bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Figure Legends from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Authors: Dunbar Karen J. , Karakasheva Tatiana A. , Tang Qiaosi , Efe Gizem , Lin Eric W. , Harris Michael , Sahu Varun , Sachdeva Uma M. , Hu Jianhua , Klein-Szanto Andres J. , Henick Brian , Diehl J. Alan , Nakagawa Hiroshi , Rustgi Anil K.
Published: September 2024

Supplementary Figure Legends 1-4
Supplementary Figure 2 from Tumor-derived CCL5 recruits cancer-associated fibroblasts and promotes tumor cell proliferation in esophageal squamous cell carcinoma
Authors: Dunbar Karen J. , Karakasheva Tatiana A. , Tang Qiaosi , Efe Gizem , Lin Eric W. , Harris Michael , Sahu Varun , Sachdeva Uma M. , Hu Jianhua , Klein-Szanto Andres J. , Henick Brian , Diehl J. Alan , Nakagawa Hiroshi , Rustgi Anil K.
Published: September 2024

Loss of tumor-derived CCL5 reduces tumor cell proliferation in TE-1 cells.
Supplementary Table 1 from Truncation of GalNAc-type O-glycans suppresses CD44-mediated osteoclastogenesis and bone metastasis in breast cancer
Authors: Lin Neng-Yu , Lee Jian-Jr , Chen Syue-Ting , Lin Jung-An , Lin Chia-Hsuan , Lin Hsuan-Yu , Su Yong-Han , Chen Cheng-Chang , Lin Mei-Chun , Kuo Ching-Ying , Haung Min-Chuan
Published: September 2024

The abundance ratio of O-glycosylated proteins from mock and C1GALT1 knockdown breast cancer cells identified by mass spectrometry.
Supplementary Data from MDM2 inhibition enhances immune checkpoint inhibitor efficacy by increasing IL-15 and MHC class II production
Authors: Langenbach Marlene , Giesler Sophie , Richtsfeld Stefan , da Costa-Pereira Sara , Rindlisbacher Lukas , Wertheimer Tobias , Braun Lukas M. , Andrieux Geoffroy , Duquesne Sandra , Pfeifer Dietmar , Woessner Nadine M. , Menssen Hans D. , Taromi Sanaz , Duyster Justus , Boerries Melanie , Brummer Tilman , Blazar Bruce R. , Minguet Susana , Turko Patrick , Levesque Mitchell P. , Becher Burkhard , Zeiser Robert
Published: September 2024

Supplementary Figures Legends and Methods
Supplementary Figure 2 from Desmoglein 2 Functions As A Receptor for Fatty Acid Binding Protein 4 in Breast Cancer Epithelial Cells
Authors: Chen Dongmei , Wirth Keith M. , Kizy Scott , Muretta Joseph M. , Markowski Todd W. , Yong Peter , Sheka Adam , Abdelwahab Hisham , Hertzel Ann V. , Ikramuddin Sayeed , Yamamoto Masato , Bernlohr David A.
Published: September 2024

S2. Predicted orientation of the F57 side chain in the apoFABP4 form.
Supplementary Figure S1 from Overlaid transcriptome and proteome analyses identify mitotic kinesins as important targets of arylsulfonamide-mediated RBM39 degradation
Authors: Coomar Seemon , Mota Pedro , Penson Alexander , Schwaller Juerg , Abdel-Wahab Omar , Gillingham Dennis
Published: September 2024

Supplementary Figure S1
Supplementary Data from Overlaid transcriptome and proteome analyses identify mitotic kinesins as important targets of arylsulfonamide-mediated RBM39 degradation
Authors: Coomar Seemon , Mota Pedro , Penson Alexander , Schwaller Juerg , Abdel-Wahab Omar , Gillingham Dennis
Published: September 2024

Supplementary Data
Figure S5 from A comparative study of neuroendocrine heterogeneity in small cell lung cancer and neuroblastoma
Authors: Cai Ling , DeBerardinis Ralph J. , Xie Yang , Minna John D. , Xiao Guanghua
Published: September 2024

A meta-analysis example that summarizes the association between MEK inhibitor resistance and NE scores.
Figure S1 from A comparative study of neuroendocrine heterogeneity in small cell lung cancer and neuroblastoma
Authors: Cai Ling , DeBerardinis Ralph J. , Xie Yang , Minna John D. , Xiao Guanghua
Published: September 2024

Intratumoral NE heterogeneity in SCLC patient tumors and intra-cell line NE heterogeneity in SCLC and NBL cell lines.
Supplementary Table 2 from Absence of either Ripk3 or Mlkl reduces incidence of hepatocellular carcinoma independent of liver fibrosis
Authors: Mohammed Sabira , Thadathil Nidheesh , Ohene-Marfo Phoebe , Tran Albert L. , Van Der Veldt Michael , Georgescu Constantin , Oh Sangphil , Nicklas Evan H. , Wang Dawei , Haritha Nair Hariprasad , Luo Wenyi , Janknecht Ralf , Miller Benjamin F. , Wren Jonathan D. , Freeman Willard M. , Deepa Sathyaseelan S.
Published: September 2024

