bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from hENT1 Expression Predicts Response to Gemcitabine and Nab-Paclitaxel in Advanced Pancreatic Ductal Adenocarcinoma
Authors: Perera Sheron , Jang Gun Ho , Wang Yifan , Kelly Deirdre , Allen Michael , Zhang Amy , Denroche Robert E. , Dodd Anna , Ramotar Stephanie , Hutchinson Shawn , Tehfe Mustapha , Ramjeesingh Ravi , Biagi James , Lam Bernard , Wilson Julie , Fischer Sandra E. , Zogopoulos George , Notta Faiyaz , Gallinger Steven , Grant Robert C. , Knox Jennifer J. , O'Kane Grainne M.
Published: April 2023

AbstractPurpose:
Modified FOLFIRINOX (mFFX) and gemcitabine/nab-paclitaxel (GnP) remain standard first-line options for patients with advanced pancreatic ductal adenocarcinoma (PDAC). Human equilibrative nucleoside transporter 1 (hENT1) was hypothesized to be a biomarker of gemcitabine in the adjuvant setting, with conflicting results. In this study, we explore hENT1 mRNA expression as a predictive biomarker in advanced PDAC.
Experimental Design:
COMPASS was a prospective observational trial of patients with advanced PDAC. A biopsy was required prior to initiating chemotherapy, as determined by treating physician. Biopsies underwent laser capture microdissection prior to whole genome and RNA sequencing. The cut-off thresholds for hENT1 expression were determined using the maximal χ2 statistic.
Results:
253 patients were included in the analyses with a median follow-up of 32 months, with 138 patients receiving mFFX and 92 receiving GnP. In the intention to treat population, median overall survival (OS) was 10.0 months in hENT1high versus 7.9 months in hENT1low (P = 0.02). In patients receiving mFFX, there was no difference in overall response rate (ORR; 35% vs. 28%, P = 0.56) or median OS (10.6 vs. 10.5 months, P = 0.45). However, in patients treated with GnP, the ORR was significantly higher in hENT1high compared with hENT1low tumors (43% vs. 21%, P = 0.038). Median OS in this GnP-treated cohort was 10.6 months in hENT1high versus 6.7 months hENT1low (P < 0.001). In an interaction analysis, hENT1 was predictive of treatment response to GnP (interaction P = 0.002).
Conclusions:
In advanced PDAC, hENT1 mRNA expression predicts ORR and OS in patients receiving GnP.
Data from Molecularly Defined Subsets of Ewing Sarcoma Tumors Differ in Their Responses to IGF1R and WEE1 Inhibition
Authors: Soni Upendra Kumar , Wang Yuhua , Pandey Ram Naresh , Roberts Ryan , Pressey Joseph G. , Hegde Rashmi S.
Published: April 2023

AbstractPurpose:
Targeted cancer therapeutics have not significantly benefited patients with Ewing sarcoma with metastatic or relapsed disease. Understanding the molecular underpinnings of drug resistance can lead to biomarker-driven treatment selection.
Experimental Design:
Receptor tyrosine kinase (RTK) pathway activation was analyzed in tumor cells derived from a panel of Ewing sarcoma tumors, including primary and metastatic tumors from the same patient. Phospho-RTK arrays, Western blots, and IHC were used. Protein localization and the levels of key markers were determined using immunofluorescence. DNA damage tolerance was measured through PCNA ubiquitination levels and the DNA fiber assay. Effects of pharmacologic inhibition were assessed in vitro and key results validated in vivo using patient-derived xenografts.
Results:
Ewing sarcoma tumors fell into two groups. In one, IGF1R was predominantly nuclear (nIGF1R), DNA damage tolerance pathway was upregulated, and cells had low replication stress and RRM2B levels and high levels of WEE1 and RAD21. These tumors were relatively insensitive to IGF1R inhibition. The second group had high replication stress and RRM2B, low levels of WEE1 and RAD21, membrane-associated IGF1R (mIGF1R) signaling, and sensitivity to IGF1R or WEE1-targeted inhibitors. Moreover, the matched primary and metastatic tumors differed in IGF1R localization, levels of replication stress, and inhibitor sensitivity. In all instances, combined IGF1R and WEE1 inhibition led to tumor regression.
Conclusions:
IGF1R signaling mechanisms and replication stress levels can vary among Ewing sarcoma tumors (including in the same patient), influencing the effects of IGF1R and WEE1 treatment. These findings make the case for using biopsy-derived predictive biomarkers at multiple stages of Ewing sarcoma disease management.
Data from A Blood-Based Metabolite Panel for Distinguishing Ovarian Cancer from Benign Pelvic Masses
Authors: Irajizad Ehsan , Han Chae Y. , Celestino Joseph , Wu Ranran , Murage Eunice , Spencer Rachelle , Dennison Jennifer B. , Vykoukal Jody , Long James P. , Do Kim Anh , Drescher Charles , Lu Karen , Lu Zhen , Bast Robert C. , Hanash Sam , Fahrmann Johannes F.
Published: April 2023

AbstractPurpose:
To assess the contributions of circulating metabolites for improving upon the performance of the risk of ovarian malignancy algorithm (ROMA) for risk prediction of ovarian cancer among women with ovarian cysts.
Experimental Design:
Metabolomic profiling was performed on an initial set of sera from 101 serous and nonserous ovarian cancer cases and 134 individuals with benign pelvic masses (BPM). Using a deep learning model, a panel consisting of seven cancer-related metabolites [diacetylspermine, diacetylspermidine, N-(3-acetamidopropyl)pyrrolidin-2-one, N-acetylneuraminate, N-acetyl-mannosamine, N-acetyl-lactosamine, and hydroxyisobutyric acid] was developed for distinguishing early-stage ovarian cancer from BPM. The performance of the metabolite panel was evaluated in an independent set of sera from 118 ovarian cancer cases and 56 subjects with BPM. The contributions of the panel for improving upon the performance of ROMA were further assessed.
Results:
A 7-marker metabolite panel (7MetP) developed in the training set yielded an AUC of 0.86 [95% confidence interval (CI): 0.76–0.95] for early-stage ovarian cancer in the independent test set. The 7MetP+ROMA model had an AUC of 0.93 (95% CI: 0.84–0.98) for early-stage ovarian cancer in the test set, which was improved compared with ROMA alone [0.91 (95% CI: 0.84–0.98); likelihood ratio test P: 0.03]. In the entire specimen set, the combined 7MetP+ROMA model yielded a higher positive predictive value (0.68 vs. 0.52; one-sided P < 0.001) with improved specificity (0.89 vs. 0.78; one-sided P < 0.001) for early-stage ovarian cancer compared with ROMA alone.
Conclusions:
A blood-based metabolite panel was developed that demonstrates independent predictive ability and complements ROMA for distinguishing early-stage ovarian cancer from benign disease to better inform clinical decision making.
Data from Safety, Outcomes, and T-Cell Characteristics in Patients with Relapsed or Refractory MDS or CMML Treated with Atezolizumab in Combination with Guadecitabine
Authors: O'Connell Casey L. , Baer Maria R. , Ørskov Andreas Due , Saini Sunil Kumar , Duong Vu H. , Kropf Patricia , Hansen Jakob Werner , Tsao-Wei Denice , Jang Hyo Sik , Emadi Ashkan , Holmberg-Thyden Staffan , Cowland Jack , Brinker Brett T. , Horwood Kristin , Burgos Ryan , Hostetter Galen , Youngblood Benjamin A. , Hadrup Sine Reker , Issa Jean-Pierre , Jones Peter , Baylin Stephen B. , Siddiqi Imran , Grønbaek Kirsten
Published: April 2023

