Justin H. , Drake Justin M.
Published: May 2024

Supplementary Table 26. LuCaP Proteome VSN Normalized Differential Expression ROTS AdCa CR vs AdCa NCR
Supplementary Figure Legends 1-8 from Coregulation of NDC80 Complex Subunits Determines the Fidelity of the Spindle-Assembly Checkpoint and Mitosis
Authors: Kim Sehong , Lau Thomas T.Y. , Liao Man Kit , Ma Hoi Tang , Poon Randy Y.C.
Published: May 2024

Supplemental Figure legends
Supplementary Table 2 from Unraveling the Global Proteome and Phosphoproteome of Prostate Cancer Patient-Derived Xenografts
Authors: Sychev Zoi E. , Day Abderrahman , Bergom Hannah E. , Larson Gabrianne , Ali Atef , Ludwig Megan , Boytim Ella , Coleman Ilsa , Corey Eva , Plymate Stephen R. , Nelson Peter S. , Hwang Justin H. , Drake Justin M.
Published: May 2024

Supplementary Table 2. LuCaP Proteome Imputed Data
Supplementary Figure 9 from An Endosomal Acid-Regulatory Feedback System Rewires Cytosolic cAMP Metabolism and Drives Tumor Progression
Authors: Prasad Hari , Mandal Susmita , Mathew John Kandam Kulathu , Cherukunnath Aparna , Duddu Atchuta Srinivas , Banerjee Mallar , Ramani Harini , Bhat Ramray , Jolly Mohit Kumar , Visweswariah Sandhya S.
Published: May 2024

Supplementary Figure 9 shows data supporting the role of NHE9 on expression of MMP1 in colorectal cancer.
Supplementary Figure 3 from Unraveling the Global Proteome and Phosphoproteome of Prostate Cancer Patient-Derived Xenografts
Authors: Sychev Zoi E. , Day Abderrahman , Bergom Hannah E. , Larson Gabrianne , Ali Atef , Ludwig Megan , Boytim Ella , Coleman Ilsa , Corey Eva , Plymate Stephen R. , Nelson Peter S. , Hwang Justin H. , Drake Justin M.
Published: May 2024

Supplementary Figure 3. Overall linear regression plot
Supplementary Figure 8 from An Endosomal Acid-Regulatory Feedback System Rewires Cytosolic cAMP Metabolism and Drives Tumor Progression
Authors: Prasad Hari , Mandal Susmita , Mathew John Kandam Kulathu , Cherukunnath Aparna , Duddu Atchuta Srinivas , Banerjee Mallar , Ramani Harini , Bhat Ramray , Jolly Mohit Kumar , Visweswariah Sandhya S.
Published: May 2024

Supplementary Figure 8 shows data supporting the role of NHE9 in cytosolic cAMP homeostasis in colorectal cancer.
Supplementary Figure 6 from An Endosomal Acid-Regulatory Feedback System Rewires Cytosolic cAMP Metabolism and Drives Tumor Progression
Authors: Prasad Hari , Mandal Susmita , Mathew John Kandam Kulathu , Cherukunnath Aparna , Duddu Atchuta Srinivas , Banerjee Mallar , Ramani Harini , Bhat Ramray , Jolly Mohit Kumar , Visweswariah Sandhya S.
Published: May 2024

Supplementary Figure 6 shows data from Ingenuity Pathway Analysis of colorectal cancer cells expressing NHE9, and the association between enrichment scores for Ca2+ signaling and NHE9 expression in colorectal cancer samples.
Supplementary Figure 3 from An Endosomal Acid-Regulatory Feedback System Rewires Cytosolic cAMP Metabolism and Drives Tumor Progression
Authors: Prasad Hari , Mandal Susmita , Mathew John Kandam Kulathu , Cherukunnath Aparna , Duddu Atchuta Srinivas , Banerjee Mallar , Ramani Harini , Bhat Ramray , Jolly Mohit Kumar , Visweswariah Sandhya S.
Published: May 2024

Supplementary Figure 3 shows the experimental protocol for measuring endosomal pH in colorectal cancer cells.
Supplementary Figure 1 from An Endosomal Acid-Regulatory Feedback System Rewires Cytosolic cAMP Metabolism and Drives Tumor Progression
Authors: Prasad Hari , Mandal Susmita , Mathew John Kandam Kulathu , Cherukunnath Aparna , Duddu Atchuta Srinivas , Banerjee Mallar , Ramani Harini , Bhat Ramray , Jolly Mohit Kumar , Visweswariah Sandhya S.
Published: May 2024

