bluuebunny/crossref_metadata_2025 huggingface dataset:
Data from Risk of Prostate Cancer–related Death Following a Low PSA Level in the PLCO Trial
Authors: Landy Rebecca , Houghton Lauren C. , Berg Christine D. , Grubb Robert L. , Katki Hormuzd A. , Black Amanda
Published: April 2023

Abstract
Longer-than-annual screening intervals have been suggested to improve the balance of benefits and harms in prostate cancer screening. Many researchers, societies, and guideline committees have suggested that screening intervals could depend on the prostate-specific antigen (PSA) result. We analyzed data from men (N = 33,897) ages 55–74 years with a baseline PSA test in the intervention arm of the Prostate, Lung, Colorectal and Ovarian Cancer Screening trial (United States, 1993–2001). We estimated 5- and 10-year risks of aggressive cancer (Gleason ≥8 and/or stage III/IV) and 15-year risks of prostate cancer–related mortality for men with baseline PSA ≤ 0.5 ng/mL (N = 4,862), ≤1 ng/mL (N = 15,110), and 1.01–2.5 ng/mL (N = 12,422). A total of 217 men died from prostate cancer through 15 years, although no men with PSA ≤ 1 ng/mL died from prostate cancer within 5 years [95% confidence interval (CI), 0.00%–0.03%]. The 5-year incidence of aggressive disease was low (0.08%; 95% CI, 0.03%–0.12%) for men with PSA ≤ 1 ng/mL, and higher for men with baseline PSA 1.01–2.5 ng/mL (0.51%; 95% CI, 0.38%–0.74%). No men aged ≥65 years with PSA ≤ 0.5 ng/mL died from prostate cancer within 15 years (95% CI, 0.00%–0.32%), and their 10-year incidence of aggressive disease was low (0.25%; 95% CI, 0.00%–0.53%). Compared with white men, black men with PSA ≤ 1 ng/mL had higher 10-year rates of aggressive disease (1.6% vs. 0.4%; P < 0.01). Five-year screening intervals may be appropriate for the 45% of men with PSA ≤ 1 ng/mL. Men ages ≥65 years with PSA ≤ 0.5 ng/mL could consider stopping screening. Substantial risk disparities suggest appropriate screening intervals could depend on race/ethnicity.
Data from Immune Checkpoint Inhibition is Safe and Effective for Liver Cancer Prevention in a Mouse Model of Hepatocellular Carcinoma
Authors: Chung Andrew S. , Mettlen Marcel , Ganguly Debolina , Lu Tianshi , Wang Tao , Brekken Rolf A. , Hsiehchen David , Zhu Hao
Published: April 2023

Abstract
Cirrhosis is a high-risk state for hepatocellular carcinoma (HCC) development and represents an opportunity to prevent cancer. In the precancerous state of cirrhosis, there is an accumulation of neoantigens that may be specifically targetable through immunotherapy. We asked whether immune checkpoint inhibition could prevent tumorigenesis in a mouse model of diethylnitrosamine and carbon tetrachloride–induced HCC. We found that initiation of anti-PD-1 therapy prior to tumorigenesis could prevent up to 46% of liver tumors. This significant reduction in tumor burden was accompanied by infiltration of CD4+ Th cells and CD8+ cytotoxic T cells into the liver parenchyma. Importantly, anti-PD-1 therapy did not exacerbate liver dysfunction or worsen overall health in this liver disease model. Given the safety and preservation of quality of life observed with long-term immunotherapy use, an immunotherapy chemoprevention strategy is likely associated with a low risk-to-benefit ratio and high value care in select patients. These results encourage a prevention trial in cirrhotic patients with the highest risk of developing HCC.

See related Spotlight by Mohammed et al., p. 897
Data from Predicting Progression of Low-Grade Oral Dysplasia Using Brushing-Based DNA Ploidy and Chromatin Organization Analysis
Authors: Datta Madhurima , Laronde Denise M. , Rosin Miriam P. , Zhang Lewei , Chan Bertrand , Guillaud Martial
Published: April 2023

Abstract
Most oral cancers arise from oral potentially malignant lesions, which show varying grades of dysplasia. Risk of progression increases with increasing grade of dysplasia; however, risk prediction among oral low-grade dysplasia (LGD), that is, mild and moderate dysplasia can be challenging as only 5%–15% transform. Moreover, grading of dysplasia is subjective and varies with the area of the lesion being biopsied. To date, no biomarkers or tools are used clinically to triage oral LGDs. This study uses a combination of DNA ploidy and chromatin organization (CO) scores from cells obtained from lesion brushings to identify oral LGDs at high-risk of progression. A total of 130 lesion brushings from patients with oral LGDs were selected of which 16 (12.3%) lesions progressed to severe dysplasia or cancer. DNA ploidy and CO scores were analyzed from nuclear features measured by our in-house DNA image cytometry (DNA-ICM) system and used to classify brushings into low-risk and high-risk. A total of 57 samples were classified as high-risk of which 13 were progressors. High-risk DNA brushing was significant for progression (P = 0.001) and grade of dysplasia (P = 0.004). Multivariate analysis showed high-risk DNA brushing showed 5.1- to 8-fold increased risk of progression, a stronger predictor than dysplasia grading and lesion clinical features. DNA-ICM can serve as a non-invasive, high-throughput tool to identify high-risk lesions several years before transformation. This will help clinicians focus on such lesions whereas low-risk lesions may be spared from unnecessary biopsies.