AbstractPurpose:
We hypothesized that resistance to hypomethylating agents (HMA) among patients with myelodysplastic syndrome (MDS) and chronic myelomonocytic leukemia (CMML) would be overcome by combining a programmed death-ligand 1 antibody with an HMA.
Patients and Methods:
We conducted a Phase I/II, multicenter clinical trial for patients with MDS not achieving an International Working Group response after at least 4 cycles of an HMA (“refractory”) or progressing after a response (“relapsed”) with 3+ or higher risk MDS by the revised International Prognostic Scoring System (IPSS-R) and CMML-1 or -2. Phase I consisted of a 3+3 dose-escalation design beginning with guadecitabine at 30 mg/m2 and escalating to 60 mg/m2 Days 1 to 5 with fixed-dose atezolizumab: 840 mg intravenously Days 8 and 22 of a 28-day cycle. Primary endpoints were safety and tolerability; secondary endpoints were overall response rate (ORR) and survival.
Results:
Thirty-three patients, median age 73 (range 54–85), were treated. Thirty patients had MDS and 3 had CMML, with 30% relapsed and 70% refractory. No dose-limiting toxicities were observed in Phase I. There were 3 (9%) deaths in ≤ 30 days. Five patients (16%) came off study for drug-related toxicity. Immune-related adverse events (IRAE) occurred in 12 (36%) patients (4 grade 3, 3 grade 2, and 5 grade1). ORR was 33% [95% confidence interval (CI), 19%–52%] with 2 complete remission (CR), 3 hematologic improvement, 5 marrow CR, and 1 partial remission. Median overall survival was 15.1 (95% CI, 8.5–25.3) months.
Conclusions:
Guadecitabine with atezolizumab has modest efficacy with manageable IRAEs and typical cytopenia-related safety concerns for patients with relapsed or refractory MDS and CMML.
Data from Gallium-68–labeled Peptide PET Quantifies Tumor Exposure of PD-L1 Therapeutics
Authors: Mishra Akhilesh , Kumar Dhiraj , Gupta Kuldeep , Lofland Gabriela , Sharma Ajay Kumar , Banka Dhanush S. , Hobbs Robert F. , Dannals Robert F. , Rowe Steven P. , Gabrielson Edward , Nimmagadda Sridhar
Published: April 2023

AbstractPurpose:
Immune checkpoint therapy (ICT) is currently ineffective in a majority of patients. Tumor drug exposure measurements can provide vital insights into mechanisms involved in the resistance of solid tumors to those therapeutics; however, tools to quantify in situ drug exposure are few. We have investigated the potential of programmed death-ligand 1 (PD-L1) pharmacodynamics, quantified using PET, to inform on the tumor exposure of anti–PD-L1 (aPD-L1) therapeutics.
Experimental Design:
To noninvasively quantify PD-L1 levels, we first developed a novel peptide-based gallium-68–labeled binder, [68Ga]Ga-DK223, and evaluated its in vivo distribution, pharmacokinetics, and PD-L1 specificity in preclinical models of triple-negative breast cancer and urothelial carcinoma with variable PD-L1 expression. We then quantified baseline and accessible PD-L1 levels in tumors as a noninvasive pharmacodynamic measure to assess tumor exposure to two aPD-L1 antibodies (avelumab and durvalumab).
Results:
DK223 exhibited a KD of 1.01±0.83 nmol/L for PD-L1 and inhibited the PD-1:PD-L1 interaction in a dose-dependent manner. [68Ga]Ga-DK223 provides high-contrast PET images within 60 minutes of administration and detects PD-L1 in an expression-dependent manner in xenograft models. PD-L1 pharmacodynamics measured using [68Ga]Ga-DK223-PET revealed that avelumab and durvalumab had similar exposure early during therapy, but only durvalumab exhibited sustained exposure at the tumor.
Conclusions:
[68Ga]Ga-DK223 detected variable PD-L1 levels and exhibited salient features required for clinical translation. [68Ga]Ga-DK223-PET could be useful for quantifying total PD-L1 levels at baseline and accessible PD-L1 levels during therapy to understand drug exposure at the tumor, thus supporting its use for guiding and optimizing ICT.
Data from Zinc Finger MYND-Type Containing 8 (ZMYND8) Is Epigenetically Regulated in Mutant Isocitrate Dehydrogenase 1 (IDH1) Glioma to Promote Radioresistance
Authors: Carney Stephen V. , Banerjee Kaushik , Mujeeb Anzar , Zhu Brandon , Haase Santiago , Varela Maria L. , Kadiyala Padma , Tronrud Claire E. , Zhu Ziwen , Mukherji Devarshi , Gorla Preethi , Sun Yilun , Tagett Rebecca , Núñez Felipe J. , Luo Maowu , Luo Weibo , Ljungman Mats , Liu Yayuan , Xia Ziyun , Schwendeman Anna , Qin Tingting , Sartor Maureen A. , Costello Joseph F. , Cahill Daniel P. , Lowenstein Pedro R. , Castro Maria G.
Published: April 2023