Supplementary Figure 1 shows NHE9 immunohistochemistry in colorectal cancer and normal colon and rectal samples, and data analyzing gender differences in patient survival based on NHE9 expression.
Data from Unraveling the Global Proteome and Phosphoproteome of Prostate Cancer Patient-Derived Xenografts
Authors: Sychev Zoi E. , Day Abderrahman , Bergom Hannah E. , Larson Gabrianne , Ali Atef , Ludwig Megan , Boytim Ella , Coleman Ilsa , Corey Eva , Plymate Stephen R. , Nelson Peter S. , Hwang Justin H. , Drake Justin M.
Published: May 2024

Abstract
Resistance to androgen-deprivation therapies leads to metastatic castration-resistant prostate cancer (mCRPC) of adenocarcinoma (AdCa) origin that can transform into emergent aggressive variant prostate cancer (AVPC), which has neuroendocrine (NE)-like features. In this work, we used LuCaP patient-derived xenograft (PDX) tumors, clinically relevant models that reflect and retain key features of the tumor from advanced prostate cancer patients. Here we performed proteome and phosphoproteome characterization of 48 LuCaP PDX tumors and identified over 94,000 peptides and 9,700 phosphopeptides corresponding to 7,738 proteins. We compared 15 NE versus 33 AdCa samples, which included six different PDX tumors for each group in biological replicates, and identified 309 unique proteins and 476 unique phosphopeptides that were significantly altered and corresponded to proteins that are known to distinguish these two phenotypes. Assessment of concordance from PDX tumor-matched protein and mRNA revealed increased dissonance in transcriptionally regulated proteins in NE and metabolite interconversion enzymes in AdCa.
Implications:
Overall, our study highlights the importance of protein-based identification when compared with RNA and provides a rich resource of new and feasible targets for clinical assay development and in understanding the underlying biology of these tumors.
Supplementary Table S6 from Examining the Association between Abstinence from Smoking and Healthcare Costs among Patients with Cancer
Authors: Kypriotakis George , Kim Seokhun , Karam-Hage Maher , Robinson Jason D. , Minnix Jennifer A. , Blalock Janice A. , Cui Yong , Beneventi Diane , Kim Bumyang , Pan I.-Wen , Shih Ya-Chen Tina , Cinciripini Paul M.
Published: May 2024

Supplementary Table S6: Effects of insurance on abstinence and on cost, and abstinence on cost controlling for insurance
Supplementary Figure S4 from Combination of an Autoantibody Panel and Alpha-Fetoprotein for Early Detection of Hepatitis B Virus-Associated Hepatocellular Carcinoma
Authors: Shen Yajing , Chen Jiajun , Wu Jinyu , Li Tiandong , Yi Chuncheng , Wang Keyan , Wang Peng , Sun Changqing , Ye Hua
Published: May 2024

Supplementary Figure S4: These four candidate TAAbs were further confirmed by indirect ELISA with two testing cohorts. In the initial verification of candidate TAAbs in 120 sera, the expression of all four TAAbs was significantly different between the HBV-HCC and CHB groups (P<0.001) (Supplementary Figure S4A). These four TAAbs were further validated in a large dataset (663 sera). The results showed that the expression of four TAAbs was significantly different in the pairwise comparisons between the three groups (P<0.01), and the expression was highest in the HBV-HCC group and lowest in the CHB group (Supplementary Figure S4B).
Data from Germline and Somatic Fumarate Hydratase Testing in Atypical Uterine Leiomyomata
Authors: Kipnis Lindsay M. , Breen Katelyn M. , Koeller Diane R. , Levine Alison Schwartz , Yang Zelei , Jun Hyeji , Tayob Nabihah , Stokes Samantha M. , Hayes Connor P. , Ghazani Arezou A. , Hill Sarah J. , Rana Huma Q.
Published: May 2024

