bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Association of Aspirin, Metformin, and Statin Use with Gastric Cancer Incidence and Mortality: A Nationwide Cohort Study
Authors: Cho Mi Hee , Yoo Tae Gon , Jeong Su-Min , Shin Dong Wook
Published: April 2023

Abstract
Anticancer effects of aspirin, metformin, and statins against gastric cancer, one of the most common cancers in the world, have been reported. This retrospective cohort study aimed to investigate independent associations of aspirin, metformin, and statin use with gastric cancer incidence and mortality after adjustment for concomitant use of other drugs, using pooled cohort data extracted from the Korean National Health Insurance claim database. Follow-up started on January 1, 2004 and ended at the date of gastric cancer diagnosis, death, or December 31, 2013. Exposures to drugs were defined as cumulative duration of use for aspirin and cumulative defined daily dose for metformin and statin, and were entered as time-dependent variables in Cox analysis models to avoid immortal time bias. Use of aspirin for longer than 182.5 and 547.5 days during 2-year interval was associated with reduced risks of gastric cancer incidence and mortality, respectively. Patients with diabetes were at higher risk of gastric cancer incidence and mortality than nondiabetic people, regardless of metformin treatment. However, metformin use among patients with diabetes was associated with a reduction in gastric cancer mortality in a dose-response manner. Statin use was also associated with a reduction of gastric cancer mortality in the general population, but not with gastric cancer incidence. In conclusion, long-term use of aspirin was independently associated with reduced incidence and mortality of gastric cancer in the general population, but metformin or statin use was only associated with a reduction of gastric cancer mortality in patients with diabetes and in the general population, respectively.
Prevention Relevance:
Long-term use of aspirin was independently associated with reduced incidence and mortality of gastric cancer in the general population. Metformin or statin use, however, was only associated with a reduction of gastric cancer mortality in diabetic patients and in the general population in a dose-response manner, respectively.
Data from Inhibition of the Biosynthesis of Prostaglandin E2 By Low-Dose Aspirin: Implications for Adenocarcinoma Metastasis
Authors: Boutaud Olivier , Sosa I. Romina , Amin Taneem , Oram Denise , Adler David , Hwang Hyun S. , Crews Brenda C. , Milne Ginger , Harris Bradford K. , Hoeksema Megan , Knollmann Bjorn C. , Lammers Philip E. , Marnett Lawrence J. , Massion Pierre P. , Oates John A.
Published: April 2023

Abstract
Meta-analyses have demonstrated that low-dose aspirin reduces the risk of developing adenocarcinoma metastasis, and when colon cancer is detected during aspirin treatment, there is a remarkable 83% reduction in risk of metastasis. As platelets participate in the metastatic process, the antiplatelet action of low-dose aspirin likely contributes to its antimetastatic effect. Cycloxooxygenase-2 (COX-2)–derived prostaglandin E2 (PGE2) also contributes to metastasis, and we addressed the hypothesis that low-dose aspirin also inhibits PGE2 biosynthesis. We show that low-dose aspirin inhibits systemic PGE2 biosynthesis by 45% in healthy volunteers (P < 0.0001). Aspirin is found to be more potent in colon adenocarcinoma cells than in the platelet, and in lung adenocarcinoma cells, its inhibition is equivalent to that in the platelet. Inhibition of COX by aspirin in colon cancer cells is in the context of the metastasis of colon cancer primarily to the liver, the organ exposed to the same high concentrations of aspirin as the platelet. We find that the interaction of activated platelets with lung adenocarcinoma cells upregulates COX-2 expression and PGE2 biosynthesis, and inhibition of platelet COX-1 by aspirin inhibits PGE2 production by the platelet–tumor cell aggregates. In conclusion, low-dose aspirin has a significant effect on extraplatelet cyclooxygenase and potently inhibits COX-2 in lung and colon adenocarcinoma cells. This supports a hypothesis that the remarkable prevention of metastasis from adenocarcinomas, and particularly from colon adenocarcinomas, by low-dose aspirin results from its effect on platelet COX-1 combined with inhibition of PGE2 biosynthesis in metastasizing tumor cells. Cancer Prev Res; 9(11); 855–65. ©2016 AACR.
Data from Low Colorectal Cancer Screening Uptake and Persistent Disparities in an Underserved Urban Population
Authors: Ni Katherine , O'Connell Kelli , Anand Sanya , Yakoubovitch Stephanie C. , Kwon Simona C. , de Latour Rabia Ali , Wallach Andrew B. , Sherman Scott E. , Du Mengmeng , Liang Peter S.
Published: April 2023

Abstract
Colorectal cancer screening has increased substantially in New York City in recent years. However, screening uptake measured by telephone surveys may not fully capture rates among underserved populations. We measured screening completion within 1 year of a primary care visit among previously unscreened patients in a large urban safety-net hospital and identified sociodemographic and health-related predictors of screening.

We identified 21,256 patients ages 50 to 75 who were seen by primary care providers (PCP) in 2014, of whom 14,425 (67.9%) were not up-to-date with screening. Because PCPs facilitate the majority of screening, we compared patients who received screening within 1 year of an initial PCP visit to those who remained unscreened using multivariable logistic regression.

Among patients not up-to-date with screening at study outset, 11.5% (1,658 patients) completed screening within 1 year of a PCP visit. Asian race, more PCP visits, and higher area-level income were associated with higher screening completion. Factors associated with remaining unscreened included morbid obesity, ever smoking, Elixhauser comorbidity index of 0, and having Medicaid/Medicare insurance. Age, sex, language, and travel time to the hospital were not associated with screening status. Overall, 39.9% of patients were up-to-date with screening by 2015.

In an underserved urban population, colorectal cancer screening disparities remain, and overall screening uptake was low. Because more PCP visits were associated with modestly higher screening completion at 1 year, additional community-level education and outreach may be crucial to increase colorectal cancer screening in underserved populations.
Data from Association of IgG Glycosylation and Esophageal Precancerosis Beyond Inflammation
Authors: Wu Zhiyuan , Pan Huiying , Liu Di , Zhou Di , Tao Lixin , Zhang Jie , Wang Xiaonan , Wang Youxin , Wang Wei , Guo Xiuhua
Published: April 2023

Abstract
This study aimed to investigate the association of IgG glycosylation and esophageal precancerosis for squamous cell carcinoma and determine its role in inflammation. Primary glycans selected by the least absolute shrinkage and selection operator (LASSO) algorithm were validated using univariate and multivariate logistics models plus restricted cubic spline functions. In total, 24 direct glycans and 27 derived traits were detected, among which four glycans and three derived traits were primarily selected. Then, GP5 (adjusted OR: 0.805), GP17 (adjusted OR: 1.305), G12n (adjusted OR: 1.271), Gal_1 (adjusted OR: 0.776) and Fuc (adjusted OR: 0.737) were validated and significantly associated with esophageal precancerosis. In addition, there was a consistent positive association in GP17 and G12n and a negative association in GP5, Gal_1, and Fuc by restricted cubic spline function. Compared with esophageal inflammation, GP17, G12n, and Fuc were still independently associated with precancerosis. In brief, the IgG glycosylation profile was independently associated with esophageal precancerosis beyond inflammation, which could be an early biomarker for esophageal cancer.