AbstractPurpose:
Mutant isocitrate dehydrogenase 1 (mIDH1) alters the epigenetic regulation of chromatin, leading to a hypermethylation phenotype in adult glioma. This work focuses on identifying gene targets epigenetically dysregulated by mIDH1 to confer therapeutic resistance to ionizing radiation (IR).
Experimental Design:
We evaluated changes in the transcriptome and epigenome in a radioresistant mIDH1 patient-derived glioma cell culture (GCC) following treatment with an mIDH1-specific inhibitor, AGI-5198. We identified Zinc Finger MYND-Type Containing 8 (ZMYND8) as a potential target of mIDH1 reprogramming. We suppressed ZMYND8 expression by shRNA knockdown and genetic knockout (KO) in mIDH1 glioma cells and then assessed cellular viability to IR. We assessed the sensitivity of mIDH1 GCCS to pharmacologic inhibition of ZMYND8-interacting partners: HDAC, BRD4, and PARP.
Results:
Inhibition of mIDH1 leads to an upregulation of gene networks involved in replication stress. We found that the expression of ZMYND8, a regulator of DNA damage response, was decreased in three patient-derived mIDH1 GCCs after treatment with AGI-5198. Knockdown of ZMYND8 expression sensitized mIDH1 GCCs to radiotherapy marked by decreased cellular viability. Following IR, mIDH1 glioma cells with ZMYND8 KO exhibit significant phosphorylation of ATM and sustained γH2AX activation. ZMYND8 KO mIDH1 GCCs were further responsive to IR when treated with either BRD4 or HDAC inhibitors. PARP inhibition further enhanced the efficacy of radiotherapy in ZMYND8 KO mIDH1 glioma cells.
Conclusions:
These findings indicate the impact of ZMYND8 in the maintenance of genomic integrity and repair of IR-induced DNA damage in mIDH1 glioma.

See related commentary by Sachdev et al., p. 1648
Data from Humoral and Cellular Immune Responses against SARS-CoV-2 after Third Dose BNT162b2 following Double-Dose Vaccination with BNT162b2 versus ChAdOx1 in Patients with Cancer
Authors: Debie Yana , Van Audenaerde Jonas R.M. , Vandamme Timon , Croes Lieselot , Teuwen Laure-Anne , Verbruggen Lise , Vanhoutte Greetje , Marcq Elly , Verheggen Lisa , Le Blon Debbie , Peeters Bart , Goossens Maria E. , Pannus Pieter , Ariën Kevin K. , Anguille Sébastien , Janssens Annelies , Prenen Hans , Smits Evelien L.J. , Vulsteke Christof , Lion Eva , Peeters Marc , van Dam Peter A.
Published: April 2023

Purpose:
Patients with cancer display reduced humoral responses after double-dose COVID-19 vaccination, whereas their cellular response is more comparable with that in healthy individuals. Recent studies demonstrated that a third vaccination dose boosts these immune responses, both in healthy people and patients with cancer. Because of the availability of many different COVID-19 vaccines, many people have been boosted with a different vaccine from the one used for double-dose vaccination. Data on such alternative vaccination schedules are scarce. This prospective study compares a third dose of BNT162b2 after double-dose BNT162b2 (homologous) versus ChAdOx1 (heterologous) vaccination in patients with cancer.
Experimental Design:
A total of 442 subjects (315 patients and 127 healthy) received a third dose of BNT162b2 (230 homologous vs. 212 heterologous). Vaccine-induced adverse events (AE) were captured up to 7 days after vaccination. Humoral immunity was assessed by SARS-CoV-2 anti-S1 IgG antibody levels and SARS-CoV-2 50% neutralization titers (NT50) against Wuhan and BA.1 Omicron strains. Cellular immunity was examined by analyzing CD4+ and CD8+ T-cell responses against SARS-CoV-2–specific S1 and S2 peptides.
Results:
Local AEs were more common after heterologous boosting. SARS-CoV-2 anti-S1 IgG antibody levels did not differ significantly between homologous and heterologous boosted subjects [GMT 1,755.90 BAU/mL (95% CI, 1,276.95–2,414.48) vs. 1,495.82 BAU/mL (95% CI, 1,131.48–1,977.46)]. However, homologous-boosted subjects show significantly higher NT50 values against BA.1 Omicron. Subjects receiving heterologous boosting demonstrated increased spike-specific CD8+ T cells, including higher IFNγ and TNFα levels.
Conclusions:
In patients with cancer who received double-dose ChAdOx1, a third heterologous dose of BNT162b2 was able to close the gap in antibody response.
Data from Novel Lymphocyte-Independent Antitumor Activity by PD-1 Blocking Antibody against PD-1+ Chemoresistant Lung Cancer Cells
Authors: Rotolo Ramona , Leuci Valeria , Donini Chiara , Galvagno Federica , Massa Annamaria , De Santis Maria Chiara , Peirone Serena , Medico Giovanni , Sanlorenzo Martina , Vujic Igor , Gammaitoni Loretta , Basiricò Marco , Righi Luisella , Riganti Chiara , Salaroglio Iris Chiara , Napoli Francesca , Tabbò Fabrizio , Mariniello Annapaola , Vigna Elisa , Modica Chiara , D’Ambrosio Lorenzo , Grignani Giovanni , Taulli Riccardo , Hirsch Emilio , Cereda Matteo , Aglietta Massimo , Scagliotti Giorgio Vittorio , Novello Silvia , Bironzo Paolo , Sangiolo Dario
Published: April 2023

AbstractPurpose:
Antibodies against the lymphocyte PD-1 (aPD-1) receptor are cornerstone agents for advanced non–small cell lung cancer (NSCLC), based on their ability to restore the exhausted antitumor immune response. Our study reports a novel, lymphocyte-independent, therapeutic activity of aPD-1 against NSCLC, blocking the tumor-intrinsic PD-1 receptors on chemoresistant cells.
Experimental Design:
PD-1 in NSCLC cells was explored in vitro at baseline, including stem-like pneumospheres, and following treatment with cisplatin both at transcriptional and protein levels. PD-1 signaling and RNA sequencing were assessed. The lymphocyte-independent antitumor activity of aPD-1 was explored in vitro, by PD-1 blockade and stimulation with soluble ligand (PD-L1s), and in vivo within NSCLC xenograft models.
Results:
We showed the existence of PD-1+ NSCLC cell subsets in cell lines and large in silico datasets (Cancer Cell Line Encyclopedia and The Cancer Genome Atlas). Cisplatin significantly increased PD-1 expression on chemo-surviving NSCLC cells (2.5-fold P = 0.0014), while the sequential treatment with anti–PD-1 Ab impaired their recovery after chemotherapy. PD-1 was found to be associated with tumor stemness features. PD-1 expression was enhanced in NSCLC stem-like pneumospheres (P < 0.0001), significantly promoted by stimulation with soluble PD-L1 (+27% ± 4, P < 0.0001) and inhibited by PD-1 blockade (−30% ± 3, P < 0.0001). The intravenous monotherapy with anti–PD-1 significantly inhibited tumor growth of NSCLC xenografts in immunodeficient mice, without the contribution of the immune system, and delayed the occurrence of chemoresistance when combined with cisplatin.
Conclusions:
We report first evidence of a novel lymphocyte-independent activity of anti–PD-1 antibodies in NSCLC, capable of inhibiting chemo-surviving NSCLC cells and exploitable to contrast disease relapses following chemotherapy.