List of significantly altered transcripts from RNA Seq analysis
Fig. S7 from Absence of either Ripk3 or Mlkl reduces incidence of hepatocellular carcinoma independent of liver fibrosis
Authors: Mohammed Sabira , Thadathil Nidheesh , Ohene-Marfo Phoebe , Tran Albert L. , Van Der Veldt Michael , Georgescu Constantin , Oh Sangphil , Nicklas Evan H. , Wang Dawei , Haritha Nair Hariprasad , Luo Wenyi , Janknecht Ralf , Miller Benjamin F. , Wren Jonathan D. , Freeman Willard M. , Deepa Sathyaseelan S.
Published: September 2024

Figure S7 shows western blots for p-AKT/AKT, p-S6/S6, b tubulin, p-ERK/ERK, P-p-38/p-38, b catenin, p62 and b tubulin
Fig. S1 from Absence of either Ripk3 or Mlkl reduces incidence of hepatocellular carcinoma independent of liver fibrosis
Authors: Mohammed Sabira , Thadathil Nidheesh , Ohene-Marfo Phoebe , Tran Albert L. , Van Der Veldt Michael , Georgescu Constantin , Oh Sangphil , Nicklas Evan H. , Wang Dawei , Haritha Nair Hariprasad , Luo Wenyi , Janknecht Ralf , Miller Benjamin F. , Wren Jonathan D. , Freeman Willard M. , Deepa Sathyaseelan S.
Published: September 2024

Figure S1 shows the experimental plan of the study, IHC staining for Ripk3, Transcript levels of Mlkl and Ripk3, Western blots for Cleaved and Total Caspase 3
Figure S7 from Fibronectin contributes to a BRAF inhibitor-driven invasive phenotype in thyroid cancer through EGR1, which can be blocked by inhibition of ERK1/2.
Authors: Hicks Hannah M. , Pozdeyev Nikita , Sams Sharon B. , Pugazhenthi Umarani , Bales Elise S. , Hofmann Marie-Claude , McKenna Logan R. , Schweppe Rebecca E.
Published: September 2024

Figure S7. In the CUTC60-PDX model, BRAF and ERK1/2 inhibition have no significant effect on invasion.
Supplementary Table S8 from Single-Cell Evolutionary Analysis Reveals Drivers of Plasticity and Mediators of Chemoresistance in Small Cell Lung Cancer
Authors: Wollenzien Hannah , Tecleab Yohannes Afeworki A. , Szczepaniak-Sloane Robert , Restaino Anthony , Kareta Michael S.
Published: September 2024

Oligos and Primer Sequences
Supplementary Table S2 from Single-Cell Evolutionary Analysis Reveals Drivers of Plasticity and Mediators of Chemoresistance in Small Cell Lung Cancer
Authors: Wollenzien Hannah , Tecleab Yohannes Afeworki A. , Szczepaniak-Sloane Robert , Restaino Anthony , Kareta Michael S.
Published: September 2024

Description of samples in the xenograft study
Supplementary Figure S9 from Single-Cell Evolutionary Analysis Reveals Drivers of Plasticity and Mediators of Chemoresistance in Small Cell Lung Cancer
Authors: Wollenzien Hannah , Tecleab Yohannes Afeworki A. , Szczepaniak-Sloane Robert , Restaino Anthony , Kareta Michael S.
Published: September 2024

In silico removal and characterization of isolation of murine cells.
Supplementary Figure S8 from Single-Cell Evolutionary Analysis Reveals Drivers of Plasticity and Mediators of Chemoresistance in Small Cell Lung Cancer
Authors: Wollenzien Hannah , Tecleab Yohannes Afeworki A. , Szczepaniak-Sloane Robert , Restaino Anthony , Kareta Michael S.
Published: September 2024

Validation of the LBC labeling and xenograft growth.
Supplementary Figure S4 from Single-Cell Evolutionary Analysis Reveals Drivers of Plasticity and Mediators of Chemoresistance in Small Cell Lung Cancer
Authors: Wollenzien Hannah , Tecleab Yohannes Afeworki A. , Szczepaniak-Sloane Robert , Restaino Anthony , Kareta Michael S.
Published: September 2024

Gene counts and filtering.
Supplementary Figure S3 from Single-Cell Evolutionary Analysis Reveals Drivers of Plasticity and Mediators of Chemoresistance in Small Cell Lung Cancer
Authors: Wollenzien Hannah , Tecleab Yohannes Afeworki A. , Szczepaniak-Sloane Robert , Restaino Anthony , Kareta Michael S.
Published: September 2024

SCLC Subtype-specific marker expression from the RPR2-Cas9 mouse model.
Supplementary Figure S14 from Single-Cell Evolutionary Analysis Reveals Drivers of Plasticity and Mediators of Chemoresistance in Small Cell Lung Cancer
Authors: Wollenzien Hannah , Tecleab Yohannes Afeworki A. , Szczepaniak-Sloane Robert , Restaino Anthony , Kareta Michael S.
Published: September 2024

Validation of GAGE2A and PAGE5 shRNAs and overexpression vectors.
Supplementary Figure S1 from Single-Cell Evolutionary Analysis Reveals Drivers of Plasticity and Mediators of Chemoresistance in Small Cell Lung Cancer
Authors: Wollenzien Hannah , Tecleab Yohannes Afeworki A. , Szczepaniak-Sloane Robert , Restaino Anthony , Kareta Michael S.
Published: September 2024