Prevention Relevance: IgG glycosylation profile is associated with esophageal precancerosis and specific IgG glycans involves in the early stage of esophageal cancer, which is independent of inflammation.
Data from Obesity-Associated Alterations in Inflammation, Epigenetics, and Mammary Tumor Growth Persist in Formerly Obese Mice
Authors: Rossi Emily L. , de Angel Rebecca E. , Bowers Laura W. , Khatib Subreen A. , Smith Laura A. , Van Buren Eric , Bhardwaj Priya , Giri Dilip , Estecio Marcos R. , Troester Melissa A. , Hair Brionna Y. , Kirk Erin L. , Gong Ting , Shen Jianjun , Dannenberg Andrew J. , Hursting Stephen D.
Published: April 2023

Abstract
Using a murine model of basal-like breast cancer, we tested the hypothesis that chronic obesity, an established breast cancer risk and progression factor in women, induces mammary gland epigenetic reprogramming and increases mammary tumor growth. Moreover, we assessed whether the obesity-induced epigenetic and protumor effects are reversed by weight normalization. Ovariectomized female C57BL/6 mice were fed a control diet or diet-induced obesity (DIO) regimen for 17 weeks, resulting in a normal weight or obese phenotype, respectively. Mice on the DIO regimen were then randomized to continue the DIO diet or were switched to the control diet, resulting in formerly obese (FOb) mice with weights comparable with control mice. At week 24, all mice were orthotopically injected with MMTV-Wnt-1 mouse mammary tumor cells. Mean tumor volume, serum IL6 levels, expression of proinflammatory genes in the mammary fat pad, and mammary DNA methylation profiles were similar in DIO and FOb mice and higher than in controls. Many of the genes found to have obesity-associated hypermethylation in mice were also found to be hypermethylated in the normal breast tissue of obese versus nonobese human subjects, and nearly all of these concordant genes remained hypermethylated after significant weight loss in the FOb mice. Our findings suggest that weight normalization may not be sufficient to reverse the effects of chronic obesity on epigenetic reprogramming and inflammatory signals in the microenvironment that are associated with breast cancer progression. Cancer Prev Res; 9(5); 339–48. ©2016 AACR.
Data from Unmetabolized Folic Acid, Tetrahydrofolate, and Colorectal Adenoma Risk
Authors: Rees Judy R. , Morris Carolyn B. , Peacock Janet L. , Ueland Per M. , Barry Elizabeth L. , McKeown-Eyssen Gail E. , Figueiredo Jane C. , Snover Dale C. , Baron John A.
Published: April 2023

Abstract
In a randomized trial of folic acid supplementation for the prevention of colorectal adenomas, we previously found indications of increased risk during later treatment and follow-up. This could have been due to the unmetabolized folic acid (UFA) or natural reduced and methylated folates (mF) to which it is metabolized. In post hoc analyses, we measured mF (the sum of 5-methyl-tetrahydrofolate and 4-alfa-hydroxy-5-methyl-THF) and UFA concentrations in the serum of 924 participants. Using binomial regression models with a log link, we assessed the associations between plasma mF or UFA and adenoma occurrence. We found no association between plasma mF or UFA and overall adenoma risk. However, during later follow-up, the prespecified, composite endpoint of high-risk findings (advanced or multiple adenomas) was positively associated with plasma mF (Plinear trend = 0.009), with a 58% increased risk for participants in the upper versus lowest quartile. An irregular association was seen with plasma UFA, with suggestions of an inverse trend (Plinear trend=0.049). A modest, significant inverse association was also seen between mF and risk of serrated lesions, with a 39% lower risk for upper versus lower quartile participants (Plinear trend = 0.03). In conclusion, during the later follow-up period in which folic acid supplementation was previously seen to increase the risk of advanced and multiple adenomas, higher serum mF was associated with a higher risk of multiple and/or advanced adenomas, but no clear indication that UFA played a direct role. There were indications that higher mF was associated with reduced risk of serrated polyps. Cancer Prev Res; 10(8); 451–8. ©2017 AACR.
Data from Physical Activity Plus Energy Restriction Prevents 4T1.2 Mammary Tumor Progression, MDSC Accumulation, and an Immunosuppressive Tumor Microenvironment
Authors: Turbitt William J. , Xu Yitong , Sosnoski Donna M. , Collins Shawntawnee D. , Meng Huicui , Mastro Andrea M. , Rogers Connie J.
Published: April 2023

Abstract
Physical activity and the prevention of weight gain decrease breast cancer incidence and improve survival. Unraveling the biological mechanisms underlying these cancer prevention effects is difficult because activity and dietary restriction are often linked. The goal of this study was to determine whether physical activity (PA), preventing weight gain via energy restriction (ER), or the combination was most effective in delaying tumor growth, reducing metastatic progression, and improving survival in the 4T1.2 mammary tumor model. Furthermore, we determined whether any of these interventions prevented the expansion of protumor immunosuppressive cells and altered the tumor microenvironment (TME). Female BALB/c mice (n = 7–20/group) were randomized to sedentary (SED) or PA wheel cages and fed ad libitum (AL) or 90% of control food intake (ER). After 8 weeks on the interventions, mice were inoculated with 5 × 104 4T1.2luc cells into the 4th mammary fat pad and continued on their respective intervention. PA+ER significantly delayed primary tumor growth (final tumor volume, 0.193 ± 0.042 vs. 0.369 ± 0.049 cm3, P < 0.001), reduced metastatic burden in the lungs (0.72 ± 0.36 vs. 16.27 ± 6.98, P = 0.054) and increased survival (median survival, 68 vs 40 days, P = 0.043) compared with SED+AL mice. PA+ER also reduced the expression level of metastatic and immunosuppressive genes and resulted in favorable changes in immune cell infiltrates in the tumor. These data suggest that both PA and ER are needed to reduce tumor growth, delay metastatic progression, and improve survival, and that this protection is associated with changes in immune-mediated mechanisms.
Data from Effect of Green Tea Supplements on Liver Enzyme Elevation: Results from a Randomized Intervention Study in the United States
Authors: Yu Zheming , Samavat Hamed , Dostal Allison M. , Wang Renwei , Torkelson Carolyn J. , Yang Chung S. , Butler Lesley M. , Kensler Thomas W. , Wu Anna H. , Kurzer Mindy S. , Yuan Jian-Min
Published: April 2023