See related commentary by Augustin et al., p. 505
Data from A Phase II Clinical Trial of Nivolumab and Temozolomide for Neuroendocrine Neoplasms
Authors: Owen Dwight H. , Benner Brooke , Wei Lai , Sukrithan Vineeth , Goyal Ashima , Zhou Ye , Pilcher Carly , Suffren Sheryl-Ann , Christenson Gwen , Curtis Nancy , Jukich Megan , Schwarz Emily , Savardekar Himanshu , Norman Ruthann , Ferguson Sarah , Kleiber Barbara , Wesolowski Robert , Carson William E. , Otterson Gregory A. , Verschraegen Claire F. , Shah Manisha H. , Konda Bhavana
Published: April 2023

AbstractPurpose:
Treatment options are limited in patients with metastatic neuroendocrine neoplasms (NEN). We present the results for a phase II trial of combination nivolumab and temozolomide in patients with advanced NEN along with results of immune changes in peripheral blood.
Patients and Methods:
NCT03728361 is a nonrandomized, phase II study of nivolumab and temozolomide in patients with NEN. The primary endpoint was response rate using RECIST 1.1. Secondary endpoints included progression-free survival (PFS), overall survival (OS), and safety. Immune profiling was performed by mass cytometry to evaluate the effect on peripheral blood immune cell subsets.
Results:
Among all 28 patients with NEN, the confirmed response rate was 9/28 [32.1%, 95% confidence interval (CI): 15.9–52.4]. Of 11 patients with lung NEN, the response rate was 64% (n = 7); there was a significant difference in responses by primary tumor location (lung vs. others, P = 0.020). The median PFS was 8.8 months (95% CI: 3.9–11.1 months), and median OS was 32.3 months (95% CI: 20.7—not reached months). Exploratory blood immune cell profiling revealed an increase in circulating CD8+ T cells (27.9% ± 13.4% vs. 31.7% ± 14.6%, P = 0.03) and a decrease in CD4+ T cells (59.6% ± 13.1% vs. 56.5% ± 13.0%, P = 0.001) after 2 weeks of treatment. LAG-3–expressing total T cells were lower in patients experiencing a partial response (0.18% ± 0.24% vs. 0.83% ± 0.55%, P = 0.028). Myeloid-derived suppressor cell levels increased during the study and did not correlate with response.
Conclusions:
Combination nivolumab and temozolomide demonstrated promising activity in NEN.

See related commentary by Velez and Garon, p. 691
Data from Genomic Complexity Predicts Resistance to Endocrine Therapy and CDK4/6 Inhibition in Hormone Receptor–Positive (HR+)/HER2-Negative Metastatic Breast Cancer
Authors: Davis Andrew A. , Luo Jingqin , Zheng Tiantian , Dai Chao , Dong Xiaoxi , Tan Lu , Suresh Rama , Ademuyiwa Foluso O. , Rigden Caron , Rearden Timothy P. , Clifton Katherine , Weilbaecher Katherine , Frith Ashley , Tandra Pavan K. , Summa Tracy , Haas Brittney , Thomas Shana , Hernandez-Aya Leonel F. , Peterson Lindsay L. , Wang Xiaohong , Luo Shujun J. , Zhou Kemin , Du Pan , Jia Shidong , King Bonnie L. , Krishnamurthy Jairam , Ma Cynthia X.
Published: April 2023

AbstractPurpose:
Clinical biomarkers to identify patients unlikely to benefit from CDK4/6 inhibition (CDK4/6i) in combination with endocrine therapy (ET) are lacking. We implemented a comprehensive circulating tumor DNA (ctDNA) analysis to identify genomic features for predicting and monitoring treatment resistance.
Experimental Design:
ctDNA was isolated from 216 plasma samples collected from 51 patients with hormone receptor–positive (HR+)/HER2-negative (HER2−) metastatic breast cancer (MBC) on a phase II trial of palbociclib combined with letrozole or fulvestrant (NCT03007979). Boosted whole-exome sequencing (WES) was performed at baseline and clinical progression to evaluate genomic alterations, mutational signatures, and blood tumor mutational burden (bTMB). Low-pass whole-genome sequencing was performed at baseline and serial timepoints to assess blood copy-number burden (bCNB).
Results:
High bTMB and bCNB were associated with lack of clinical benefit and significantly shorter progression-free survival (PFS) compared with patients with low bTMB or low bCNB (all P < 0.05). Dominant APOBEC signatures were detected at baseline exclusively in cases with high bTMB (5/13, 38.5%) versus low bTMB (0/37, 0%; P = 0.0006). Alterations in ESR1 were enriched in samples with high bTMB (P = 0.0005). There was a high correlation between bTMB determined by WES and bTMB determined using a 600-gene panel (R = 0.98). During serial monitoring, an increase in bCNB score preceded radiographic progression in 12 of 18 (66.7%) patients.
Conclusions:
Genomic complexity detected by noninvasive profiling of bTMB and bCNB predicted poor outcomes in patients treated with ET and CDK4/6i and identified early disease progression before imaging. Novel treatment strategies including immunotherapy-based combinations should be investigated in this population.
Data from Clinical Features Associated with Outcomes and Biomarker Analysis of Dabrafenib plus Trametinib Treatment in Patients with BRAF-Mutant Melanoma Brain Metastases
Authors: Wilmott James S. , Tawbi Hussein , Engh Johnathan A. , Amankulor Nduka M. , Shivalingam Brindha , Banerjee Hiya , Vergara Ismael A. , Lee Hansol , Johansson Peter A. , Ferguson Peter M. , Saiag Philippe , Robert Caroline , Grob Jean-Jacques , Butterfield Lisa H. , Scolyer Richard A. , Kirkwood John M. , Long Georgina V. , Davies Michael A.
Published: April 2023

AbstractPurpose:
This study aimed to identify baseline clinical features associated with the outcomes of patients enrolled in the COMBI-MB phase II study of dabrafenib and trametinib treatment in patients with V600 BRAF-mutant metastatic melanoma with melanoma brain metastases (MBM). Exploratory biomarker analysis was also conducted as part of the synergistic COMBI-BRV trial (BRV116521), to identify molecular and immunologic changes associated with dabrafenib in MBMs and extracranial metastases (ECM).
Patients and Methods:
Post hoc analysis was performed for baseline features of patients (n = 125) enrolled in COMBI-MB. Analyses were performed to identify baseline clinical features associated with intracranial response rate (ICRR), progression-free survival (PFS), and overall survival (OS).