Validation of the autochthonous barcoding model.
Supplementary Table S1 from Identification of a ΔNp63-Dependent Basal-Like A Subtype-Specific Transcribed Enhancer Program (B-STEP) in Aggressive Pancreatic Ductal Adenocarcinoma
Authors: Wang Xin , Kutschat Ana P. , Aggrey-Fynn Joana , Hamdan Feda H. , Graham Rondell P. , Wixom Alexander Q. , Souto Yara , Ladigan-Badura Swetlana , Yonkus Jennifer A. , Abdelrahman Amro M. , Alva-Ruiz Roberto , Gaedcke Jochen , Strobel Philipp , Kosinsky Robyn Laura , Wegwitz Florian , Hermann Patrick , Truty Mark J. , Siveke Jens T. , Hahn Stephan A. , Hessmann Elisabeth , Johnsen Steven A. , Najafova Zeynab
Published: September 2024

Supplementary Table S1 contains list of crRNAs used in the study.
Supplementary Methods from Identification of a ΔNp63-Dependent Basal-Like A Subtype-Specific Transcribed Enhancer Program (B-STEP) in Aggressive Pancreatic Ductal Adenocarcinoma
Authors: Wang Xin , Kutschat Ana P. , Aggrey-Fynn Joana , Hamdan Feda H. , Graham Rondell P. , Wixom Alexander Q. , Souto Yara , Ladigan-Badura Swetlana , Yonkus Jennifer A. , Abdelrahman Amro M. , Alva-Ruiz Roberto , Gaedcke Jochen , Strobel Philipp , Kosinsky Robyn Laura , Wegwitz Florian , Hermann Patrick , Truty Mark J. , Siveke Jens T. , Hahn Stephan A. , Hessmann Elisabeth , Johnsen Steven A. , Najafova Zeynab
Published: September 2024

The file contains additional supplementary methods
Supplementary Figure 6 from Targeting c-Jun is a potential therapy for luminal breast cancer bone metastasis
Authors: Han Yuxuan , Katayama Shota , Futakuchi Mitsuru , Nakamichi Kazuya , Wakabayashi Yutaro , Sakamoto Mai , Nakayama Jun , Semba Kentaro
Published: September 2024

Mineralization assay co-cultured with MCF7 cells.
Supplementary Figure 4 from Targeting c-Jun is a potential therapy for luminal breast cancer bone metastasis
Authors: Han Yuxuan , Katayama Shota , Futakuchi Mitsuru , Nakamichi Kazuya , Wakabayashi Yutaro , Sakamoto Mai , Nakayama Jun , Semba Kentaro
Published: September 2024

Extraction of c-Jun-regulated bone metastasis gene signatures from the MCF7 cell lines.
Supplementary Figure 8 from Targeting the ATF6-mediated ER stress response and autophagy blocks integrin-driven prostate cancer progression
Authors: Macke Amanda J. , Pachikov Artem N. , Divita Taylor E. , Morris Mary E. , LaGrange Chad A. , Holzapfel Melissa S. , Kubyshkin Anatoly V. , Zyablitskaya Evgeniya Y. , Makalish Tatiana P. , Eremenko Sergey N. , Qiu Haowen , Riethoven Jean-Jack M. , Hemstreet George P. , Petrosyan Armen
Published: September 2024

Figure S8. AST (A) and ALT (B) serum activity from the indicated mice. ALT and AST activity were examined using the ALT Assay Kit (Abcam, ab241035) and the AST Assay Kit (Abcam, ab105135), respectively, per the manufacturer's protocol. Kruskal-Wallis test, all p>0.05, mean ± SD; n represents number of mice tested.
Supplementary Figure 7 from Targeting the ATF6-mediated ER stress response and autophagy blocks integrin-driven prostate cancer progression
Authors: Macke Amanda J. , Pachikov Artem N. , Divita Taylor E. , Morris Mary E. , LaGrange Chad A. , Holzapfel Melissa S. , Kubyshkin Anatoly V. , Zyablitskaya Evgeniya Y. , Makalish Tatiana P. , Eremenko Sergey N. , Qiu Haowen , Riethoven Jean-Jack M. , Hemstreet George P. , Petrosyan Armen
Published: September 2024

Figure S7. (A, B) Alcohol dehydrogenase (ADH1A) and Aldehyde dehydrogenase (ALDH2) W-B of the lysate of PC-3 (A) and DU145 (B) cells. Asterisks indicate the bands corresponding to the appropriate proteins.
Supplementary Figure 8 from Continuous administration of anti-VEGFA antibody upregulates PAI-1 secretion from ovarian cancer cells via miR-143-3p downregulation
Authors: Yagi Taro , Sawada Kenjiro , Miyamoto Mayuko , Shimizu Aasa , Oui Yukako , Toda Aska , Nakamura Koji , Kinose Yasuto , Kodama Michiko , Hashimoto Kae , Kimura Tadashi
Published: September 2024

Supplementary Figure 8 shows the representative images of immunohistochemical staining of a human normal kidney for PAI-1 and CD31.
Fig S3 from HCK promotes high-grade serous ovarian cancer tumorigenesis through CD44 and NOTCH3 signaling
Authors: Khella Christen A. , Franciosa Lucyann , Rodriguez-Rodriguez Lorna , Rajkarnikar Resha , Mythreye Karthikeyan , Gatza Michael L.
Published: September 2024

Cell line selection and engineering
Supplementary Figure 5 from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Authors: Sullivan-Reed Katherine , Toma Monika M. , Drzewiecka Malgorzata , Nieborowska-Skorska Margaret , Nejati Reza , Karami Adam , Wasik Mariusz A. , Sliwinski Tomasz , Skorski Tomasz
Published: September 2024