Abstract
Liver injury effects of green tea–based products have been reported in sporadic case reports. However, no study has examined systematically such adverse effects in an unbiased manner. We examined the potential effects of a high, sustained oral dose of green tea extract (GTE) on liver injury measures in a randomized, placebo-controlled, double-blinded phase II clinical trial, which enrolled 1,075 women with the original aim to assess the effect of daily GTE consumption for 12 months on biomarkers of breast cancer risk. The current analysis examined the effect of GTE consumption on liver injury in 1,021 participants (513 in GTE and 508 in placebo arm) with normal baseline levels of liver enzymes. Among women in the GTE arm, alanine aminotransferase (ALT) increased by 5.4 U/L [95% confidence interval (CI), 3.6–7.1] and aspartate aminotransferase increased by 3.8 U/L (95% CI, 2.5–5.1), which were significantly higher than those among women in the placebo arm (both P < 0.001). Overall, 26 (5.1%) women in GTE developed moderate or more severe abnormalities in any liver function measure during the intervention period, yielding an OR of 7.0 (95% CI, 2.4–20.3) for developing liver function abnormalities as compared with those in the placebo arm. ALT returned to normal after dechallenge and increased again after one or more rechallenges with GTE. The rise–fall pattern of liver enzyme values following the challenge–dechallenge cycles of GTE consumption strongly implicates the effect of high-dose GTE on liver enzyme elevations. Cancer Prev Res; 10(10); 571–9. ©2017 AACR.
Data from Obesity-associated Breast Inflammation among Hispanic/Latina Breast Cancer Patients
Authors: Greenlee Heather , Shi Zaixing , Hibshoosh Hanina , Giri Dilip D. , Ahmed Aqeel , Williams Samantha , Falcone Domenick J. , Winston Lisle A. , Zhou Xi K. , Hudis Clifford A. , Hershman Dawn L. , Dannenberg Andrew J. , Iyengar Neil M.
Published: April 2023

Abstract
Breast white adipose tissue inflammation (BWATi) is associated with obesity and higher breast cancer risk among non-Hispanic white women. Obesity is prevalent in Hispanic/Latina patients with breast cancer, and the occurrence of BWATi in this population is not well-characterized. The association between BWATi and body mass index (BMI) was evaluated in Hispanic/Latina patients with breast cancer who underwent mastectomy. BWATi was defined as the presence of crown-like structures of the breast (CLS-B), detected by CD68 IHC in nontumor breast tissue. BWATi severity was quantified as number of CLS-B/cm2. Adipocyte diameter was measured using hematoxylin and eosin-stained breast tissue sections. Preoperative BMI (within 1 week prior to mastectomy) was categorized as normal (18.5–<25.0 kg/m2), overweight (25.0–<30.0 kg/m2), class I obesity (30.0–<35.0 kg/m2), and class II–III obesity (35.0 kg/m2 or above). Patient charts were abstracted to record clinicopathologic features and liver function tests <90 days before mastectomy. The study included 91 women (mean age 69 years; range 36–96 years). Prevalence of BWATi increased with BMI (24% in normal weight, 34% in overweight, 57% in class I obesity, and 65% in class II–III obesity; Ptrend <0.01). Severe BWATi (>0.27 CLS-B/cm2) was associated with higher BMI (Ptrend = 0.046) and greater adipocyte diameter (P = 0.04). Adjusting for BMI, neoadjuvant chemotherapy, and elevated alanine aminotransferase were associated with severe BWATi, and current smoking was associated with mild BWATi (all P < 0.05). BWATi was associated with higher BMI in Hispanic/Latina patients with breast cancer, consistent with previously described associations in other populations.
Data from Chemopreventive Effect of Cinnamon and Its Bioactive Compounds in a Rat Model of Premalignant Prostate Carcinogenesis
Authors: Gopalakrishnan Srividya , Dhaware Mahamaya , Sudharma Athira Anilkumar , Mullapudi Surekha Venkata , Siginam Siva Ramakrishna , Gogulothu Ramesh , Mir Irfan Ahmad , Ismail Ayesha
Published: April 2023

Abstract
Cinnamon and its bioactive compounds inhibit prostate cancer cell proliferation in vitro. The aim of the current study was to assess the chemopreventive efficacy of cinnamon (CN) and its bioactive compounds in vivo using N-methyl-N-nitrosourea (MNU) and testosterone (T) to induce prostate carcinogenesis in male Wistar/National Institute of Nutrition rats. Cancer-induced (CI) rats (n = 10) developed prostatic hyperplasia and prostatic intraepithelial neoplasia. These histopathologic changes were diminished in CI rats fed for 4 months with diets supplemented with either CN (n = 20) or its bioactive compounds (cinnamaldehyde, n = 10 and procyanidin B2, n = 10). Androgen receptor (AR) expression was lower in the prostates of CI rats than in control, but the AR target gene, probasin, was robustly upregulated. Treatment of CI rats with CN or its bioactive compounds upregulated AR expression but inhibited the expression of the 5-alpha reductase genes (Srd5a1 and Srd5a2) and did not further increase probasin expression, suggesting blunted transcriptional activity of AR due to the limited availability of dihydrotestosterone. MNU+T induced an altered oxidant status in rat prostate, which was reflected by an increase in lipid peroxidation and DNA oxidation. These changes were completely or partially corrected by treatment with CN or the bioactive compounds. CN and its active components increased the activity of the apoptotic enzymes caspase-8 and caspase-3 in the prostates of CI rats. In conclusion, our data demonstrate that CN and its bioactive compounds have inhibitory effects on premalignant prostate lesions induced by MNU + T and, therefore, may be considered for the chemoprevention of prostate cancer.
Prevention Relevance:
The research work presented in this article demonstrates the chemopreventive efficacy of CN and its bioactive compounds in a rat model of premalignant prostate cancer.
Supplementary Figure 3 from IDO Is a Nodal Pathogenic Driver of Lung Cancer and Metastasis Development
Authors: Smith Courtney , Chang Mee Young , Parker Katherine H. , Beury Daniel W. , DuHadaway James B. , Flick Hollie E. , Boulden Janette , Sutanto-Ward Erika , Soler Alejandro Peralta , Laury-Kleintop Lisa D. , Mandik-Nayak Laura , Metz Richard , Ostrand-Rosenberg Suzanne , Prendergast George C. , Muller Alexander J.
Published: April 2023

PDF file - 661K, Additional MDSC evaluation for the phenotypic impact of IDO1 loss and for IDO1 expression
Supplementary Figure Legends 1-5, Methods, Discussion from Functional Metabolic Screen Identifies 6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase 4 as an Important Regulator of Prostate Cancer Cell Survival
Authors: Ros Susana , Santos Claudio R. , Moco Sofia , Baenke Franziska , Kelly Gavin , Howell Michael , Zamboni Nicola , Schulze Almut
Published: April 2023