Prevention Relevance: DNA ploidy and chromatin organization of cells collected from oral potentially malignant lesions (OPMLs) can identify lesions at high-risk of progression several years prior. This non-invasive test would enable clinicians to triage high-risk (OPMLs) for closer follow-up while low-risk lesions can undergo less frequent biopsies reducing burden on healthcare resources.
Data from The COX-2–PGE2 Pathway Promotes Tumor Evasion in Colorectal Adenomas
Authors: Wei Jie , Zhang Jinyu , Wang Dingzhi , Cen Bo , Lang Jessica D. , DuBois Raymond N.
Published: April 2023

Abstract
The mechanisms underlying the regulation of a checkpoint receptor, PD-1, in tumor-infiltrating immune cells during the development of colorectal cancer are not fully understood. Here we demonstrate that COX-2–derived PGE2, an inflammatory mediator and tumor promoter, induces PD-1 expression by enhancing NFκB's binding to the PD-1 promoter via an EP4–PI3K–Akt signaling pathway in both CD8+ T cells and macrophages. Moreover, PGE2 suppresses CD8+ T-cell proliferation and cytotoxicity against tumor cells and impairs macrophage phagocytosis of cancer cells via an EP4–PI3K–Akt–NFκB–PD-1 signaling pathway. In contrast, inhibiting the COX-2–PGE2–EP4 pathway increases intestinal CD8+ T-cell activation and proliferation and enhances intestinal macrophage phagocytosis of carcinoma cells accompanied by reduction of PD-1 expression in intestinal CD8+ T cells and macrophages in ApcMin/+ mice. PD-1 expression correlates well with COX-2 levels in human colorectal cancer specimens. Both elevated PD-1 and COX-2 are associated with poorer overall survival in patients with colorectal cancer. Our results uncover a novel role of PGE2 in tumor immune evasion. They may provide the rationale for developing new therapeutic approaches to subvert this process by targeting immune checkpoint pathways using EP4 antagonists. In addition, our findings reveal a novel mechanism explaining how NSAIDs reduce colorectal cancer risk by suppressing tumor immune evasion.
Prevention Relevance:
These findings provide a potential explanation underlying the chemopreventive effect of NSAIDs on reducing colorectal cancer incidence during premalignancy and provide a rationale for developing EP4 antagonists for colorectal cancer prevention and treatment. Simply targeting PGE2 signaling alone may be efficacious in colorectal cancer prevention and treatment, avoiding side effects associated with NSAIDs.
Data from Baseline Oral Microbiome and All-cancer Incidence in a Cohort of Nonsmoking Mexican American Women
Authors: Zhang Xiaotao , Hoffman Kristi L. , Wei Peng , Elhor Gbito Kplola Y. , Joseph Reji , Li Fangyu , Scheet Paul , Chang Shine , Petrosino Joseph F. , Daniel Carrie R.
Published: April 2023

Abstract
Given the increasing evidence that the oral microbiome is involved in obesity, diabetes, and cancer risk, we investigated baseline oral microbiota profiles in relation to all-cancer incidence among nonsmoking women enrolled in a Texas cohort of first- and second-generation immigrants of Mexican origin. We characterized the 16Sv4 rDNA microbiome in oral mouthwash samples collected at baseline from a representative subset of 305 nonsmoking women, ages 20–75 years. We evaluated within- (alpha) and between-sample (beta) diversity by incident cancer status and applied linear discriminant analysis (LDA) effect size analysis to assess differentially abundant taxa. Diversity and candidate taxa in relation to all-cancer incidence were evaluated in multivariable-adjusted Cox regression models. Over 8.8 median years of follow-up, 31 incident cancer cases were identified and verified. Advanced age, greater acculturation, and cardiometabolic risk factors were associated with all-cancer incidence. Higher alpha diversity (age-adjusted Pdifference < 0.01) and distinct biological communities (Pdifference = 0.002) were observed by incident cancer status. Each unit increase in the Shannon diversity index yielded >8-fold increase in all-cancer and obesity-related cancer risk [multivariable-adjusted HR (95% confidence interval), 8.11 (3.14–20.94) and 10.72 (3.30–34.84), respectively] with similar findings for the inverse Simpson index. Streptococcus was enriched among women who did not develop cancer, while Fusobacterium, Prevotella, Mogibacterium, Campylobacter, Lachnoanaerobaculum, Dialister, and Atopobium were higher among women who developed cancer (LDA score ≥ 3; q-value < 0.01). This initial study of oral microbiota and overall cancer risk in nonsmoking Mexican American women suggests the readily accessible oral microbiota as a promising biomarker.
Prevention Relevance:
Mexican American women suffer a disproportionate burden of chronic health conditions that increase cancer risk. Few investigations of the microbiome, a key determinant of host health, have been conducted among this group. Oral microbiota profiles may provide early and accessible cancer biomarker data on invasive bacteria or community disruptions.
Data from Circulating Receptor Activator of Nuclear Factor-κB (RANK), RANK ligand (RANKL), and Mammographic Density in Premenopausal Women
Authors: Toriola Adetunji T. , Appleton Catherine M. , Zong Xiaoyu , Luo Jingqin , Weilbaecher Katherine , Tamimi Rulla M. , Colditz Graham A.
Published: April 2023