Abstract
Women with germline pathogenic variants (PV) in the fumarate hydratase (FH) gene develop cutaneous and uterine leiomyomata and have an increased risk of developing aggressive renal cell carcinomas. Many of these women are unaware of their cancer predisposition until an atypical uterine leiomyoma is diagnosed during a myomectomy or hysterectomy, making a streamlined genetic counseling process after a pathology-based atypical uterine leiomyoma diagnosis critical. However, the prevalence of germline pathogenic/likely PVs in FH among atypical uterine leiomyomata cases is unknown. To better understand FH germline PV prevalence and current patterns of genetic counseling and germline genetic testing, we undertook a retrospective review of atypical uterine leiomyomata cases at a single large center. We compared clinical characteristics between the FH PV, FH wild-type (WT), and unknown genetic testing cohorts. Of the 144 cases with atypical uterine leiomyomata with evaluable clinical data, only 49 (34%) had documented genetic test results, and 12 (8.3%) had a germline FH PV. There were 48 IHC-defined FH-deficient cases, of which 41 (85%) had FH testing and nine had a germline FH PV, representing 22% of the tested cohort and 18.8% of the FH-deficient cohort. Germline FH PVs were present in 8.3% of evaluable patients, representing 24.5% of the cohort that completed genetic testing. These data highlight the disconnect between pathology and genetic counseling, and help to refine risk estimates that can be used when counseling patients with atypical uterine leiomyomata.
Prevention Relevance:
Women diagnosed with fumarate hydratase (FH)-deficient uterine leiomyomata are at increased risk of renal cancer. This work suggests a more standardized pathology-genetic counseling referral pathway for these patients, and that research on underlying causes of FH-deficient uterine leiomyomata in the absence of germline FH pathogenic/likely pathogenic variants is needed.
Figure S5 from PVRL2 Suppresses Antitumor Immunity through PVRIG- and TIGIT-independent Pathways
Authors: Yang Jiuling , Wang Li , Byrnes James R. , Kirkemo Lisa L. , Driks Hannah , Belair Cassandra D. , Aguilar Oscar A. , Lanier Lewis L. , Wells James A. , Fong Lawrence , Blelloch Robert
Published: May 2024

Supplementary Figure S5: Combined loss of PVRL2 and PVR loss does not further inhibit tumor growth.
Figure S8 from High-Dimensional Analyses Reveal IL15 Enhances Activation of Sipuleucel-T Lymphocyte Subsets and Reverses Immunoresistance
Authors: Saeed Muhammad A. , Peng Bo , Kim Kevin , Rawat Kavita , Kuehm Lindsey M. , Siegel Zoe R. , Borkowski Ariel , Habib Nabih , Van Tine Brian , Sheikh Nadeem , Tuyen Vu , Thorek Daniel L.J. , Fehniger Todd A. , Pachynski Russell K.
Published: May 2024

IL-15 significantly improves sip-T mediated suppression of tumor growth in vivo
Figure S5 from High-Dimensional Analyses Reveal IL15 Enhances Activation of Sipuleucel-T Lymphocyte Subsets and Reverses Immunoresistance
Authors: Saeed Muhammad A. , Peng Bo , Kim Kevin , Rawat Kavita , Kuehm Lindsey M. , Siegel Zoe R. , Borkowski Ariel , Habib Nabih , Van Tine Brian , Sheikh Nadeem , Tuyen Vu , Thorek Daniel L.J. , Fehniger Todd A. , Pachynski Russell K.
Published: May 2024

IL-15 expands antigen-specific T-cell subsets of sip-T
Figure S7 from ILT2 and ILT4 Drive Myeloid Suppression via Both Overlapping and Distinct Mechanisms
Authors: Tian Jane , Ashique Amir M. , Weeks Sabrina , Lan Tian , Yang Hong , Chen Hung-I Harry , Song Christina , Koyano Kikuye , Mondal Kalyani , Tsai Daniel , Cheung Isla , Moshrefi Mehrdad , Kekatpure Avantika , Fan Bin , Li Betty , Qurashi Samir , Rocha Lauren , Aguayo Jonathan , Rodgers Col , Meza Marchelle , Heeke Darren , Medfisch Sara M. , Chu Chun , Starck Shelley , Basak Nandini Pal , Sankaran Satish , Malhotra Mohit , Crawley Suzanne , Tran Thomas-Toan , Duey Dana Y. , Ho Carmence , Mikaelian Igor , Liu Wenhui , Rivera Lee B. , Huang Jiawei , Paavola Kevin J. , O'Hollaren Kyle , Blum Lisa K. , Lin Vicky Y. , Chen Peirong , Iyer Anjushree , He Sisi , Roda Julie M. , Wang Yan , Sissons James , Kutach Alan K. , Kaplan Daniel D. , Stone Geoffrey W.
Published: May 2024

Supplementary Figure S7
Supplementary Table S3 from Machine Learning Links T-cell Function and Spatial Localization to Neoadjuvant Immunotherapy and Clinical Outcome in Pancreatic Cancer
Authors: Blise Katie E. , Sivagnanam Shamilene , Betts Courtney B. , Betre Konjit , Kirchberger Nell , Tate Benjamin J. , Furth Emma E. , Dias Costa Andressa , Nowak Jonathan A. , Wolpin Brian M. , Vonderheide Robert H. , Goecks Jeremy , Coussens Lisa M. , Byrne Katelyn T.
Published: May 2024