PDF file - 186K
Supplementary Figure 5 from Functional Metabolic Screen Identifies 6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase 4 as an Important Regulator of Prostate Cancer Cell Survival
Authors: Ros Susana , Santos Claudio R. , Moco Sofia , Baenke Franziska , Kelly Gavin , Howell Michael , Zamboni Nicola , Schulze Almut
Published: April 2023

PDF file - 399K
Supplementary Figure 3 from Functional Metabolic Screen Identifies 6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase 4 as an Important Regulator of Prostate Cancer Cell Survival
Authors: Ros Susana , Santos Claudio R. , Moco Sofia , Baenke Franziska , Kelly Gavin , Howell Michael , Zamboni Nicola , Schulze Almut
Published: April 2023

PDF file - 259K
Supplementary Table 6 from Proteomic Profiling Identifies Dysregulated Pathways in Small Cell Lung Cancer and Novel Therapeutic Targets Including PARP1
Authors: Byers Lauren Averett , Wang Jing , Nilsson Monique B. , Fujimoto Junya , Saintigny Pierre , Yordy John , Giri Uma , Peyton Michael , Fan You Hong , Diao Lixia , Masrorpour Fatemeh , Shen Li , Liu Wenbin , Duchemann Boris , Tumula Praveen , Bhardwaj Vikas , Welsh James , Weber Stephanie , Glisson Bonnie S. , Kalhor Neda , Wistuba Ignacio I. , Girard Luc , Lippman Scott M. , Mills Gordon B. , Coombes Kevin R. , Weinstein John N. , Minna John D. , Heymach John V.
Published: April 2023

PDF file, 35K, IC50 values for AZD2281 and AG01469 after 14d treatment.
Supplementary Table 4 from Proteomic Profiling Identifies Dysregulated Pathways in Small Cell Lung Cancer and Novel Therapeutic Targets Including PARP1
Authors: Byers Lauren Averett , Wang Jing , Nilsson Monique B. , Fujimoto Junya , Saintigny Pierre , Yordy John , Giri Uma , Peyton Michael , Fan You Hong , Diao Lixia , Masrorpour Fatemeh , Shen Li , Liu Wenbin , Duchemann Boris , Tumula Praveen , Bhardwaj Vikas , Welsh James , Weber Stephanie , Glisson Bonnie S. , Kalhor Neda , Wistuba Ignacio I. , Girard Luc , Lippman Scott M. , Mills Gordon B. , Coombes Kevin R. , Weinstein John N. , Minna John D. , Heymach John V.
Published: April 2023

PDF file, 53K, mRNA transcripts significantly different between SCLC and NSCLC cell lines.
Supplementary Methods and Figure Legend from Noncovalent Wild-type–Sparing Inhibitors of EGFR T790M
Authors: Lee Ho-June , Schaefer Gabriele , Heffron Timothy P. , Shao Lily , Ye Xiaofen , Sideris Steve , Malek Shiva , Chan Emily , Merchant Mark , La Hank , Ubhayakar Savita , Yauch Robert L. , Pirazzoli Valentina , Politi Katerina , Settleman Jeff
Published: April 2023

PDF file - 130K
Supplementary Figure 2 from Proteomic Profiling Identifies Dysregulated Pathways in Small Cell Lung Cancer and Novel Therapeutic Targets Including PARP1
Authors: Byers Lauren Averett , Wang Jing , Nilsson Monique B. , Fujimoto Junya , Saintigny Pierre , Yordy John , Giri Uma , Peyton Michael , Fan You Hong , Diao Lixia , Masrorpour Fatemeh , Shen Li , Liu Wenbin , Duchemann Boris , Tumula Praveen , Bhardwaj Vikas , Welsh James , Weber Stephanie , Glisson Bonnie S. , Kalhor Neda , Wistuba Ignacio I. , Girard Luc , Lippman Scott M. , Mills Gordon B. , Coombes Kevin R. , Weinstein John N. , Minna John D. , Heymach John V.
Published: April 2023

PDF file, 94K, PARP1 and other proteins associated with AZD2281 response.
Supplementary Table 1 from Hypoxia Induces Phenotypic Plasticity and Therapy Resistance in Melanoma via the Tyrosine Kinase Receptors ROR1 and ROR2
Authors: O'Connell Michael P. , Marchbank Katie , Webster Marie R. , Valiga Alexander A. , Kaur Amanpreet , Vultur Adina , Li Ling , Herlyn Meenhard , Villanueva Jessie , Liu Qin , Yin Xiangfan , Widura Sandy , Nelson Janelle , Ruiz Nivia , Camilli Tura C. , Indig Fred E. , Flaherty Keith T. , Wargo Jennifer A. , Frederick Dennie T. , Cooper Zachary A. , Nair Suresh , Amaravadi Ravi K. , Schuchter Lynn M. , Karakousis Giorgos C. , Xu Wei , Xu Xiaowei , Weeraratna Ashani T.
Published: April 2023

PDF file 283K, Table of patient characteristics, and Wnt5A staining, pre-therapy
Supplementary Figure S3 from Hypoxia Induces Phenotypic Plasticity and Therapy Resistance in Melanoma via the Tyrosine Kinase Receptors ROR1 and ROR2
Authors: O'Connell Michael P. , Marchbank Katie , Webster Marie R. , Valiga Alexander A. , Kaur Amanpreet , Vultur Adina , Li Ling , Herlyn Meenhard , Villanueva Jessie , Liu Qin , Yin Xiangfan , Widura Sandy , Nelson Janelle , Ruiz Nivia , Camilli Tura C. , Indig Fred E. , Flaherty Keith T. , Wargo Jennifer A. , Frederick Dennie T. , Cooper Zachary A. , Nair Suresh , Amaravadi Ravi K. , Schuchter Lynn M. , Karakousis Giorgos C. , Xu Wei , Xu Xiaowei , Weeraratna Ashani T.
Published: April 2023

PDF file 255K, The Wnt5A mediated degradation of ROR1 is PKC-dependent
Supplementary Dataset 1 from Noncovalent Wild-type–Sparing Inhibitors of EGFR T790M
Authors: Lee Ho-June , Schaefer Gabriele , Heffron Timothy P. , Shao Lily , Ye Xiaofen , Sideris Steve , Malek Shiva , Chan Emily , Merchant Mark , La Hank , Ubhayakar Savita , Yauch Robert L. , Pirazzoli Valentina , Politi Katerina , Settleman Jeff
Published: April 2023

XLSX file - 109K, Tumor cell line profiling of G�6976 sensitivity.
Supplementary Figure S2 from Hypoxia Induces Phenotypic Plasticity and Therapy Resistance in Melanoma via the Tyrosine Kinase Receptors ROR1 and ROR2
Authors: O'Connell Michael P. , Marchbank Katie , Webster Marie R. , Valiga Alexander A. , Kaur Amanpreet , Vultur Adina , Li Ling , Herlyn Meenhard , Villanueva Jessie , Liu Qin , Yin Xiangfan , Widura Sandy , Nelson Janelle , Ruiz Nivia , Camilli Tura C. , Indig Fred E. , Flaherty Keith T. , Wargo Jennifer A. , Frederick Dennie T. , Cooper Zachary A. , Nair Suresh , Amaravadi Ravi K. , Schuchter Lynn M. , Karakousis Giorgos C. , Xu Wei , Xu Xiaowei , Weeraratna Ashani T.
Published: April 2023