Abstract
The receptor activator of nuclear factor-κB (RANK) pathway plays essential roles in breast development. Mammographic density is a strong risk factor for breast cancer, especially in premenopausal women. We, therefore, investigated the associations of circulating RANK and soluble RANK ligand (sRANKL) with mammographic density in premenopausal women. Mammographic density was measured as volumetric percent density in 365 cancer-free premenopausal women (mean age, 47.5 years) attending screening mammogram at the Washington University School of Medicine (St. Louis, MO). We used linear regression models adjusted for confounders, to compare the least-square means of volumetric percent density across tertiles of circulating RANK and sRANKL. Furthermore, because RANKL levels in mammary tissue are modulated by progesterone, we stratified analyses by progesterone levels. The mean volumetric percent density increased across tertiles of circulating RANK from 8.6% in tertile 1, to 8.8% in tertile 2, and 9.5% in tertile 3 (Ptrend = 0.02). For sRANKL, the mean volumetric percent density was 8.5% in tertile 1, 9.4% in tertile 2, and 9.0% in tertile 3 (Ptrend = 0.30). However, when restricted to women with higher progesterone levels, the mean volumetric percent density increased from 9.1% in sRANKL tertile 1 to 9.5% in tertile 2, and 10.1% in tertile 3 (Ptrend = 0.01). Circulating RANK was positively associated with volumetric percent density, while circulating sRANKL was positively associated with volumetric percent density among women with higher progesterone levels. These findings support the inhibition of RANKL signaling as a pathway to reduce mammographic density and possibly breast cancer incidence in high-risk women with dense breasts.
Data from Colonoscopy and Sigmoidoscopy Use among the Average-Risk Population for Colorectal Cancer: A Systematic Review and Trend Analysis
Authors: Cardoso Rafael , Niedermaier Tobias , Chen Chen , Hoffmeister Michael , Brenner Hermann
Published: April 2023

Abstract
Monitoring population-level colonoscopy and sigmoidoscopy use is crucial to estimate the future burden of colorectal cancer and guide screening efforts. We conducted a systematic literature search on colonoscopy and sigmoidoscopy use, published between November 2016 and December 2018 in the databases PubMed and Web of Science to update previous reviews and analyze time trends for various countries. In addition, we used data from the German and European Health Interview Surveys and the National Health Interview Survey to explore recent time trends for Germany and the US, respectively. The literature search yielded 23 new articles: fourteen from the US and nine from Australia, Canada, England, Germany, Saudi Arabia, and South Korea. Colonoscopy use within 10 years was highest and, apart from the youngest age groups eligible for colorectal cancer screening, kept increasing to levels close to 60% in the US and Germany. A recent steep increase was also observed for South Korea. Limited data were available on sigmoidoscopy use; regional studies from the US suggest that sigmoidoscopy has become rarely used. Despite high uptake and ongoing increase in the US, Germany, and South Korea, use of colonoscopy and sigmoidoscopy has either remained low or essentially unknown for the majority of countries.
Data from Does Mutated K-RAS Oncogene Attenuate the Effect of Sulindac in Colon Cancer Chemoprevention?
Authors: Rice Photini F.S. , Ehrichs Kevin G. , Jones Mykella S. , Chen Hwudarw , Hsu Chiu-Hsieh , Abril Edward R. , Nagle Raymond B. , Besselsen David G. , Barton Jennifer K. , Ignatenko Natalia A.
Published: April 2023

Abstract
The NSAID sulindac has been successfully used alone or in combination with other agents to suppress colon tumorigenesis in patients with genetic predisposition and also showed its efficacy in prevention of sporadic colon adenomas. At the same time, some experimental and clinical reports suggest that a mutant K-RAS oncogene may negate sulindac antitumor efficacy. To directly assess sulindac activity at suppressing premalignant lesions carrying K-RAS mutation, we utilized a novel mouse model with an inducible colon-specific expression of the mutant K-ras oncogene (K-rasG12D). Tumor development and treatment effects were monitored by minimally invasive endoscopic Optical coherence tomography. Expression of the mutant K-ras allele accelerated azoxymethane (AOM)-induced colon carcinogenesis in C57BL/6 mice, a strain otherwise resistant to this carcinogen. Sulindac completely prevented AOM-induced tumor formation in K-ras wild-type (K-ras wt) animals. In K-rasG12D–mutant mice, a 38% reduction in tumor number, an 83% reduction in tumor volume (P ≤ 0.01) and an increase in the number of adenoma-free mice (P = 0.04) were observed. The partial response of K-RasG12D animals to sulindac treatment was evident by the decrease in mucosal thickness (P < 0.01) and delay in progression of the precancerous aberrant crypt foci to adenomas. Molecular analyses showed significant induction in cyclooxygenase 2 (COX-2), cleaved caspase-3 (CC3), and Ki-67 expression by AOM, but not sulindac treatment, in all genotypes. Our data underscore the importance of screening for K-RAS mutations in individuals with colon polyps to provide more personalized interventions targeting mutant K-RAS signaling pathways. Cancer Prev Res; 11(1); 16–26. ©2017 AACR.
Data from Effects of Walnut Consumption on Colon Carcinogenesis and Microbial Community Structure
Authors: Nakanishi Masako , Chen Yanfei , Qendro Veneta , Miyamoto Shingo , Weinstock Erica , Weinstock George M. , Rosenberg Daniel W.
Published: April 2023