S5. Targeting Polθ + PARP1 and Polθ + RAD52 induced dual synthetic lethality against HR-deficient leukemia cells.
Supplemental Figure 5 from Mitochondrial uncoupling inhibits reductive carboxylation in cancer cells
Authors: Jiang Haowen , He Clifford Jiajun , Li Albert M. , He Bo , Li Yang , Zhou Meng-Ning , Ye Jiangbin
Published: September 2024

S5. Mitochondrial uncoupler NEN, FCCP and BAM15 inhibit reductive carboxylation under hypoxia.
Supplemental Figure 3 from Mitochondrial uncoupling inhibits reductive carboxylation in cancer cells
Authors: Jiang Haowen , He Clifford Jiajun , Li Albert M. , He Bo , Li Yang , Zhou Meng-Ning , Ye Jiangbin
Published: September 2024

S3. Mitochondrial uncoupler FCCP and BAM5 inhibit reductive carboxylation.
Supplemental Table 1 from Allele-specific gene regulation, phenotypes, and therapeutic vulnerabilities in estrogen receptor alpha mutant endometrial cancer
Authors: Blanchard Zannel , Rush Craig M. , Arnesen Spencer , Vahrenkamp Jeffery M. , Rodriguez Adriana C. , Jarboe Elke A. , Brown Callie , Chang Matthew E.K. , Flory Mark R. , Mohammed Hisham , Modzelewska Katarzyna , Lum David H. , Gertz Jason
Published: September 2024

Differentially expressed genes from in vitro RNA-seq experiments
Supplemental Figure 4 from Allele-specific gene regulation, phenotypes, and therapeutic vulnerabilities in estrogen receptor alpha mutant endometrial cancer
Authors: Blanchard Zannel , Rush Craig M. , Arnesen Spencer , Vahrenkamp Jeffery M. , Rodriguez Adriana C. , Jarboe Elke A. , Brown Callie , Chang Matthew E.K. , Flory Mark R. , Mohammed Hisham , Modzelewska Katarzyna , Lum David H. , Gertz Jason
Published: September 2024

ER mutants do not affect proliferation, but down-regulate proteins associated with movement and impact migration
Supplementary Figure 2 from Hierarchical phosphorylation of HOXB13 by mTOR dictates its activity and oncogenic function in prostate cancer
Authors: Chen Yonghong , Dufour Catherine R. , Han Lingwei , Li Ting , Xia Hui , Giguere Vincent
Published: September 2024

Supplementary Figure 2. HOXB13 additional phosphorylation at S31 is still dependent on mTOR activity.
Supplementary Figure 1 from Hierarchical phosphorylation of HOXB13 by mTOR dictates its activity and oncogenic function in prostate cancer
Authors: Chen Yonghong , Dufour Catherine R. , Han Lingwei , Li Ting , Xia Hui , Giguere Vincent
Published: September 2024

Supplementary Figure 1. mTOR negatively regulates HOXB13 protein stability
Figure S2 from TRIM50 inhibits gastric cancer progression by regulating the ubiquitination and nuclear translocation of JUP
Authors: Hu Jiajia , Huang Runjie , Liang Chengcai , Wang Yingnan , Wang Min , Chen Yanxing , Wu Chenyi , Zhang Jinling , Liu Zekun , Zhao Qi , Liu Zexian , Wang Feng , Yuan Shuqiang
Published: September 2024

Figure S2: Immunoblotting assay of TRIM50 expression in GC cells.
Supplementary Figure 8 from Podoplanin drives amoeboid invasion in canine and human mucosal melanoma
Authors: Shinada Masahiro , Kato Daiki , Motegi Tomoki , Tsuboi Masaya , Ikeda Namiko , Aoki Susumu , Iguchi Takaaki , Li Toshio , Kodera Yuka , Ota Ryosuke , Hashimoto Yuko , Takahashi Yosuke , Chambers James , Uchida Kazuyuki , Kato Yukinari , Nishimura Ryohei , Nakagawa Takayuki
Published: September 2024

PDPN promotes tumor growth and amoeboid invasion in vivo.
Supplementary Figure 5 from Podoplanin drives amoeboid invasion in canine and human mucosal melanoma
Authors: Shinada Masahiro , Kato Daiki , Motegi Tomoki , Tsuboi Masaya , Ikeda Namiko , Aoki Susumu , Iguchi Takaaki , Li Toshio , Kodera Yuka , Ota Ryosuke , Hashimoto Yuko , Takahashi Yosuke , Chambers James , Uchida Kazuyuki , Kato Yukinari , Nishimura Ryohei , Nakagawa Takayuki
Published: September 2024

ROCK inhibition suppresses cell proliferation, survival, and migration.
Supplementary Figure 1 from A Novel Role of Prostate-Specific Membrane Antigen in Telomere Stability in Prostate Cancer Cells
Authors: Reddy Vidyavathi , Hwang Clara , Reddy G. Prem-Veer , Kim Sahn-Ho
Published: September 2024

Supplementary Figure 1
Supplementary Table and Figure Legends from Telomerase upregulation induces progression of mouse BrafV600E-driven thyroid cancers and triggers non-telomeric effects
Authors: Landa Inigo , Thornton Caitlin EM , Xu Bin , Haase Jacob , Krishnamoorthy Gnana P. , Hao Jingzhu , Knauf Jeffrey A. , Herbert Zachary T. , Martínez Paula , Blasco Maria A. , Ghossein Ronald , Fagin James A.
Published: September 2024