Exploratory biomarker analysis was performed on biospecimen collected in the COMBI-BRV trial in which patients with BRAF-mutant, resectable MBM were treated with dabrafenib for 10 to 14 days prior to craniotomy. Accessible ECM were resected or biopsied at the time of craniotomy. Biospecimens underwent molecular and immunologic profiling for comparative analyses.
Results:
In COMBI-MB baseline treatment with corticosteroids was independently associated with lower ICRR [39% vs. 63%; OR, 0.323; 95 % confidence interval (CI), 0.105–0.996; P = 0.049] and shorter PFS (HR, 1.93; 95% CI, 1.06–3.51; P = 0.031). Additional significant associations identified in the multivariate analysis were improved PFS in patients with a BRAFV600E genotype (HR, 0.565; 95% CI, 0.321–0.996; P = 0.048) and improved OS in patients with Eastern Cooperative Oncology Group 0 (HR, 0.44; 95% CI, 0.25–0.78; P = 0.005).
Conclusions:
Corticosteroid treatment was associated with reduced ICRR and PFS in COMBI-MB, similar to results with immunotherapy for MBMs. Baseline corticosteroid treatment is a key factor to consider in MBM patient management and clinical trial design/interpretation.
Data from A Phase Ib/II Trial of Combined BRAF and EGFR Inhibition in BRAF V600E Positive Metastatic Colorectal Cancer and Other Cancers: The EVICT (Erlotinib and Vemurafenib In Combination Trial) Study
Authors: Tan Lavinia , Tran Ben , Tie Jeanne , Markman Ben , Ananda Sumi , Tebbutt Niall C. , Michael Michael , Link Emma , Wong Stephen Q. , Chandrashekar Sushma , Guinto Jerick , Ritchie David , Koldej Rachel , Solomon Benjamin J. , McArthur Grant A. , Hicks Rodney J. , Gibbs Peter , Dawson Sarah-Jane , Desai Jayesh
Published: April 2023

AbstractPurpose:
BRAF V600E mutant metastatic colorectal cancer represents a significant clinical problem, with combination approaches being developed clinically with oral BRAF inhibitors combined with EGFR-targeting antibodies. While compelling preclinical data have highlighted the effectiveness of combination therapy with vemurafenib and small-molecule EGFR inhibitors, gefitinib or erlotinib, in colorectal cancer, this therapeutic strategy has not been investigated in clinical studies.
Patients and Methods:
We conducted a phase Ib/II dose-escalation/expansion trial investigating the safety/efficacy of the BRAF inhibitor vemurafenib and EGFR inhibitor erlotinib.
Results:
Thirty-two patients with BRAF V600E positive metastatic colorectal cancer (mCRC) and 7 patients with other cancers were enrolled. No dose-limiting toxicities were observed in escalation, with vemurafenib 960 mg twice daily with erlotinib 150 mg daily selected as the recommended phase II dose. Among 31 evaluable patients with mCRC and 7 with other cancers, overall response rates were 32% [10/31, 16% (5/31) confirmed] and 43% (3/7), respectively, with clinical benefit rates of 65% and 100%. Early ctDNA dynamics were predictive of treatment efficacy, and serial ctDNA monitoring revealed distinct patterns of convergent genomic evolution associated with acquired treatment resistance, with frequent emergence of MAPK pathway alterations, including polyclonal KRAS, NRAS, and MAP2K1 mutations, and MET amplification.
Conclusions:
The Erlotinib and Vemurafenib In Combination Trial study demonstrated a safe and novel combination of two oral inhibitors targeting BRAF and EGFR. The dynamic assessment of serial ctDNA was a useful measure of underlying genomic changes in response to this combination and in understanding potential mechanisms of resistance.
Data from BRD9 Degradation Disrupts Ribosome Biogenesis in Multiple Myeloma
Authors: Kurata Keiji , Samur Mehmet K. , Liow Priscilla , Wen Kenneth , Yamamoto Leona , Liu Jiye , Morelli Eugenio , Gulla Annamaria , Tai Yu-Tzu , Qi Jun , Hideshima Teru , Anderson Kenneth C.
Published: April 2023

AbstractPurpose:
BRD9 is a defining component of the noncanonical SWI/SNF complex, which regulates gene expression by controlling chromatin dynamics. Although recent studies have found an oncogenic role for BRD9 in multiple cancer types including multiple myeloma, its clinical significance and oncogenic mechanism have not yet been elucidated. Here, we sought to identify the clinical and biological impact of BRD9 in multiple myeloma, which may contribute to the development of novel therapeutic strategies.
Experimental Design:
We performed integrated analyses of BRD9 in vitro and in vivo using multiple myeloma cell lines and primary multiple myeloma cells in established preclinical models, which identified the molecular functions of BRD9 contributing to multiple myeloma cell survival.
Results:
We found that high BRD9 expression was a poor prognostic factor in multiple myeloma. Depleting BRD9 by genetic (shRNA) and pharmacologic (dBRD9-A; proteolysis-targeting chimera; BRD9 degrader) approaches downregulated ribosome biogenesis genes, decreased the expression of the master regulator MYC, and disrupted the protein-synthesis maintenance machinery, thereby inhibiting multiple myeloma cell growth in vitro and in vivo in preclinical models. Importantly, we identified that the expression of ribosome biogenesis genes was associated with the disease progression and prognosis of patients with multiple myeloma. Our results suggest that BRD9 promotes gene expression by predominantly occupying the promoter regions of ribosome biogenesis genes and cooperating with BRD4 to enhance the transcriptional function of MYC.
Conclusions:
Our study identifies and validates BRD9 as a novel therapeutic target in preclinical models of multiple myeloma, which provides the framework for the clinical evaluation of BRD9 degraders to improve patient outcome.
Supplementary Fig. S2 from Heparin-binding epidermal growth factor–like growth factor promotes transcoelomic metastasis in ovarian cancer through epithelial-mesenchymal transition
Authors: Yagi Hiroshi , Yotsumoto Fusanori , Miyamoto Shingo
Published: April 2023

Supplementary Fig. S2 from Heparin-binding epidermal growth factor–like growth factor promotes transcoelomic metastasis in ovarian cancer through epithelial-mesenchymal transition
Supplementary Material from Anti-CD30 diabody-drug conjugates with potent antitumor activity
Authors: Kim Kristine M. , McDonagh Charlotte F. , Westendorf Lori , Brown Lindsay L. , Sussman Django , Feist Tiffany , Lyon Robert , Alley Stephen C. , Okeley Nicole M. , Zhang Xinqun , Thompson Melissa C. , Stone Ivan , Gerber Hans-Peter , Carter Paul J.
Published: April 2023