Abstract
Walnuts are composed of a complex array of biologically active constituents with individual cancer-protective properties. Here, we assessed the potential benefit of whole walnut consumption in a mouse tumor bioassay using azoxymethane. In study 1, a modest reduction (1.3-fold) in tumor numbers was observed in mice fed a standard diet (AIN-76A) containing 9.4% walnuts (15% of total fat). In study 2, the effects of walnut supplementation was tested in the Total Western Diet (TWD). There was a significant reduction (2.3-fold; P < 0.02) in tumor numbers in male mice fed TWD containing 7% walnuts (10.5% of total fat). Higher concentrations of walnuts lacked inhibitory effects, particularly in female mice, indicating there may be optimal levels of dietary walnut intake for cancer prevention. Since components of the Mediterranean diet have been shown to affect the gut microbiome, the effects of walnuts were therefore tested in fecal samples using 16S rRNA gene sequencing. Carcinogen treatment reduced the diversity and richness of the gut microbiome, especially in male mice, which exhibited lower variability and greater sensitivity to environmental changes. Analysis of individual operational taxonomic units (OTU) identified specific groups of bacteria associated with carcinogen exposure, walnut consumption, and/or both variables. Correlation analysis also identified specific OTU clades that were strongly associated with the presence and number of tumors. Taken together, our results indicate that walnuts afford partial protection to the colon against a potent carcinogenic insult, and this may be due, in part, to walnut-induced changes to the gut microbiome. Cancer Prev Res; 9(8); 692–703. ©2016 AACR.
Data from Metabolomics Profiles of Hepatocellular Carcinoma in a Korean Prospective Cohort: The Korean Cancer Prevention Study-II
Authors: Jee Sun Ha , Kim Minjoo , Kim Minkyung , Yoo Hye Jin , Kim Hyungyoon , Jung Keum Ji , Hong Seri , Lee Jong Ho
Published: April 2023

Abstract
In the prospective Korean Cancer Prevention Study-II (KCPS-II), we investigated the application of metabolomics to differentiate subjects with incident hepatocellular carcinoma (HCC group) from subjects who remained free of cancer (control group) during a mean follow-up period of 7 years with the aim of identifying valuable metabolic biomarkers for HCC. We used baseline serum samples from 75 subjects with incident HCC and 134 age- and gender-matched cancer-free subjects. Serum metabolic profiles associated with HCC incidence were investigated via metabolomics analysis. Compared with the control group, the HCC group showed significantly higher serum levels of aspartate aminotransferase (AST), alanine aminotransferase, and γ-glutamyl transpeptidase. At baseline, compared with the control group, the HCC group showed significantly higher levels of 9 metabolites, including leucine, 5-hydroxyhexanoic acid, phenylalanine, tyrosine, arachidonic acid, and tauroursodeoxycholic acid (TUDCA), but lower levels of 28 metabolites, including oleamide, androsterone sulfate, L-palmitoylcarnitine, lysophosphatidic acid (LPA) 16:0, LPA 18:1, and lysophosphatidylcholines (lysoPC). Multiple linear regression revealed that the incidence of HCC was associated with the levels of tyrosine, AST, lysoPCs (16:1, 20:3), oleamide, 5-hydroxyhexanoic acid, androsterone sulfate, and TUDCA (adjusted R2 = 0.514, P = 0.036). This study showed the clinical relevance of the dysregulation of not only branched amino acids, aromatic amino acids, and lysoPCs but also bile acid biosynthesis and linoleic acid, arachidonic acid, and fatty acid metabolism. In addition, tyrosine, AST, lysoPCs (16:1, 20:3), oleamide, 5-hydroxyhexanoic acid, androsterone sulfate, and TUDCA were identified as independent variables associated with the incidence of HCC. Cancer Prev Res; 11(5); 303–12. ©2018 AACR.
Data from Vitamin D Signaling Suppresses Early Prostate Carcinogenesis in TgAPT121 Mice
Authors: Fleet James C. , Kovalenko Pavlo L. , Li Yan , Smolinski Justin , Spees Colleen , Yu Jun-Ge , Thomas-Ahner Jennifer M. , Cui Min , Neme Antonio , Carlberg Carsten , Clinton Steven K.
Published: April 2023