Supplementary TableS 1-7 and Figure Legends 1-5
Supplementary Table 1 from Telomerase upregulation induces progression of mouse BrafV600E-driven thyroid cancers and triggers non-telomeric effects
Authors: Landa Inigo , Thornton Caitlin EM , Xu Bin , Haase Jacob , Krishnamoorthy Gnana P. , Hao Jingzhu , Knauf Jeffrey A. , Herbert Zachary T. , Martínez Paula , Blasco Maria A. , Ghossein Ronald , Fagin James A.
Published: September 2024

List of primers used for quantitative PCR.
Supplementary Data File S2 from USP1 expression driven by EWS::FLI1 transcription factor stabilizes Survivin and mitigates replication stress in Ewing sarcoma
Authors: Mallard Halle J. , Wan Shibiao , Nidhi Prakriti , Hanscom-Trofy Yvan D. , Mohapatra Bhopal , Woods Nicholas T. , Lopez-Guerrero Jose Antonio , Llombart-Bosch Antonio , Machado Isidro , Scotlandi Katia , Kreiling Natasha F. , Perry Megan C. , Mirza Sameer , Coulter Donald W. , Band Vimla , Band Hamid , Ghosal Gargi
Published: September 2024

Analysis of TMT-MS data; Page 2: DAVID pathway analysis of differentially expressed proteins identified by TMT-MS.
Figure S5 from USP1 expression driven by EWS::FLI1 transcription factor stabilizes Survivin and mitigates replication stress in Ewing sarcoma
Authors: Mallard Halle J. , Wan Shibiao , Nidhi Prakriti , Hanscom-Trofy Yvan D. , Mohapatra Bhopal , Woods Nicholas T. , Lopez-Guerrero Jose Antonio , Llombart-Bosch Antonio , Machado Isidro , Scotlandi Katia , Kreiling Natasha F. , Perry Megan C. , Mirza Sameer , Coulter Donald W. , Band Vimla , Band Hamid , Ghosal Gargi
Published: September 2024

Figure S5 shows EWS cells are sensitive to doxorubicin and etoposide treatment.
Figure S6 from CBF-beta mitigates PI3K-alpha-specific inhibitor killing through PIM1 in PIK3CA mutant gastric cancer
Authors: Stanland Lyla J. , Ang Hazel X. , Hoj Jacob P. , Chu Yunqiang , Tan Patrick , Wood Kris C. , Luftig Micah A.
Published: September 2024

Figure S6 shows down-regulation of RUNX1 in BYL719 resistant cells
Table S6 from Stromal DDR2 promotes ovarian cancer metastasis through regulation of metabolism and secretion of extracellular matrix proteins
Authors: Schab Angela M. , Greenwade Molly M. , Stock Elizabeth , Lomonosova Elena , Cho Kevin , Grither Whitney R. , Noia Hollie , Wilke Daniel , Mullen Mary M. , Hagemann Andrea R. , Hagemann Ian S. , Thaker Premal H. , Kuroki Lindsay M. , McCourt Carolyn K. , Khabele Dineo , Powell Matthew A. , Mutch David G. , Zhao Peinan , Shriver Leah P. , Patti Gary J. , Longmore Gregory D. , Fuh Katherine C.
Published: September 2024

Cell line sequencing
Table S1 from Stromal DDR2 promotes ovarian cancer metastasis through regulation of metabolism and secretion of extracellular matrix proteins
Authors: Schab Angela M. , Greenwade Molly M. , Stock Elizabeth , Lomonosova Elena , Cho Kevin , Grither Whitney R. , Noia Hollie , Wilke Daniel , Mullen Mary M. , Hagemann Andrea R. , Hagemann Ian S. , Thaker Premal H. , Kuroki Lindsay M. , McCourt Carolyn K. , Khabele Dineo , Powell Matthew A. , Mutch David G. , Zhao Peinan , Shriver Leah P. , Patti Gary J. , Longmore Gregory D. , Fuh Katherine C.
Published: September 2024

Primer Sequences
Figure S2 from Stromal DDR2 promotes ovarian cancer metastasis through regulation of metabolism and secretion of extracellular matrix proteins
Authors: Schab Angela M. , Greenwade Molly M. , Stock Elizabeth , Lomonosova Elena , Cho Kevin , Grither Whitney R. , Noia Hollie , Wilke Daniel , Mullen Mary M. , Hagemann Andrea R. , Hagemann Ian S. , Thaker Premal H. , Kuroki Lindsay M. , McCourt Carolyn K. , Khabele Dineo , Powell Matthew A. , Mutch David G. , Zhao Peinan , Shriver Leah P. , Patti Gary J. , Longmore Gregory D. , Fuh Katherine C.
Published: September 2024

Stromal cell expression of DDR2 is critical for clearance, related to Figure 3
Table S3 from FBXO24 suppresses breast cancer tumorigenesis by targeting LSD1 for Ubiquitination
Authors: Dong Bo , Song Xiang , Wang Xinzhao , Dai Tao , Wang Jianlin , Yu Zhiyong , Deng Jiong , Evers B. Mark , Wu Yadi
Published: September 2024