PDF file 165K, Wnt5A mediated degradation of ROR1 is not mediated through the lysosome
Supplementary Figure S1 from Hypoxia Induces Phenotypic Plasticity and Therapy Resistance in Melanoma via the Tyrosine Kinase Receptors ROR1 and ROR2
Authors: O'Connell Michael P. , Marchbank Katie , Webster Marie R. , Valiga Alexander A. , Kaur Amanpreet , Vultur Adina , Li Ling , Herlyn Meenhard , Villanueva Jessie , Liu Qin , Yin Xiangfan , Widura Sandy , Nelson Janelle , Ruiz Nivia , Camilli Tura C. , Indig Fred E. , Flaherty Keith T. , Wargo Jennifer A. , Frederick Dennie T. , Cooper Zachary A. , Nair Suresh , Amaravadi Ravi K. , Schuchter Lynn M. , Karakousis Giorgos C. , Xu Wei , Xu Xiaowei , Weeraratna Ashani T.
Published: April 2023

PDF file 136K, Gene expression analysis of markers of proliferative and metastatic phenotypes
Supplementary Figure 2 from HER2 Amplification: A Potential Mechanism of Acquired Resistance to EGFR Inhibition in EGFR-Mutant Lung Cancers That Lack the Second-Site EGFRT790M Mutation
Authors: Takezawa Ken , Pirazzoli Valentina , Arcila Maria E. , Nebhan Caroline A. , Song Xiaoling , de Stanchina Elisa , Ohashi Kadoaki , Janjigian Yelena Y. , Spitzler Paula J. , Melnick Mary Ann , Riely Greg J. , Kris Mark G. , Miller Vincent A. , Ladanyi Marc , Politi Katerina , Pao William
Published: April 2023

PDF file - 155K, The effects of combination therapy with afatinib and cetuximab (continued)
Supplementary Figure 1 from HER2 Amplification: A Potential Mechanism of Acquired Resistance to EGFR Inhibition in EGFR-Mutant Lung Cancers That Lack the Second-Site EGFRT790M Mutation
Authors: Takezawa Ken , Pirazzoli Valentina , Arcila Maria E. , Nebhan Caroline A. , Song Xiaoling , de Stanchina Elisa , Ohashi Kadoaki , Janjigian Yelena Y. , Spitzler Paula J. , Melnick Mary Ann , Riely Greg J. , Kris Mark G. , Miller Vincent A. , Ladanyi Marc , Politi Katerina , Pao William
Published: April 2023

PDF file - 190K, The effects of combination therapy with afatinib and cetuximab
Supplementary Figures 1-5 from Genome-wide DNA Methylation Events in TMPRSS2–ERG Fusion-Negative Prostate Cancers Implicate an EZH2-Dependent Mechanism with miR-26a Hypermethylation
Authors: Börno Stefan T. , Fischer Axel , Kerick Martin , Fälth Maria , Laible Mark , Brase Jan C. , Kuner Ruprecht , Dahl Andreas , Grimm Christina , Sayanjali Behnam , Isau Melanie , Röhr Christina , Wunderlich Andrea , Timmermann Bernd , Claus Rainer , Plass Christoph , Graefen Markus , Simon Ronald , Demichelis Francesca , Rubin Mark A. , Sauter Guido , Schlomm Thorsten , Sültmann Holger , Lehrach Hans , Schweiger Michal R.
Published: April 2023

PDF file - 947K, Supplementary Fig. S1. Differential methylations in PCa validated by BS-MS experiments. Supplementary Fig. S2. DNA-Methylomes of prostate cancer differ significantly from normal tissues. Supplementary Fig. S3. Global differences in DNA methylation patterns between tumor, normal, FUS+ and FUS- samples. Supplementary Fig. S4 Patientwise patterns of promoter hypermethylation and corresponding gene expression of EZH2 target genes. Supplementary Fig. S5 Methylation of the miRNA-26a genomic region
Supplementary Figure Legends 1-5, Table Legends 1-4 from Genome-wide DNA Methylation Events in TMPRSS2–ERG Fusion-Negative Prostate Cancers Implicate an EZH2-Dependent Mechanism with miR-26a Hypermethylation
Authors: Börno Stefan T. , Fischer Axel , Kerick Martin , Fälth Maria , Laible Mark , Brase Jan C. , Kuner Ruprecht , Dahl Andreas , Grimm Christina , Sayanjali Behnam , Isau Melanie , Röhr Christina , Wunderlich Andrea , Timmermann Bernd , Claus Rainer , Plass Christoph , Graefen Markus , Simon Ronald , Demichelis Francesca , Rubin Mark A. , Sauter Guido , Schlomm Thorsten , Sültmann Holger , Lehrach Hans , Schweiger Michal R.
Published: April 2023

PDF file - 64K
Supplementary Tables 1-3 and Table 5 from Rescue Screens with Secreted Proteins Reveal Compensatory Potential of Receptor Tyrosine Kinases in Driving Cancer Growth
Authors: Harbinski Fred , Craig Vanessa J. , Sanghavi Sneha , Jeffery Douglas , Liu Lijuan , Sheppard Kelly Ann , Wagner Sabrina , Stamm Christelle , Buness Andreas , Chatenay-Rivauday Christian , Yao Yao , He Feng , Lu Chris X. , Guagnano Vito , Metz Thomas , Finan Peter M. , Hofmann Francesco , Sellers William R. , Porter Jeffrey A. , Myer Vic E. , Graus-Porta Diana , Wilson Christopher J. , Buckler Alan , Tiedt Ralph
Published: April 2023

PDF file - 59K, This file contains additional experimental data relating to the profile of JAA120, secretome screening results, gene expression data, and in vivo MET/FGR inhibitor synergy
Supplementary Table 4 from Rescue Screens with Secreted Proteins Reveal Compensatory Potential of Receptor Tyrosine Kinases in Driving Cancer Growth
Authors: Harbinski Fred , Craig Vanessa J. , Sanghavi Sneha , Jeffery Douglas , Liu Lijuan , Sheppard Kelly Ann , Wagner Sabrina , Stamm Christelle , Buness Andreas , Chatenay-Rivauday Christian , Yao Yao , He Feng , Lu Chris X. , Guagnano Vito , Metz Thomas , Finan Peter M. , Hofmann Francesco , Sellers William R. , Porter Jeffrey A. , Myer Vic E. , Graus-Porta Diana , Wilson Christopher J. , Buckler Alan , Tiedt Ralph
Published: April 2023