Abstract
We tested whether lifelong modification of vitamin D signaling can alter the progression of early prostate carcinogenesis in studies using mice that develop high-grade prostatic intraepithelial neoplasia that is similar to humans. Two tissue-limited models showed that prostate vitamin D receptor (VDR) loss increased prostate carcinogenesis. In another study, we fed diets with three vitamin D3 levels (inadequate = 25 IU/kg diet, adequate for bone health = 150 IU/kg, or high = 1,000 IU/kg) and two calcium levels (adequate for bone health = 0.5% and high = 1.5%). Dietary vitamin D caused a dose-dependent increase in serum 25-hydroxyvitamin D levels and a reduction in the percentage of mice with adenocarcinoma but did not improve bone mass. In contrast, high calcium suppressed serum 1,25-dihydroxyvitamin D levels and improved bone mass but increased the incidence of adenocarcinoma. Analysis of the VDR cistrome in RWPE1 prostate epithelial cells revealed vitamin D–mediated regulation of multiple cancer-relevant pathways. Our data support the hypothesis that the loss of vitamin D signaling accelerates the early stages of prostate carcinogenesis, and our results suggest that different dietary requirements may be needed to support prostate health or maximize bone mass.
Significance:
This work shows that disrupting vitamin D signaling through diet or genetic deletion increases early prostate carcinogenesis through multiple pathways. Higher-diet vitamin D levels are needed for cancer than bone.
Data from Estrogen-DNA Adducts and Breast Cancer Risk in Premenopausal Asian Women
Authors: Lin Ching-Hung , Zahid Muhammad , Kuo Wen-Hung , Hu Fu-Chang , Wang Ming-Yang , Chen I-Chun , Beseler Cheryl L. , Mondal Bodhisattwa , Lu Yen-Shen , Rogan Eleanor G. , Cheng Ann-Lii
Published: April 2023

Abstract
The incidence of breast cancer among premenopausal women has been increasing rapidly in recent decades in East Asia. This case–control study investigated whether estrogen-DNA adducts were associated with breast cancer risk in Taiwan. The control group (n = 146) comprised healthy female volunteers and women with non-proliferative breast disease. The case group (n = 221) comprised women either with proliferative benign breast disease or breast cancer. The ratios of estrogen-DNA adducts to their respective metabolites and conjugates in plasma were analyzed using ultraperformance LC/MS-MS. The SNPs of CYP1A1, CYP1B1, and COMT were genotyped. Logistic regression model was used to compare the estrogen-DNA adduct ratios between the two groups. The estrogen-DNA adduct ratio in the case group was significantly higher than that in the control group (median ratio: 58.52 vs. 29.36, P = 0.004). A multiple logistic regression model demonstrated that a unit increase in the natural log of the estrogen-DNA adduct ratio in premenopausal women was a significant predictor of breast cancer risk, with an estimated hazard ratio of 1.718 (1.444−2.046, P < 0.001). However, the CYP1A1, CYP1B1, and COMT SNPs were not associated with the estrogen-DNA adduct ratios. In conclusion, plasma estrogen-DNA adduct ratio was associated with the presence of breast cancer or proliferating benign breast disease in premenopausal women in Taiwan.
Prevention Relevance:
This study provides evidence that endogenous estrogen-induced genotoxicity may contribute to the carcinogenesis of breast cancer in premenopausal Asian women. This work could have important preventive implication for the emerging disease in East Asia.
Data from Three-Year Interval for the Multi-Target Stool DNA Test for Colorectal Cancer Screening: A Longitudinal Study
Authors: Imperiale Thomas F. , Lavin Philip T. , Marti Tara N. , Jakubowski Debbie , Itzkowitz Steven H. , May Folasade P. , Limburg Paul J. , Sweetser Seth , Daghestani Anas , Berger Barry M.
Published: April 2023

Abstract
Data supporting the clinical utility of multi-target stool DNA (mt-sDNA) at the guideline-recommended 3-year interval have not been reported.

Between April 2015 and July 2016, candidates for colorectal cancer screening whose providers prescribed the mt-sDNA test were enrolled. Participants with a positive baseline test were recommended for colonoscopy and completed the study. Those with a negative baseline test were followed annually for 3 years. In year 3, the mt-sDNA test was repeated and colonoscopy was recommended independent of results. Data were analyzed using the Predictive Summary Index (PSI), a measure of the gain in certainty for dichotomous diagnostic tests (where a positive value indicates a net gain), and by comparing observed versus expected colorectal cancers and advanced precancerous lesions.

Of 2,404 enrolled subjects, 2,044 (85%) had a valid baseline mt-sDNA result [284 (13.9%) positive and 1,760 (86.1%) negative]. Following participant attrition, the year 3 intention to screen cohort included 591 of 1,760 (33.6%) subjects with valid mt-sDNA and colonoscopy results, with no colorectal cancers and 63 advanced precancerous lesions [22 (34.9%) detected by mt-sDNA] and respective PSI values of 0% (P = 1) and 9.3% (P = 0.01). The observed 3-year colorectal cancer yield was lower than expected (one-sided P = 0.09), while that for advanced precancerous lesions was higher than expected (two-sided P = 0.009).