Supplemental Table S3. Tumor samples used for analysis
Supplementary Figure 2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Authors: Cismas Sonia , Pasca Sylvya , Crudden Caitrin , Troccoli Drakensjo Iara , Suleymanova Naida , Zhang Simin , Gebhard Benjamin , Song Dawei , Neo Shiyong , Shibano Takashi , Smith Terry J. , Calin George A. , Girnita Ada , Girnita Leonard
Published: September 2024

Effect of β-arrestin imbalance on MDM2 localization
Data from Interdependence of SS18-SSX-driven YAP1 and β-catenin activation in synovial sarcoma
Authors: Isfort Ilka , Berthold Ruth , Heinst Lorena , Wardelmann Eva , Larsson Olle , Trautmann Marcel , Hartmann Wolfgang
Published: September 2024

Abstract
Synovial sarcoma (SySa), a rare malignant soft tissue tumor, is characterized by a specific chromosomal translocation t(X;18). The resulting chimeric SS18-SSX fusion protein drives SySa pathogenesis by integrating into the BAF complex and dysregulating gene transcription. Since previous functional analyses revealed a connection between SS18-SSX and the activity of the transcriptional co-regulators YAP1/TAZ and β-catenin, respectively, this study examined a potential interdependence between these essential effector proteins in SySa. In a large cohort of SySa tissue specimens, immunohistochemical analyses revealed a substantial subset of SySa with concurrent nuclear accumulation of YAP1/TAZ and β‑catenin. In vitro, small molecule inhibitor treatment, RNAi-mediated knockdown and vector-based overexpression assays demonstrated that YAP1, TAZ and β-catenin transcriptional activity is not only stimulated by the SS18-SSX fusion protein, but that they also mutually enhance each other’s activation. These analyses showed the highest cooperative effect with overexpression of YAP1 in combination with β-catenin. Co-immunoprecipitation experiments detected nuclear interactions between YAP1, β-catenin and the SS18-SSX fusion protein, the latter being an integral part of the BAF complex. Disruption of BAF complex assembly affected the coregulation of YAP1 and β-catenin, indicating that this chromatin remodeling complex plays a crucial role for interdependent YAP1 and β-catenin activation in SySa cells.

Implications: This study provides deeper insights into SySa tumor biology demonstrating a mutual dependence between YAP1/TAZ and β-catenin transcriptional activity and a complex interplay with the SS18-SSX fusion protein within the BAF complex.
Data from MACdb: A curated knowledgebase for metabolic associations across human cancers
Authors: Sun Yanling , Zheng Xinchang , Wang Guoliang , Wang Yibo , Chen Xiaoning , Sun Jiani , Xiong Zhuang , Zhang Sisi , Wang Tianyi , Fan Zhuojing , Bu Congfan , Bao Yiming , Zhao Wenming
Published: September 2024

Abstract
Cancer is one of the leading causes of human death. As metabolomics techniques become more and more widely used in cancer research, metabolites are increasingly recognized as crucial factors in both cancer diagnosis and treatment. In this study, we developed MACdb (https://ngdc.cncb.ac.cn/macdb), a curated knowledgebase to recruit the metabolic associations between metabolites and cancers. Unlike conventional data-driven resources, MACdb integrates cancer-metabolic knowledge from extensive publications, providing high quality metabolite associations and tools to support multiple research purposes. In the current implementation, MACdb has integrated 40,710 cancer-metabolite associations, covering 267 traits from 17 categories of cancers with high incidence or mortality, based entirely on manual curation from 1,127 studies reported in 462 publications (screened from 5,153 research papers). MACdb offers intuitive browsing functions to explore associations at multi-dimensions (metabolite, trait, study, and publication), and constructs knowledge graph to provide overall landscape among cancer, trait, and metabolite. Furthermore, NameToCid (map metabolite name to PubChem Cid) and Enrichment tools are developed to help users enrich the association of metabolites with various cancer types and traits. Implications: MACdb paves an informative and practical way to evaluate cancer-metabolite associations and has a great potential to help researchers identify key predictive metabolic markers in cancers.
Data from Critical role of 6-phosphogluconate dehydrogenase in TAp73-mediated cancer cell proliferation
Authors: Qiao Rui , Wei Mengmeng , Chen Hui , Zhang Xianhong , Zhang Jie , Gao Liyang , Ma Haijun , Wang Yujiong , Li Le
Published: September 2024

Abstract
Cancer cells frequently alter their metabolism to support biogenesis and proliferation and survive specific metabolic stressors. The glucose-associated pentose phosphate pathway (PPP) is crucial for cancer cell proliferation. In particular, 6-phosphogluconate dehydrogenase (6PGD), the second dehydrogenase in the PPP, catalyzes the decarboxylation of 6-phosphogluconate into ribulose 5-phosphate (Ru5P). However, the mechanisms controlling 6PGD expression in cancer cells remain unclear. Herein, we show that TAp73 increases Ru5P and NADPH production through 6PGD activation to counteract reactive oxygen species and protects cells from apoptosis. Moreover, 6PGD overexpression rescues the proliferation and tumorigenic ability of TAp73-deficient cells. These findings further establish the critical role of TAp73 on glucose metabolism regulation, demonstrating that TAp73 can activate 6PGD expression to support oncogenic cell growth.