XLS file - 147K, Expression of selected RTKs and cognate ligands in cancer cell lines as a basis for selecting models for testing of FGFR/MET inhibitor combinations
Supplementary Tables 1-2 from The mTORC1 Inhibitor Everolimus Prevents and Treats Eμ-Myc Lymphoma by Restoring Oncogene-Induced Senescence
Authors: Wall Meaghan , Poortinga Gretchen , Stanley Kym L. , Lindemann Ralph K. , Bots Michael , Chan Christopher J. , Bywater Megan J. , Kinross Kathryn M. , Astle Megan V. , Waldeck Kelly , Hannan Katherine M. , Shortt Jake , Smyth Mark J. , Lowe Scott W. , Hannan Ross D. , Pearson Richard B. , Johnstone Ricky W. , McArthur Grant A.
Published: April 2023

PDF file - 28K, Primer sequences. ST2: Baseline characteristics of randomized mice
Supplementary Methods from Rescue Screens with Secreted Proteins Reveal Compensatory Potential of Receptor Tyrosine Kinases in Driving Cancer Growth
Authors: Harbinski Fred , Craig Vanessa J. , Sanghavi Sneha , Jeffery Douglas , Liu Lijuan , Sheppard Kelly Ann , Wagner Sabrina , Stamm Christelle , Buness Andreas , Chatenay-Rivauday Christian , Yao Yao , He Feng , Lu Chris X. , Guagnano Vito , Metz Thomas , Finan Peter M. , Hofmann Francesco , Sellers William R. , Porter Jeffrey A. , Myer Vic E. , Graus-Porta Diana , Wilson Christopher J. , Buckler Alan , Tiedt Ralph
Published: April 2023

PDF file - 75K, This file contains detailed descriptions of materials and methods that had to be omitted from the main manuscript due to space limitations
Supplementary Figures 4-6 from The mTORC1 Inhibitor Everolimus Prevents and Treats Eμ-Myc Lymphoma by Restoring Oncogene-Induced Senescence
Authors: Wall Meaghan , Poortinga Gretchen , Stanley Kym L. , Lindemann Ralph K. , Bots Michael , Chan Christopher J. , Bywater Megan J. , Kinross Kathryn M. , Astle Megan V. , Waldeck Kelly , Hannan Katherine M. , Shortt Jake , Smyth Mark J. , Lowe Scott W. , Hannan Ross D. , Pearson Richard B. , Johnstone Ricky W. , McArthur Grant A.
Published: April 2023

PDF file - 2.3MB, Bone marrow cellularity. SF5: Heightened sensitivity of B-cells. SF6. Survival benefit of everolimus
Supplementary Figure Legends from A Hormone–DNA Repair Circuit Governs the Response to Genotoxic Insult
Authors: Goodwin Jonathan F. , Schiewer Matthew J. , Dean Jeffry L. , Schrecengost Randy S. , de Leeuw Renée , Han Sumin , Ma Teng , Den Robert B. , Dicker Adam P. , Feng Felix Y. , Knudsen Karen E.
Published: April 2023

Supplementary Figure Legends - PDF file 66K, Figure legends corresponding to supplemental figures
Supplementary Figure 12 from The mTORC1 Inhibitor Everolimus Prevents and Treats Eμ-Myc Lymphoma by Restoring Oncogene-Induced Senescence
Authors: Wall Meaghan , Poortinga Gretchen , Stanley Kym L. , Lindemann Ralph K. , Bots Michael , Chan Christopher J. , Bywater Megan J. , Kinross Kathryn M. , Astle Megan V. , Waldeck Kelly , Hannan Katherine M. , Shortt Jake , Smyth Mark J. , Lowe Scott W. , Hannan Ross D. , Pearson Richard B. , Johnstone Ricky W. , McArthur Grant A.
Published: April 2023

PDF file - 121K, Full lenght Western blots
Supplementary Figure 3,4 from A Hormone–DNA Repair Circuit Governs the Response to Genotoxic Insult
Authors: Goodwin Jonathan F. , Schiewer Matthew J. , Dean Jeffry L. , Schrecengost Randy S. , de Leeuw Renée , Han Sumin , Ma Teng , Den Robert B. , Dicker Adam P. , Feng Felix Y. , Knudsen Karen E.
Published: April 2023

Supplementary Figure 3,4 - PDF file 443K, Supplemental data demonstrating that exposure to IR promotes cell cycle arrest and AR activity regulates genes required for DNA damage repair
Supplementary Table S1 from Individualized Systems Medicine Strategy to Tailor Treatments for Patients with Chemorefractory Acute Myeloid Leukemia
Authors: Pemovska Tea , Kontro Mika , Yadav Bhagwan , Edgren Henrik , Eldfors Samuli , Szwajda Agnieszka , Almusa Henrikki , Bespalov Maxim M. , Ellonen Pekka , Elonen Erkki , Gjertsen Bjørn T. , Karjalainen Riikka , Kulesskiy Evgeny , Lagström Sonja , Lehto Anna , Lepistö Maija , Lundán Tuija , Majumder Muntasir Mamun , Marti Jesus M. Lopez , Mattila Pirkko , Murumägi Astrid , Mustjoki Satu , Palva Aino , Parsons Alun , Pirttinen Tero , Rämet Maria E. , Suvela Minna , Turunen Laura , Västrik Imre , Wolf Maija , Knowles Jonathan , Aittokallio Tero , Heckman Caroline A. , Porkka Kimmo , Kallioniemi Olli , Wennerberg Krister
Published: April 2023

- XLSX file 452K, DSRT Oncology drug collection
Supplementary Figures 1-9 from Dual Roles of PARP-1 Promote Cancer Growth and Progression
Authors: Schiewer Matthew J. , Goodwin Jonathan F. , Han Sumin , Brenner J. Chad , Augello Michael A. , Dean Jeffry L. , Liu Fengzhi , Planck Jamie L. , Ravindranathan Preethi , Chinnaiyan Arul M. , McCue Peter , Gomella Leonard G. , Raj Ganesh V. , Dicker Adam P. , Brody Jonathan R. , Pascal John M. , Centenera Margaret M. , Butler Lisa M. , Tilley Wayne D. , Feng Felix Y. , Knudsen Karen E.
Published: April 2023

PDF file - 410K, Dose responses, transcriptional, biological, biochemical, and in vivo supplemental data
Supplementary Table S6 from Inhibiting EGF Receptor or SRC Family Kinase Signaling Overcomes BRAF Inhibitor Resistance in Melanoma
Authors: Girotti Maria R. , Pedersen Malin , Sanchez-Laorden Berta , Viros Amaya , Turajlic Samra , Niculescu-Duvaz Dan , Zambon Alfonso , Sinclair John , Hayes Andrew , Gore Martin , Lorigan Paul , Springer Caroline , Larkin James , Jorgensen Claus , Marais Richard
Published: April 2023