Repeat mt-sDNA screening at a 3-year interval resulted in a statistically significant gain in detection of advanced precancerous lesions. Due to absence of year 3 colorectal cancers, the PSI estimate for colorectal cancer was underpowered and could not be reliably quantified. Larger studies are required to assess the colorectal cancer study findings.
Prevention Relevance:
Understanding the 3-year yield of mt-sDNA for colorectal cancer and advanced precancerous polyps is required to ensure the clinical appropriateness of the 3-year interval and to optimize mt-sDNA's screening effectiveness.
Data from Simple Prediction Model for Colorectal Serrated Polyps: Development and External Validation Study in US Prospective Cohorts
Authors: Lyu Zhangyan , Hang Dong , He Xiaosheng , Wu Kana , Cao Yin , Rosner Bernard , Chan Andrew T. , Ogino Shuji , Li Ni , Dai Min , Giovannucci Edward L. , Song Mingyang
Published: April 2023

Abstract
Serrated polyps (SPs) are precursors for colorectal cancer (CRC) and contribute disproportionately to post-colonoscopy cancers. Leveraging three US cohorts (43974 women and 5322 men), we developed prediction models for high-risk SPs (sized ≥10 mm or ≥3) among individuals undergoing their first colonoscopy screening. We then validated the model in the Partners Colonoscopy Cohort (51203 women and 39077 men). We evaluated discrimination and calibration using the C-statistic and Hosmer–Lemeshow test, respectively. The age & family history model generated a C-statistic (95% CI) of 0.57 (0.56-0.58) in women and 0.58 (0.55-0.61) in men. Further inclusion of smoking, alcohol, and body mass index (the simple model) increased the C-statistic (95% CI) to 0.68 (0.67-0.69) in women and 0.68 (0.66-0.71) in men (all P<0.001). Adding more predictors did not provide much incremental predictivity. In the validation cohort, moderate discrimination was observed in both women (0.60, 0.58-0.61) and men (0.60, 0.59-0.62). Notably, the simple model also yielded similar C-statistics for a composite endpoint of SPs and high-risk conventional adenomas (HRAs) (women, 0.62, 0.62-0.63; men, 0.63, 0.61-0.64). The model was adequately calibrated in both sets of cohorts. In summary, we developed and externally validated a simple prediction model based on five major risk factors for high-risk SPs that may be useful for healthy lifestyle recommendations and tailored CRC screening.
Data from Breastfeeding and Mammographic Breast Density: A Cross-sectional Study
Authors: Getz Kayla R. , Adedokun Babatunde , Xu Shuai , Toriola Adetunji T.
Published: April 2023

Abstract
Breastfeeding is inversely associated with breast cancer risk but the associations of breastfeeding with mammographic breast density (MBD) are not clear. We investigated the association between breastfeeding and volumetric measures of MBD (volumetric percent density (VPD), dense volume (DV) and non-dense volume (NDV)) and evaluated whether it differs by race, menopausal status, and body mass index (BMI).
The study population was comprised of 964 women (67% non-Hispanic white, 29% non-Hispanic black) who had screening mammography at Washington University School of Medicine, St. Louis, MO. VPD, DV and NDV were log10 transformed. We performed multivariable linear regression models adjusted for age, BMI, family history of breast cancer, race, and age at menarche among all participants and exclusively in parous women.
Mean age was 50.7 years. VPD was 12% lower among women who breastfed 0-6 months, (10^β=0.88, 95%CI (0.79,0.98)) compared to nulliparous women. Breastfeeding was inversely associated with DV (parous never breastfed: 10^β=0.93, 95%CI (0.83,1.04), breastfed 0-6 months: 10^β=0.91, 95%CI (0.79,1.05), breastfed 7-12 months: 10^β=0.94, 95%CI (0.81,1.10), breastfed >12 months: 10^β=0.87, 95%CI (0.78,0.98), p-trend=0.03). BMI modified the association between breastfeeding and VPD. Women who breastfed for 0-6 months and had a BMI < 25kg/m2 had lower VPD compared to nulliparous women, but among women with a BMI ≥ 25kg/m2 there was no association (p-interaction=0.04).
In this diverse study population, the association of breastfeeding with VPD appears to be modified by BMI, but not by race or menopausal status. Future research exploring the associations of breastfeeding with other mammographic features are needed.
Supplementary Figure 2 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 - 291K
Supplementary Figure 5 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 - 248K, PKC412 is a reversible EGFR T790M inhibitor.
Supplementary Dataset 2 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 - 242K, Ambit kinome profiling with 0.5 μM G�6976.
Supplementary Figure 4 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 - 91K, Levels of HER2 affect the sensitivity of EGFR-mutant NSCLC cells to EGFR TKIs
Supplementary Figure 3 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 - 36K, Increased murine Her2 expression in erlotinib-resistant mutant EGFR-induced transgenic mouse tumors
Supplementary Figures 7-8 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 - 209K, Everolimus is associated with changes to the immunophenotype. SF8: Continued daily dosing with everolimus results in cell cycle arrest
Supplementary Table 1 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 Table 1 - PDF file 282K, Supplemental table listing primer sequences utilized throughout study
Supplementary Methods 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 Methods - PDF file 79K, Additional materials and methods not described in main manuscript
Supplementary Table S3 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 36K, Clinical characteristics of patients at the time of diagnosis and DSRT, and responses of previous therapies
Supplementary Figure 5,6 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 5,6 - PDF file 143K, Supplemental data demonstrating that DNAPKcs knockdown is maintained in growth studies and ATM expression and activity is regulated by DNAPKcs knockdown and inhibition
Supplementary Figure 1,2 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 1,2 - PDF file 56K, Supplemental data demonstrating that scheduling of IR and ADT treatment does not alter cell survival and DNA damage induces AR mediated gene transcription in a dose dependent fashion
Supplementary Figures, Tables and Methods 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