Supplementary Material from Anti-CD30 diabody-drug conjugates with potent antitumor activity
Supplementary Fig. S1 from Curcumin suppresses constitutive activation of nuclear factor-κB and requires functional Bax to induce apoptosis in Burkitt's lymphoma cell lines
Authors: Hussain Azhar R. , Ahmed Maqbool , Al-Jomah Naif A. , Khan Asma S. , Manogaran Pulicat , Sultana Mehar , Abubaker Jehad , Platanias Leonidas C. , Al-Kuraya Khawla S. , Uddin Shahab
Published: April 2023

Supplementary Fig. S1 from Curcumin suppresses constitutive activation of nuclear factor-κB and requires functional Bax to induce apoptosis in Burkitt's lymphoma cell lines
Supplementary Fig. S1 from Gemcitabine sensitization by checkpoint kinase 1 inhibition correlates with inhibition of a Rad51 DNA damage response in pancreatic cancer cells
Authors: Parsels Leslie A. , Morgan Meredith A. , Tanska Daria M. , Parsels Joshua D. , Palmer Brian D. , Booth R. John , Denny William A. , Canman Christine E. , Kraker Alan J. , Lawrence Theodore S. , Maybaum Jonathan
Published: April 2023

Supplementary Fig. S1 from Gemcitabine sensitization by checkpoint kinase 1 inhibition correlates with inhibition of a Rad51 DNA damage response in pancreatic cancer cells
Supplementary Fig. S6 from Humanized ADEPT comprised of an engineered human purine nucleoside phosphorylase and a tumor targeting peptide for treatment of cancer
Authors: Afshar Sepideh , Asai Tsuneaki , Morrison Sherie L.
Published: April 2023

Supplementary Fig. S6 from Humanized ADEPT comprised of an engineered human purine nucleoside phosphorylase and a tumor targeting peptide for treatment of cancer
Supplementary Fig. S5 from Humanized ADEPT comprised of an engineered human purine nucleoside phosphorylase and a tumor targeting peptide for treatment of cancer
Authors: Afshar Sepideh , Asai Tsuneaki , Morrison Sherie L.
Published: April 2023

Supplementary Fig. S5 from Humanized ADEPT comprised of an engineered human purine nucleoside phosphorylase and a tumor targeting peptide for treatment of cancer
Supplementary Fig. S1 from Humanized ADEPT comprised of an engineered human purine nucleoside phosphorylase and a tumor targeting peptide for treatment of cancer
Authors: Afshar Sepideh , Asai Tsuneaki , Morrison Sherie L.
Published: April 2023

Supplementary Fig. S1 from Humanized ADEPT comprised of an engineered human purine nucleoside phosphorylase and a tumor targeting peptide for treatment of cancer
Supplementary Fig. S6 from UA62784, a novel inhibitor of centromere protein E kinesin-like protein
Authors: Henderson Meredith C. , Shaw Yeng-Jeng Y. , Wang Hong , Han Haiyong , Hurley Laurence H. , Flynn Gary , Dorr Robert T. , Von Hoff Daniel D.
Published: April 2023

Supplementary Fig. S6 from UA62784, a novel inhibitor of centromere protein E kinesin-like protein
Supplementary Fig. S4 from UA62784, a novel inhibitor of centromere protein E kinesin-like protein
Authors: Henderson Meredith C. , Shaw Yeng-Jeng Y. , Wang Hong , Han Haiyong , Hurley Laurence H. , Flynn Gary , Dorr Robert T. , Von Hoff Daniel D.
Published: April 2023

Supplementary Fig. S4 from UA62784, a novel inhibitor of centromere protein E kinesin-like protein
Supplementary Fig. S1 from UA62784, a novel inhibitor of centromere protein E kinesin-like protein
Authors: Henderson Meredith C. , Shaw Yeng-Jeng Y. , Wang Hong , Han Haiyong , Hurley Laurence H. , Flynn Gary , Dorr Robert T. , Von Hoff Daniel D.
Published: April 2023

Supplementary Fig. S1 from UA62784, a novel inhibitor of centromere protein E kinesin-like protein
Supplementary Fig. from Z3, a novel Jak2 tyrosine kinase small-molecule inhibitor that suppresses Jak2-mediated pathologic cell growth
Authors: Sayyah Jacqueline , Magis Andrew , Ostrov David A. , Allan Robert W. , Braylan Raul C. , Sayeski Peter P.
Published: April 2023

Supplementary Fig. from Z3, a novel Jak2 tyrosine kinase small-molecule inhibitor that suppresses Jak2-mediated pathologic cell growth
Supplementary Figure 1 from SUMOylation of HMGA2: selective destabilization of promyelocytic leukemia protein via proteasome
Authors: Cao Xuefei , Clavijo Carlos , Li Xu , Lin H. Helen , Chen Yuan , Shih Hsiu-Ming , Ann David K.
Published: April 2023

Supplementary Figure 1 from SUMOylation of HMGA2: selective destabilization of promyelocytic leukemia protein via proteasome
Supplementary Figure 4 from Lysophosphatidylcholine Pretreatment Reduces VLA-4 and P-Selectin–Mediated B16.F10 Melanoma Cell Adhesion In vitro and Inhibits Metastasis-Like Lung Invasion In vivo
Authors: Jantscheff Peter , Schlesinger Martin , Fritzsche Juliane , Taylor Lenka A. , Graeser Ralph , Kirfel Gregor , Fürst Dieter O. , Massing Ulrich , Bendas Gerd
Published: April 2023

Supplementary Figure 4 from Lysophosphatidylcholine Pretreatment Reduces VLA-4 and P-Selectin–Mediated B16.F10 Melanoma Cell Adhesion In vitro and Inhibits Metastasis-Like Lung Invasion In vivo
Supplementary Figure 2 from Lysophosphatidylcholine Pretreatment Reduces VLA-4 and P-Selectin–Mediated B16.F10 Melanoma Cell Adhesion In vitro and Inhibits Metastasis-Like Lung Invasion In vivo
Authors: Jantscheff Peter , Schlesinger Martin , Fritzsche Juliane , Taylor Lenka A. , Graeser Ralph , Kirfel Gregor , Fürst Dieter O. , Massing Ulrich , Bendas Gerd
Published: April 2023

Supplementary Figure 2 from Lysophosphatidylcholine Pretreatment Reduces VLA-4 and P-Selectin–Mediated B16.F10 Melanoma Cell Adhesion In vitro and Inhibits Metastasis-Like Lung Invasion In vivo
Supplementary Figure 1B from Lysophosphatidylcholine Pretreatment Reduces VLA-4 and P-Selectin–Mediated B16.F10 Melanoma Cell Adhesion In vitro and Inhibits Metastasis-Like Lung Invasion In vivo
Authors: Jantscheff Peter , Schlesinger Martin , Fritzsche Juliane , Taylor Lenka A. , Graeser Ralph , Kirfel Gregor , Fürst Dieter O. , Massing Ulrich , Bendas Gerd
Published: April 2023