PDF file - 48K,Histological analysis of lungs from NOD-SCID mice bearing human melanoma xenografts following vehicle or dasatinib treatment
Supplementary Table S5 from Inhibiting EGF Receptor or SRC Family Kinase Signaling Overcomes BRAF Inhibitor Resistance in Melanoma
Authors: Girotti Maria R. , Pedersen Malin , Sanchez-Laorden Berta , Viros Amaya , Turajlic Samra , Niculescu-Duvaz Dan , Zambon Alfonso , Sinclair John , Hayes Andrew , Gore Martin , Lorigan Paul , Springer Caroline , Larkin James , Jorgensen Claus , Marais Richard
Published: April 2023

PDF file - 44K,SFK phosphorylation intensity in patient sample following treatment with vehicle or dasatinib as indicated
Supplementary Material from Oncogenic EGFR Signaling Activates an mTORC2–NF-κB Pathway That Promotes Chemotherapy Resistance
Authors: Tanaka Kazuhiro , Babic Ivan , Nathanson David , Akhavan David , Guo Deliang , Gini Beatrice , Dang Julie , Zhu Shaojun , Yang Huijun , De Jesus Jason , Amzajerdi Ali Nael , Zhang Yinan , Dibble Christian C. , Dan Hancai , Rinkenbaugh Amanda , Yong William H. , Vinters Harry V. , Gera Joseph F. , Cavenee Webster K. , Cloughesy Timothy F. , Manning Brendan D. , Baldwin Albert S. , Mischel Paul S.
Published: April 2023

PDF file - 161K
Supplementary Table S1 from Inhibiting EGF Receptor or SRC Family Kinase Signaling Overcomes BRAF Inhibitor Resistance in Melanoma
Authors: Girotti Maria R. , Pedersen Malin , Sanchez-Laorden Berta , Viros Amaya , Turajlic Samra , Niculescu-Duvaz Dan , Zambon Alfonso , Sinclair John , Hayes Andrew , Gore Martin , Lorigan Paul , Springer Caroline , Larkin James , Jorgensen Claus , Marais Richard
Published: April 2023

PDF file - 201K,Differentially expressed phosphopeptides in A375(X) vs A375(X)/R cells
Supplementary Figure 4 from Preexisting MEK1 Exon 3 Mutations in V600E/KBRAF Melanomas Do Not Confer Resistance to BRAF Inhibitors
Authors: Shi Hubing , Moriceau Gatien , Kong Xiangju , Koya Richard C. , Nazarian Ramin , Pupo Gulietta M. , Bacchiocchi Antonella , Dahlman Kimberly B. , Chmielowski Bartosz , Sosman Jeffrey A. , Halaban Ruth , Kefford Richard F. , Long Georgina V. , Ribas Antoni , Lo Roger S.
Published: April 2023

PDF file - 76K, Relative expression levels of WT vs. P124SMEK1 in the YUKSI B-RAF/MEK1 double-mutant melanoma short-term culture. Genomic DNA (gDNA) and cDNA derived from YUKSI were subjected to exon 3 sequencing by the Sanger method. Relative peaks of WT vs. P124SMEK1 is shown to be 1:1 for both gDNA and cDNA based on nucleotide chromatograms, showing no allelic bias in RNA expression.
Supplementary Table 1 from PI3K Inhibition Impairs BRCA1/2 Expression and Sensitizes BRCA-Proficient Triple-Negative Breast Cancer to PARP Inhibition
Authors: Ibrahim Yasir H. , García-García Celina , Serra Violeta , He Lei , Torres-Lockhart Kristine , Prat Aleix , Anton Pilar , Cozar Patricia , Guzmán Marta , Grueso Judit , Rodríguez Olga , Calvo Maria Teresa , Aura Claudia , Díez Orland , Rubio Isabel T. , Pérez José , Rodón Jordi , Cortés Javier , Ellisen Leif W. , Scaltriti Maurizio , Baselga José
Published: April 2023

PDF file - 139K, Common BRCA1 and BRCA2 promoter putative transcription factors analysis
Supplementary Figure 9 from Cancer-Specific Requirement for BUB1B/BUBR1 in Human Brain Tumor Isolates and Genetically Transformed Cells
Authors: Ding Yu , Hubert Christopher G. , Herman Jacob , Corrin Philip , Toledo Chad M. , Skutt-Kakaria Kyobi , Vazquez Julio , Basom Ryan , Zhang Bin , Risler Jennifer K. , Pollard Steven M. , Nam Do-Hyun , Delrow Jeffery J. , Zhu Jun , Lee Jeongwu , DeLuca Jennifer , Olson James M. , Paddison Patrick J.
Published: April 2023

PDF file - 134K, Ras-Mapk signaling is inappropriately high BTICs and NHA-Ras cells
Supplementary Figure 4 from Cancer-Specific Requirement for BUB1B/BUBR1 in Human Brain Tumor Isolates and Genetically Transformed Cells
Authors: Ding Yu , Hubert Christopher G. , Herman Jacob , Corrin Philip , Toledo Chad M. , Skutt-Kakaria Kyobi , Vazquez Julio , Basom Ryan , Zhang Bin , Risler Jennifer K. , Pollard Steven M. , Nam Do-Hyun , Delrow Jeffery J. , Zhu Jun , Lee Jeongwu , DeLuca Jennifer , Olson James M. , Paddison Patrick J.
Published: April 2023

PDF file - 1.3MB, Examination of the effects of BUB1B knockdown on mitotic checkpoint activity
Supplementary Table 1 from Coordinate Direct Input of Both KRAS and IGF1 Receptor to Activation of PI3 kinase in KRAS-Mutant Lung Cancer
Authors: Molina-Arcas Miriam , Hancock David C. , Sheridan Clare , Kumar Madhu S. , Downward Julian
Published: April 2023

Supplementary Table 1 - PDF file 45K, Mutational status of twenty-five NSCLC cell lines
Supplementary Figure 6 from Coordinate Direct Input of Both KRAS and IGF1 Receptor to Activation of PI3 kinase in KRAS-Mutant Lung Cancer
Authors: Molina-Arcas Miriam , Hancock David C. , Sheridan Clare , Kumar Madhu S. , Downward Julian
Published: April 2023

Supplementary Figure 6 - PDF file 138K, Drug combinations across the NSCLC cell line panel
Supplementary Methods, Figure 1, Tables 1-6 from Inherited Variation at Chromosome 12p13.33, Including RAD52, Influences the Risk of Squamous Cell Lung Carcinoma
Authors: Shi Jianxin , Chatterjee Nilanjan , Rotunno Melissa , Wang Yufei , Pesatori Angela C. , Consonni Dario , Li Peng , Wheeler William , Broderick Peter , Henrion Marc , Eisen Timothy , Wang Zhaoming , Chen Wei , Dong Qiong , Albanes Demetrius , Thun Michael , Spitz Margaret R. , Bertazzi Pier Alberto , Caporaso Neil E. , Chanock Stephen J. , Amos Christopher I. , Houlston Richard S. , Landi Maria Teresa
Published: April 2023