- PDF file 400K, Supplementary Figures 1-9; Supplementary Tables 4-9 and Supplementary Methods
Supplementary Figures 1-13, Tables 1-2 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 - 1MB
Supplementary Table S3 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 - 49K,SFK phosphorylation in BRAF inhibitor-resistant tumours following dasatinib treatment
Supplementary Table 1 from A Genome-Scale RNA Interference Screen Implicates NF1 Loss in Resistance to RAF Inhibition
Authors: Whittaker Steven R. , Theurillat Jean-Philippe , Van Allen Eliezer , Wagle Nikhil , Hsiao Jessica , Cowley Glenn S. , Schadendorf Dirk , Root David E. , Garraway Levi A.
Published: April 2023

Supplementary Table 1 XLS file - 1881K, Ranking of genes enriched in the presence of PLX4720 compared to DMSO controls. PDF (17837KB) Source File (XLSX) 1881KB Using Gene-E and the RIGER algorithm, genes were ranked according to the 2nd-best shRNA criteria for enrichment across the PLX4720-treated replicas compared to the DMSO-treated samples
Supplementary Figure 7 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, B-RAFi and MEKi combinatorial treatments lead to strong synergistic growth inhibition of V600EB-RAF cell lines regardless of concurrent P124SMEK1 expression. M229 and M238 vector vs. MEK1 stable cell lines were cultured with different levels of doxycycline (ng/ml), treated with constant ratios of B-RAFi (vemurafenib) and MEK1/2i (selumetinib), as indicated (muM), and measured for survival after 72h. Relative synergy of indicated drug combinations (expressed as log10 of CI values) is shown. Calculations were made by CalcuSyn software using the method of Chou and Taladay. Interpretation of CI values is summarized as follows: CI < 0.1 (very strong synergy); = 0.1-0.3 (strong synergy); = 0.3-0.7 (synergy); 0.7-0.85 (moderate synergy); = 0.85-0.9 (slight synergy); = 0.90-1.10 (nearly additive); and = 1.10-1.20 (slight antagonism). The relevant correlated Log10 (CI) values are shown as follow: Log10 (CI 0.1) = -1; Log10 (CI 0.3) = -0.5228787452803376; Log10 (CI 0.7) = -0.1549019599857432, and Log10 (CI 0.85) = -0.07058107428570727.
Supplementary Figure 2 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 - 46K, Rapid symptomatic relief in patient 12 treated with GSK2118436/dabrafenib. This patient's right axillary nodal tumor was punch-biopsied at baseline (prior to B-RAFi therapy), showing concurrent B-RAF/MEK1 mutations, and became non-palpable after eleven days of continuous GSK2118436 dosing. This tumor shrinkage was associated with increased right shoulder mobility, decreased pain and right axillary and breast swelling, despite the best overall response in this patient (Table 1) not achieving partial response by RECIST criteria.
Supplementary Figure 6 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 - 190K, ERK and ETS1 downregulate BRCA1/2 expression
Supplementary Figure 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 - 195K, PI3K regulates BRCA expression
Supplementary Figure 5 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 - 1MB, Additional information showing cancer cells have added requirement on BUB1B for chromosome alignment and KT-MT attachment
Supplementary Figure 2 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 - 133K, BTIC and NSC growth phenotypes resulting from knockdown of PLK1 and pharmacological inhibition of Aurora B kinase
Supplementary Figure 1 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 - 39K, BUB1B knockdown prevents longer-term expansion BTICs and SSEA1+ BTIC subpopulations
Supplementary Figures 1-12 from Cancer-Stimulated Mesenchymal Stem Cells Create a Carcinoma Stem Cell Niche via Prostaglandin E2 Signaling
Authors: Li Hua-Jung , Reinhardt Ferenc , Herschman Harvey R. , Weinberg Robert A.
Published: April 2023