Supplementary Figure 1B from Lysophosphatidylcholine Pretreatment Reduces VLA-4 and P-Selectin–Mediated B16.F10 Melanoma Cell Adhesion In vitro and Inhibits Metastasis-Like Lung Invasion In vivo
Supplementary Figures and Table from Small molecules targeting histone H4 as potential therapeutics for chronic myelogenous leukemia
Authors: Chou C. James , Farkas Michelle E. , Tsai Sherry M. , Alvarez David , Dervan Peter B. , Gottesfeld Joel M.
Published: April 2023

Supplementary Figures and Table from Small molecules targeting histone H4 as potential therapeutics for chronic myelogenous leukemia
Supplementary Data from Nitro-chloromethylbenzindolines: hypoxia-activated prodrugs of potent adenine N3 DNA minor groove alkylators
Authors: Wilson William R. , Stribbling Stephen M. , Pruijn Frederik B. , Syddall Sophie P. , Patterson Adam V. , Liyanage H.D. Sarath , Smith Eileen , Botting K. Jane , Tercel Moana
Published: April 2023

Supplementary Data from Nitro-chloromethylbenzindolines: hypoxia-activated prodrugs of potent adenine N3 DNA minor groove alkylators
Supplementary Fig. S1 from Identification and characterization of small-molecule inhibitors of hepsin
Authors: Chevillet John R. , Park Gemma J. , Bedalov Antonio , Simon Julian A. , Vasioukhin Valeri I.
Published: April 2023

Supplementary Fig. S1 from Identification and characterization of small-molecule inhibitors of hepsin
Supplementary Fig. S1 from Therapeutic targeting of human hepatocyte growth factor with a single neutralizing monoclonal antibody reduces lung tumorigenesis
Authors: Stabile Laura P. , Rothstein Mary E. , Keohavong Phouthone , Jin Jide , Yin Jinling , Land Stephanie R. , Dacic Sanja , Luong The Minh , Kim K. Jin , Dulak Austin M. , Siegfried Jill M.
Published: April 2023

Supplementary Fig. S1 from Therapeutic targeting of human hepatocyte growth factor with a single neutralizing monoclonal antibody reduces lung tumorigenesis
Supplementary Table S6 from Antitumor activity and molecular effects of the novel heat shock protein 90 inhibitor, IPI-504, in pancreatic cancer
Authors: Song Dongweon , Chaerkady Raghothama , Tan Aik Choon , García-García Elena , Nalli Anuradha , Suárez-Gauthier Ana , López-Ríos Fernando , Zhang Xian Feng , Solomon Anna , Tong Jeffrey , Read Margaret , Fritz Christian , Jimeno Antonio , Pandey Akhilesh , Hidalgo Manuel
Published: April 2023

Supplementary Table S6 from Antitumor activity and molecular effects of the novel heat shock protein 90 inhibitor, IPI-504, in pancreatic cancer
Supplementary Table S2 from Antitumor activity and molecular effects of the novel heat shock protein 90 inhibitor, IPI-504, in pancreatic cancer
Authors: Song Dongweon , Chaerkady Raghothama , Tan Aik Choon , García-García Elena , Nalli Anuradha , Suárez-Gauthier Ana , López-Ríos Fernando , Zhang Xian Feng , Solomon Anna , Tong Jeffrey , Read Margaret , Fritz Christian , Jimeno Antonio , Pandey Akhilesh , Hidalgo Manuel
Published: April 2023

Supplementary Table S2 from Antitumor activity and molecular effects of the novel heat shock protein 90 inhibitor, IPI-504, in pancreatic cancer
Supplementary Table 4 from Global microRNA Analysis of the NCI-60 Cancer Cell Panel
Authors: Søkilde Rolf , Kaczkowski Bogumil , Podolska Agnieszka , Cirera Susanna , Gorodkin Jan , Møller Søren , Litman Thomas
Published: April 2023

Supplementary Table 4 from Global microRNA Analysis of the NCI-60 Cancer Cell Panel
Supplementary Fig. S6 from Mitogen-activated protein kinase kinase signaling promotes growth and vascularization of fibrosarcoma
Authors: Ding Yan , Boguslawski Elissa A. , Berghuis Bree D. , Young John J. , Zhang Zhongfa , Hardy Kim , Furge Kyle , Kort Eric , Frankel Arthur E. , Hay Rick V. , Resau James H. , Duesbery Nicholas S.
Published: April 2023

Supplementary Fig. S6 from Mitogen-activated protein kinase kinase signaling promotes growth and vascularization of fibrosarcoma
Supplementary Fig. S6 from Quantitative live imaging of cancer and normal cells treated with Kinesin-5 inhibitors indicates significant differences in phenotypic responses and cell fate
Authors: Orth James D. , Tang Yangzhong , Shi Jade , Loy Clement T. , Amendt Christiane , Wilm Claudia , Zenke Frank T. , Mitchison Timothy J.
Published: April 2023

Supplementary Fig. S6 from Quantitative live imaging of cancer and normal cells treated with Kinesin-5 inhibitors indicates significant differences in phenotypic responses and cell fate
Supplementary Fig. S4 from Quantitative live imaging of cancer and normal cells treated with Kinesin-5 inhibitors indicates significant differences in phenotypic responses and cell fate
Authors: Orth James D. , Tang Yangzhong , Shi Jade , Loy Clement T. , Amendt Christiane , Wilm Claudia , Zenke Frank T. , Mitchison Timothy J.
Published: April 2023

Supplementary Fig. S4 from Quantitative live imaging of cancer and normal cells treated with Kinesin-5 inhibitors indicates significant differences in phenotypic responses and cell fate
Supplementary Material from N-&-N, a new class of cell death-inducing kinase inhibitors derived from the purine roscovitine
Authors: Bettayeb Karima , Sallam Hatem , Ferandin Yoan , Popowycz Florence , Fournet Guy , Hassan Moustapha , Echalier Aude , Bernard Philippe , Endicott Jane , Joseph Benoît , Meijer Laurent
Published: April 2023

Supplementary Material from N-&-N, a new class of cell death-inducing kinase inhibitors derived from the purine roscovitine
Supplementary Figure 6 from Anticancer Activity of a Combination of Cisplatin and Fisetin in Embryonal Carcinoma Cells and Xenograft Tumors
Authors: Tripathi Rakshamani , Samadder Tanmoy , Gupta Sarika , Surolia Avadhesha , Shaha Chandrima
Published: April 2023