PDF file - 386K
Supplementary Figure 2 from Activating HER2 Mutations in HER2 Gene Amplification Negative Breast Cancer
Authors: Bose Ron , Kavuri Shyam M. , Searleman Adam C. , Shen Wei , Shen Dong , Koboldt Daniel C. , Monsey John , Goel Nicholas , Aronson Adam B. , Li Shunqiang , Ma Cynthia X. , Ding Li , Mardis Elaine R. , Ellis Matthew J.
Published: April 2023

PDF file - 86K, Flow cytometry measurements of cell-surface expression of HER2 mutants
Supplementary Figure 6 from Chimeric Transcript Generated by cis-Splicing of Adjacent Genes Regulates Prostate Cancer Cell Proliferation
Authors: Zhang Yanmei , Gong Mei , Yuan Huiling , Park Hong G. , Frierson Henry F. , Li Hui
Published: April 2023

PDF file - 68K, Expression of ELK4, SLC45A3-ELK4 and SLC45A3 in LNCaP cells with ELK4 silencing
Supplementary Figure 2 from TGF-β Receptor II Loss Promotes Mammary Carcinoma Progression by Th17-Dependent Mechanisms
Authors: Novitskiy Sergey V. , Pickup Michael W. , Gorska Agnieszka E. , Owens Philip , Chytil Anna , Aakre Mary , Wu Huiyun , Shyr Yu , Moses Harold L.
Published: April 2023

PDF file - 72K
Supplementary Figure 1 from TGF-β Receptor II Loss Promotes Mammary Carcinoma Progression by Th17-Dependent Mechanisms
Authors: Novitskiy Sergey V. , Pickup Michael W. , Gorska Agnieszka E. , Owens Philip , Chytil Anna , Aakre Mary , Wu Huiyun , Shyr Yu , Moses Harold L.
Published: April 2023

PDF file - 276K
Supplementary Figure Legends from Identifying the Ubiquitin Ligase Complex That Regulates the NF1 Tumor Suppressor and Ras
Authors: Hollstein Pablo E. , Cichowski Karen
Published: April 2023

Supplementary Figure Legends - PDF file 64K, Supplementary Figure Legends
Supplementary Figures S1-S10 from A Functional Cancer Genomics Screen Identifies a Druggable Synthetic Lethal Interaction between MSH3 and PRKDC
Authors: Dietlein Felix , Thelen Lisa , Jokic Mladen , Jachimowicz Ron D. , Ivan Laura , Knittel Gero , Leeser Uschi , van Oers Johanna , Edelmann Winfried , Heukamp Lukas C. , Reinhardt H. Christian
Published: April 2023

PDF file 3500K, Potency of KU60648 across 94 cancer cell lines (Figure S1), comparison of KU60648-sensitivity in mutant vs. wildtype lines for 9 exemplary DNA repair-associated genes (Figure S2), MSH3 variants and Sanger sequencing of BRCA1 (Figure S3), cell cycle analysis of 9 cell lines under KU60648 exposure (Figure S4), analysis of synergistic effects between KU60648 and doxorubicin in six cell lines (Figure S5), validation of PRKDC knockdown efficiency (Figure S6), analysis of XRCC5 knockdown cells (Figure S7), analysis of MSH3 knockout cells (Figure S8), monitoring of DNA double-strand break repair in 3 cell lines (Figure S9), waterfall plots of tumor volumes after 11-day treatment with KU60648 (Figure S10)
Supplementary Figure 4 from Stromal EGF and IGF-I Together Modulate Plasticity of Disseminated Triple-Negative Breast Tumors
Authors: Castaño Zafira , Marsh Timothy , Tadipatri Ramya , Kuznetsov Hanna S. , Al-Shahrour Fatima , Paktinat Mahnaz , Greene-Colozzi April , Nilsson Björn , Richardson Andrea L. , McAllister Sandra S.
Published: April 2023

PDF file - 508K, Tumor Microenvironment of Hosts with TNBC Expresses EGF and IGF-1 and Supports Responding Tumor Cell Malignancy.
Supplementary File 2 from Genomic Characterization of Brain Metastases Reveals Branched Evolution and Potential Therapeutic Targets
Authors: Brastianos Priscilla K. , Carter Scott L. , Santagata Sandro , Cahill Daniel P. , Taylor-Weiner Amaro , Jones Robert T. , Van Allen Eliezer M. , Lawrence Michael S. , Horowitz Peleg M. , Cibulskis Kristian , Ligon Keith L. , Tabernero Josep , Seoane Joan , Martinez-Saez Elena , Curry William T. , Dunn Ian F. , Paek Sun Ha , Park Sung-Hye , McKenna Aaron , Chevalier Aaron , Rosenberg Mara , Barker Frederick G. , Gill Corey M. , Van Hummelen Paul , Thorner Aaron R. , Johnson Bruce E. , Hoang Mai P. , Choueiri Toni K. , Signoretti Sabina , Sougnez Carrie , Rabin Michael S. , Lin Nancy U. , Winer Eric P. , Stemmer-Rachamimov Anat , Meyerson Matthew , Garraway Levi , Gabriel Stacey , Lander Eric S. , Beroukhim Rameen , Batchelor Tracy T. , Baselga José , Louis David N. , Getz Gad , Hahn William C.
Published: April 2023

Supplementary File 2. Detailed plots of SCNA calls in TARGET genes. The description for the plots in Supplementary File 2 can be found in the Legend of Supplementary Figure S3.
Supplementary Methods, Table S2 from Co-occurring Genomic Alterations Define Major Subsets of KRAS-Mutant Lung Adenocarcinoma with Distinct Biology, Immune Profiles, and Therapeutic Vulnerabilities
Authors: Skoulidis Ferdinandos , Byers Lauren A. , Diao Lixia , Papadimitrakopoulou Vassiliki A. , Tong Pan , Izzo Julie , Behrens Carmen , Kadara Humam , Parra Edwin R. , Canales Jaime Rodriguez , Zhang Jianjun , Giri Uma , Gudikote Jayanthi , Cortez Maria A. , Yang Chao , Fan Youhong , Peyton Michael , Girard Luc , Coombes Kevin R. , Toniatti Carlo , Heffernan Timothy P. , Choi Murim , Frampton Garrett M. , Miller Vincent , Weinstein John N. , Herbst Roy S. , Wong Kwok-Kin , Zhang Jianhua , Sharma Padmanee , Mills Gordon B. , Hong Waun K. , Minna John D. , Allison James P. , Futreal Andrew , Wang Jing , Wistuba Ignacio I. , Heymach John V.
Published: April 2023

Supplementary Methods. Supplementary Table 2. Details of the antibody used for TTF1 immunostaining.