Supplementary Table S3. Table of antibodies used in the mIHC panel.
Supplementary Figure S3 from Machine Learning Links T-cell Function and Spatial Localization to Neoadjuvant Immunotherapy and Clinical Outcome in Pancreatic Cancer
Authors: Blise Katie E. , Sivagnanam Shamilene , Betts Courtney B. , Betre Konjit , Kirchberger Nell , Tate Benjamin J. , Furth Emma E. , Dias Costa Andressa , Nowak Jonathan A. , Wolpin Brian M. , Vonderheide Robert H. , Goecks Jeremy , Coussens Lisa M. , Byrne Katelyn T.
Published: May 2024

Supplementary Figure S3. A. SHAP plot showing the top 30 features driving the IA model. Features are ordered
on the y-axis such that those with a larger impact on the model’s predictions appear at the top of the SHAP plot.
SHAP values are shown on the x-axis, with a value of zero (center) indicating no impact on the model, and
negative or positive SHAP values predicting long DFS or short DFS, respectively. Red or blue dots indicate
presence or absence, respectively, of the corresponding feature in tissues. B. Box plot showing feature values for
each of the top 15 features for the model derived from IA regions of the αCD40 cohort split by DFS group (n = 30
regions from short DFS patients per feature; n = 13 regions from long DFS patients per feature). Each dot
represents the log10+1 normalized feature value for one tissue region, which was inputted into the classifier model. Boxes = Q1 to Q3; whiskers = smallest and largest
datapoints within 1.5*IQR +/- Q3/Q1; solid line = median. Mann–Whitney U-test used to determine
statistical significance. P-values corrected using the Benjamini–Hochberg procedure. *, P ≤ 0.05; **, P ≤ 0.01;
***, P ≤ 0.001.
Figure S13 from ILT2 and ILT4 Drive Myeloid Suppression via Both Overlapping and Distinct Mechanisms
Authors: Tian Jane , Ashique Amir M. , Weeks Sabrina , Lan Tian , Yang Hong , Chen Hung-I Harry , Song Christina , Koyano Kikuye , Mondal Kalyani , Tsai Daniel , Cheung Isla , Moshrefi Mehrdad , Kekatpure Avantika , Fan Bin , Li Betty , Qurashi Samir , Rocha Lauren , Aguayo Jonathan , Rodgers Col , Meza Marchelle , Heeke Darren , Medfisch Sara M. , Chu Chun , Starck Shelley , Basak Nandini Pal , Sankaran Satish , Malhotra Mohit , Crawley Suzanne , Tran Thomas-Toan , Duey Dana Y. , Ho Carmence , Mikaelian Igor , Liu Wenhui , Rivera Lee B. , Huang Jiawei , Paavola Kevin J. , O'Hollaren Kyle , Blum Lisa K. , Lin Vicky Y. , Chen Peirong , Iyer Anjushree , He Sisi , Roda Julie M. , Wang Yan , Sissons James , Kutach Alan K. , Kaplan Daniel D. , Stone Geoffrey W.
Published: May 2024

Supplementary Figure S13
Figure S6 from Chronic Stress Exacerbates the Immunosuppressive Microenvironment and Progression of Gliomas by Reducing Secretion of CCL3
Authors: Wang Xu , Zhang Long , Zhou Yi , Wang Yan , Wang Xiang , Zhang Yining , Quan Ankang , Mao Yufei , Zhang Yu , Qi Ji , Ren Zhongyu , Gu Linbo , Yu Rutong , Zhou Xiuping
Published: May 2024

Supplementary Figure 6. CCL3 treatment improves the migration of TAMs in vitro and the immune microenvironment of gliomas caused by chronic stress in vivo (Related to Fig.5)
Figure S5 from Chronic Stress Exacerbates the Immunosuppressive Microenvironment and Progression of Gliomas by Reducing Secretion of CCL3
Authors: Wang Xu , Zhang Long , Zhou Yi , Wang Yan , Wang Xiang , Zhang Yining , Quan Ankang , Mao Yufei , Zhang Yu , Qi Ji , Ren Zhongyu , Gu Linbo , Yu Rutong , Zhou Xiuping
Published: May 2024

Supplementary Figure 5. Chronic stress inhibits the secretion of CCL3/4 (Related to Fig.4)
Figure S8 from The TOPK Inhibitor HI-TOPK-032 Enhances CAR T-cell Therapy of Hepatocellular Carcinoma by Upregulating Memory T Cells
Authors: Zhang Qunfang , Zheng Fang , Chen Yuchao , Liang Chun-Ling , Liu Huazhen , Qiu Feifei , Liu Yunshan , Huang Hongfeng , Lu Weihui , Dai Zhenhua
Published: May 2024

Activation of mTOR diminishes the effects of HI-TOPK-032 on GPC3-CAR-T therapy and reduces CD8+ TCM frequency in tumor-bearing mice.