Implications: By transcriptional upregulation of 6PGD, TAp73 promotes the generation of Ru5P and NADPH, and enhances tumor cell proliferation.
Data from Truncation of GalNAc-type O-glycans suppresses CD44-mediated osteoclastogenesis and bone metastasis in breast cancer
Authors: Lin Neng-Yu , Lee Jian-Jr , Chen Syue-Ting , Lin Jung-An , Lin Chia-Hsuan , Lin Hsuan-Yu , Su Yong-Han , Chen Cheng-Chang , Lin Mei-Chun , Kuo Ching-Ying , Haung Min-Chuan
Published: September 2024

Abstract
The glycoprotein CD44 is a key regulator of malignant behaviors in breast cancer cells. To date, hyaluronic acid (HA)-CD44 signaling pathway has been widely documented in the context of metastatic bone diseases. Core 1 β1,3-galactosyltransferase (C1GALT1) is a critical enzyme responsible for the elongation of O-glycosylation. Aberrant O-glycans are recognized as a hallmark in cancers. However, the effects of C1GALT1 on CD44 signaling and bone metastasis remain unclear. In this study, immunohistochemical analysis indicated that C1GALT1 expression positively correlates with CD44 in breast cancer. Silencing C1GALT1 accumulates the Tn antigen on CD44, which decreases CD44 levels and osteoclastogenic signaling. Mutations in the O-glycosites on the stem region of CD44 impair its surface localization as well as suppress cell-HA adhesion and osteoclastogenic effects of breast cancer cells. Furthermore, in vivo experiments demonstrated the inhibitory effect of silencing C1GALT1 on breast cancer bone metastasis and bone loss. In conclusion, our study highlights the importance of O-glycans in promoting CD44-mediated tumorigenic signals and indicates a novel function of C1GALT1 in driving breast cancer bone metastasis.

Implications: Truncation of GalNAc-type O-glycans by silencing C1GALT1 suppresses CD44-mediated osteoclastogenesis and bone metastasis in breast cancer; targeting the O-glycans on CD44 may serve as a potential therapeutic target for blocking cancer bone metastasis.
Data from Simultaneous targeting of DNA polymerase theta and PARP1 or RAD52 triggers dual synthetic lethality in homologous recombination-deficient leukemia cells
Authors: Sullivan-Reed Katherine , Toma Monika M. , Drzewiecka Malgorzata , Nieborowska-Skorska Margaret , Nejati Reza , Karami Adam , Wasik Mariusz A. , Sliwinski Tomasz , Skorski Tomasz
Published: September 2024

Abstract
DNA polymerase theta (Poltheta, encoded by POLQ gene) plays an essential role in Poltheta-mediated end-joining (TMEJ) of DNA double-strand breaks (DSBs). Inhibition of Poltheta is synthetic lethal in homologous recombination (HR)-deficient tumor cells. However, DSBs can be also repaired by PARP1 and RAD52 -mediated mechanisms. Since leukemia cells accumulate spontaneous DSBs, we tested if simultaneous targeting of Pol and PARP1 or RAD52 enhance the synthetic lethal effect in HR-deficient leukemia cells. Transformation potential of the oncogenes inducing BRCA1/2-deficiency (BCR-ABL1 and AML1-ETO) was severely limited in Polq-/-;Parp1-/- and Polq-/-;Rad52-/- cells when compared to single knockouts, which was associated with accumulation of DSBs. Small molecule inhibitor of Poltheta (Polthetai) when combined with PARP or RAD52 inhibitors (PARPi, RAD52i) caused accumulation of DSBs and exerted increased effect against HR-deficient leukemia and myeloproliferative neoplasm cells.

Implications: In conclusion, we show that PARPi or RAD52i might improve therapeutic effect of Polthetai against HR-deficient leukemias.
Data from Chromatin-associated SIN3B protects cancer cells from genotoxic stress-induced apoptosis and dictates DNA damage repair pathway choice
Authors: Morales-Valencia Jorge , Petit Coralie , Calderon Alexander , Saini Siddharth , David Gregory
Published: September 2024

Abstract
Transcription and DNA damage repair act in a coordinated manner. The scaffolding protein SIN3B serves as a transcriptional co-repressor of hundreds of cell-cycle-related genes. However, the contribution of SIN3B during the DNA damage response (DDR) remains unknown. Here, we show that SIN3B inactivation delays the resolution of DNA double-strand breaks (DSBs) and sensitizes cancer cells to DNA-damaging agents, including the chemotherapeutic drugs cisplatin and doxorubicin. Mechanistically, SIN3B is rapidly recruited to DNA damage sites where it directs the accumulation of MDC1. In addition, we show that SIN3B inactivation favors the engagement of the alternative NHEJ repair pathway over the canonical NHEJ. Altogether, our findings impute an unexpected function for the transcriptional co-repressor SIN3B as a gatekeeper of genomic integrity and a determining factor in the DNA repair choice pathway, and point to the inhibition of the SIN3B chromatin-modifying complex as a novel therapeutic vulnerability in cancer cells.