Supplementary Figure 6 from Anticancer Activity of a Combination of Cisplatin and Fisetin in Embryonal Carcinoma Cells and Xenograft Tumors
Supplementary Fig. S1 from Human colorectal tumors and metastases express Gb3 and can be targeted by an intestinal pathogen-based delivery tool
Authors: Falguières Thomas , Maak Matthias , von Weyhern Claus , Sarr Marianne , Sastre Xavier , Poupon Marie-France , Robine Sylvie , Johannes Ludger , Janssen Klaus-Peter
Published: April 2023

Supplementary Fig. S1 from Human colorectal tumors and metastases express Gb3 and can be targeted by an intestinal pathogen-based delivery tool
Supplementary Table S4 from The G-rich promoter and G-rich coding sequence of basic fibroblast growth factor are the targets of thalidomide in glioma
Authors: Mei Szu-Chieh , Wu Rong-Tsun
Published: April 2023

Supplementary Table S4 from The G-rich promoter and G-rich coding sequence of basic fibroblast growth factor are the targets of thalidomide in glioma
Supplementary Fig. S1 from The G-rich promoter and G-rich coding sequence of basic fibroblast growth factor are the targets of thalidomide in glioma
Authors: Mei Szu-Chieh , Wu Rong-Tsun
Published: April 2023

Supplementary Fig. S1 from The G-rich promoter and G-rich coding sequence of basic fibroblast growth factor are the targets of thalidomide in glioma
Supplementary Table 1 from Activated Phosphoinositide 3-Kinase/AKT Signaling Confers Resistance to Trastuzumab but not Lapatinib
Authors: O'Brien Neil A. , Browne Brigid C. , Chow Lucy , Wang Yuhua , Ginther Charles , Arboleda Jane , Duffy Michael J. , Crown John , O'Donovan Norma , Slamon Dennis J.
Published: April 2023

Supplementary Table 1 from Activated Phosphoinositide 3-Kinase/AKT Signaling Confers Resistance to Trastuzumab but not Lapatinib
Supplementary Table S1 from Comparison of biochemical and biological effects of ML858 (salinosporamide A) and bortezomib
Authors: Williamson Mark J. , Blank Jonathan L. , Bruzzese Frank J. , Cao Yueying , Daniels J. Scott , Dick Lawrence R. , Labutti Jason , Mazzola Anne M. , Patil Ashok D. , Reimer Corinne L. , Solomon Marjorie S. , Stirling Matthew , Tian Yuan , Tsu Christopher A. , Weatherhead Gabriel S. , Zhang Julie X. , Rolfe Mark
Published: April 2023

Supplementary Table S1 from Comparison of biochemical and biological effects of ML858 (salinosporamide A) and bortezomib
Supplementary Fig. S1 from Cyclin D3 is down-regulated by rapamycin in HER-2-overexpressing breast cancer cells
Authors: García-Morales Pilar , Hernando Eva , Carrasco-García Estefanía , Menéndez-Gutierrez María Piedad , Saceda Miguel , Martínez-Lacaci Isabel
Published: April 2023

Supplementary Fig. S1 from Cyclin D3 is down-regulated by rapamycin in HER-2-overexpressing breast cancer cells
Video Description from Structure-based design of an urokinase-type plasminogen activator receptor–derived peptide inhibiting cell migration and lung metastasis
Authors: Carriero Maria Vincenza , Longanesi-Cattani Immacolata , Bifulco Katia , Maglio Ornella , Lista Liliana , Barbieri Antonio , Votta Giuseppina , Masucci Maria Teresa , Arra Claudio , Franco Renato , De Rosa Mario , Stoppelli Maria Patrizia , Pavone Vincenzo
Published: April 2023

Video Description from Structure-based design of an urokinase-type plasminogen activator receptor–derived peptide inhibiting cell migration and lung metastasis
Supplementary Table S1 from CXCR3 expression is associated with poor survival in breast cancer and promotes metastasis in a murine model
Authors: Ma Xinrong , Norsworthy Kelly , Kundu Namita , Rodgers William H. , Gimotty Phyllis A. , Goloubeva Olga , Lipsky Michael , Li Yanchun , Holt Dawn , Fulton Amy
Published: April 2023

Supplementary Table S1 from CXCR3 expression is associated with poor survival in breast cancer and promotes metastasis in a murine model
Supplementary Tables 3-6 from Molecular Evolutionary Analysis of Cancer Cell Lines
Authors: Zhang Yan , Italia Michael J. , Auger Kurt R. , Halsey Wendy S. , Van Horn Stephanie F. , Sathe Ganesh M. , Magid-Slav Michal , Brown James R. , Holbrook Joanna D.
Published: April 2023

Supplementary Tables 3-6 from Molecular Evolutionary Analysis of Cancer Cell Lines
Supplementary Data from Antiangiogenic Activity of a Neutralizing Human Single-Chain Antibody Fragment against Fibroblast Growth Factor Receptor 1
Authors: Ronca Roberto , Benzoni Patrizia , Leali Daria , Urbinati Chiara , Belleri Mirella , Corsini Michela , Alessi Patrizia , Coltrini Daniela , Calza Stefano , Presta Marco , Dell'Era Patrizia
Published: April 2023

Supplementary Data from Antiangiogenic Activity of a Neutralizing Human Single-Chain Antibody Fragment against Fibroblast Growth Factor Receptor 1
Supplementary Figure 2 from The Mismatch Repair System Modulates Curcumin Sensitivity through Induction of DNA Strand Breaks and Activation of G2-M Checkpoint
Authors: Jiang Zhihua , Jin ShunQian , Yalowich Jack C. , Brown Kevin D. , Rajasekaran Baskaran
Published: April 2023

Supplementary Figure 2 from The Mismatch Repair System Modulates Curcumin Sensitivity through Induction of DNA Strand Breaks and Activation of G2-M Checkpoint
Supplementary Data from Mcl-1 Stability Determines Mitotic Cell Fate of Human Multiple Myeloma Tumor Cells Treated with the Kinesin Spindle Protein Inhibitor ARRY-520
Authors: Tunquist Brian J. , Woessner Richard D. , Walker Duncan H.
Published: April 2023

Supplementary Data from Mcl-1 Stability Determines Mitotic Cell Fate of Human Multiple Myeloma Tumor Cells Treated with the Kinesin Spindle Protein Inhibitor ARRY-520
Supplementary Table 1 from Dihydroartemisinin Induces Apoptosis by a Bak-Dependent Intrinsic Pathway
Authors: Handrick René , Ontikatze Teona , Bauer Kerstin-Daniela , Freier Florian , Rübel Amelie , Dürig Jan , Belka Claus , Jendrossek Verena
Published: April 2023

Supplementary Table 1 from Dihydroartemisinin Induces Apoptosis by a Bak-Dependent Intrinsic Pathway