PDF file - 1.4MB, Fig. S1. IL-1 secreting carcinoma cells are able to induce PGE2 from MSCs; Fig. S2. IL-1 and LoVoCM induce PGE2, IL-6, IL-8 and GRO-� expression in various mesenchymal cells; Fig. S3. MSCs are recruited to tumors in vivo; Fig. S4. LoVo cancer stem cells are ALDH-positive; Fig. S5. The frequency of tumor initiating cells is increased in ALDH1-postive HCC1806 SCCs.; Fig. S6. MSCs increase ALDH high/CD133+ CSC-enriched LoVo cells; Fig. S7. LoVo cells cultured with tdTomato-MSCs have increased numbers of tumor initiating cells; Fig. S8. PGE2-induced tumor initiation in vivo was not further potentiated by IL-6, IL-8, Gro-a and RANTES; Fig. S9. LoVoMSC cocultures secrete PGE2-dependent angiogenic factors; Fig. S10. COX2-PGE2-EP4 signaling is required for the increase of ALDH high LoVo; cells induced by MSCs. Fig. S11. LoVoCM induces fibroblast and myofibroblast markers in MSCs; Fig. S12. ALDH high CSCs are located near COX2-expressing regions in human colorectal cancer tumors.
Supplementary Figure 7 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 7 - PDF file 341K, Indicators of IGF1R or INSR depletion in NSCLC cell lines and of combination drug treatment in KrasLA2-G12D mice
Supplementary Tables 3, 5, 6, 8 from BRAFL597 Mutations in Melanoma Are Associated with Sensitivity to MEK Inhibitors
Authors: Dahlman Kimberly Brown , Xia Junfeng , Hutchinson Katherine , Ng Charles , Hucks Donald , Jia Peilin , Atefi Mohammad , Su Zengliu , Branch Suzanne , Lyle Pamela L. , Hicks Donna J. , Bozon Viviana , Glaspy John A. , Rosen Neal , Solit David B. , Netterville James L. , Vnencak-Jones Cindy L. , Sosman Jeffrey A. , Ribas Antoni , Zhao Zhongming , Pao William
Published: April 2023

XLS file - 364K, Figures summarizing the WGS analysis and validation efforts, immunoblots for BRAF L597Q and K601E, sequence confirmation of mutation in patient treated with TAK-733, and spectrum of melanoma mutations determined at Vanderbilt
Supplementary Methods from BRAFL597 Mutations in Melanoma Are Associated with Sensitivity to MEK Inhibitors
Authors: Dahlman Kimberly Brown , Xia Junfeng , Hutchinson Katherine , Ng Charles , Hucks Donald , Jia Peilin , Atefi Mohammad , Su Zengliu , Branch Suzanne , Lyle Pamela L. , Hicks Donna J. , Bozon Viviana , Glaspy John A. , Rosen Neal , Solit David B. , Netterville James L. , Vnencak-Jones Cindy L. , Sosman Jeffrey A. , Ribas Antoni , Zhao Zhongming , Pao William
Published: April 2023

PDF file - 76K, Includes a description of the patient sample used for WGS in addition to the methods for somatic SNP, indel, SV, and CNV determination by WGS
Supplementary Figure Legends 1-11 from BRAFL597 Mutations in Melanoma Are Associated with Sensitivity to MEK Inhibitors
Authors: Dahlman Kimberly Brown , Xia Junfeng , Hutchinson Katherine , Ng Charles , Hucks Donald , Jia Peilin , Atefi Mohammad , Su Zengliu , Branch Suzanne , Lyle Pamela L. , Hicks Donna J. , Bozon Viviana , Glaspy John A. , Rosen Neal , Solit David B. , Netterville James L. , Vnencak-Jones Cindy L. , Sosman Jeffrey A. , Ribas Antoni , Zhao Zhongming , Pao William
Published: April 2023

PDF file - 57K
Supplementary Methods from MicroRNAs Reprogram Normal Fibroblasts into Cancer-Associated Fibroblasts in Ovarian Cancer
Authors: Mitra Anirban K. , Zillhardt Marion , Hua Youjia , Tiwari Payal , Murmann Andrea E. , Peter Marcus E. , Lengyel Ernst
Published: April 2023

PDF file - 71K, Detailed description of methods.
Supplementary Table 8 from Genotype-Selective Combination Therapies for Melanoma Identified by High-Throughput Drug Screening
Authors: Held Matthew A. , Langdon Casey G. , Platt James T. , Graham-Steed Tisheeka , Liu Zongzhi , Chakraborty Ashok , Bacchiocchi Antonella , Koo Andrew , Haskins Jonathan W. , Bosenberg Marcus W. , Stern David F.
Published: April 2023

XLSX file - 134K, Table S8. Most effective genotype-selective combinations.
Supplementary Figures 1-8 from Cell-Selective Inhibition of NF-κB Signaling Improves Therapeutic Index in a Melanoma Chemotherapy Model
Authors: Enzler Thomas , Sano Yasuyo , Choo Min-Kyung , Cottam Howard B. , Karin Michael , Tsao Hensin , Park Jin Mo
Published: April 2023

PDF file - 674K