Implications: Identifying SIN3B as a modulator of DNA damage repair choice provides novel potential therapeutic avenues to sensitize cancer cells to cytotoxic therapies.
Data from Hierarchical phosphorylation of HOXB13 by mTOR dictates its activity and oncogenic function in prostate cancer
Authors: Chen Yonghong , Dufour Catherine R. , Han Lingwei , Li Ting , Xia Hui , Giguere Vincent
Published: September 2024

Abstract
Dysregulation of mTOR signaling plays a critical role in promoting prostate cancer growth. HOXB13, a homeodomain transcription factor, is known to influence the androgen response and prostate cancer development. Recently, HOXB13 was found to complex with mTOR on chromatin. However, the functional crosstalk between HOXB13 and mTOR remains elusive. We now report that mTOR directly interacts with and hierarchically phosphorylates HOXB13 at threonine 8 and 41 then serine 31 to promote its interaction with the E3 ligase SKP2 while enhancing its oncogenic properties. Expression of HOXB13 harboring phosphomimetic mutations at the mTOR-targeted sites stimulates prostate cancer cellular growth both in vitro and in murine xenografts. Transcriptional profiling studies revealed a phospho-HOXB13-dependent gene signature capable of robustly discriminating between normal prostate tissues, primary and metastatic prostate cancer samples. This work uncovers a previously unanticipated molecular cascade by which mTOR directly phosphorylates HOXB13 to dictate a specific gene program with oncogenic implications in prostate cancer.

Implications: Control of HOXB13 transcriptional activity via its direct phosphorylation by the mTOR kinase is a potential therapeutic avenue for the management of advanced prostate cancer.
Data from Telomerase upregulation induces progression of mouse BrafV600E-driven thyroid cancers and triggers non-telomeric effects
Authors: Landa Inigo , Thornton Caitlin EM , Xu Bin , Haase Jacob , Krishnamoorthy Gnana P. , Hao Jingzhu , Knauf Jeffrey A. , Herbert Zachary T. , Martínez Paula , Blasco Maria A. , Ghossein Ronald , Fagin James A.
Published: September 2024

Abstract
Mutations in the promoter of the telomerase reverse transcriptase (TERT) gene are the paradigm of a cross-cancer alteration in a non-coding region. TERT promoter mutations (TPMs) are biomarkers of poor prognosis in cancer, including thyroid tumors. TPMs enhance TERT transcription, which is otherwise silenced in adult tissues, thus reactivating a bona fide oncoprotein. To study TERT deregulation and its downstream consequences, we generated a Tert mutant promoter mouse model via CRISPR/Cas9 engineering of the murine equivalent locus (Tert-123C>T) and crossed it with thyroid-specific BrafV600E-mutant mice. We also employed an alternative model of Tert overexpression (K5-Tert). Whereas all BrafV600E animals developed well-differentiated papillary thyroid tumors, 29% and 36% of BrafV600E+Tert-123C>T and BrafV600E+K5-Tert mice progressed to poorly differentiated cancers at week 20, respectively. Tert-upregulated tumors showed increased mitosis and necrosis in areas of solid growth, and older animals displayed anaplastic-like features, i.e., spindle cells and macrophage infiltration. Murine Tert promoter mutation increased Tert transcription in vitro and in vivo, but temporal and intra-tumoral heterogeneity was observed. RNA-sequencing of thyroid tumor cells showed that processes other than the canonical Tert-mediated telomere maintenance role operate in these specimens. Pathway analysis showed that MAPK and PI3K/AKT signaling, as well as processes not previously associated with this tumor etiology, involving cytokine and chemokine signaling, were overactivated. These models constitute useful pre-clinical tools to understand the cell-autonomous and microenvironment-related consequences of Tert-mediated progression in advanced thyroid cancers and other aggressive tumors carrying TPMs.
Implications: Telomerase-driven cancer progression activates pathways that can be dissected and perhaps therapeutically exploited.
Data from Stromal DDR2 promotes ovarian cancer metastasis through regulation of metabolism and secretion of extracellular matrix proteins
Authors: Schab Angela M. , Greenwade Molly M. , Stock Elizabeth , Lomonosova Elena , Cho Kevin , Grither Whitney R. , Noia Hollie , Wilke Daniel , Mullen Mary M. , Hagemann Andrea R. , Hagemann Ian S. , Thaker Premal H. , Kuroki Lindsay M. , McCourt Carolyn K. , Khabele Dineo , Powell Matthew A. , Mutch David G. , Zhao Peinan , Shriver Leah P. , Patti Gary J. , Longmore Gregory D. , Fuh Katherine C.
Published: September 2024

Abstract
Ovarian cancer is the leading cause of gynecological cancer-related deaths. The propensity for metastasis within the peritoneal cavity is a driving factor for the poor outcomes associated with this disease, but there is currently no effective therapy targeting metastasis. In this study we investigate the contribution of stromal cells to ovarian cancer metastasis and identify normal stromal cell expression of the collagen receptor, Discoidin Domain Receptor 2 (DDR2), that acts to facilitate ovarian cancer metastasis. In vivo, global genetic inactivation of Ddr2 impairs the ability of Ddr2-expressing syngeneic ovarian cancer cells to spread throughout the peritoneal cavity. Specifically, DDR2 expression in mesothelial cells lining the peritoneal cavity facilitates tumor cell attachment and clearance. Subsequently, omentum fibroblast expression of DDR2 promotes tumor cell invasion. Mechanistically, we find DDR2-expressing fibroblasts are more energetically active, such that DDR2 regulates glycolysis through AKT/SNAI1 leading to suppressed fructose-1,6-bisphosphatase and increased hexokinase activity, a key glycolytic enzyme. Upon inhibition of DDR2 we find decreased protein synthesis and secretion. Consequently, when DDR2 is inhibited, there is reduction in secreted extracellular matrix proteins important for metastasis. Specifically, we find that fibroblast DDR2 inhibition leads to decreased secretion of the collagen crosslinker, LOXL2. Adding back LOXL2 to DDR2 deficient fibroblasts rescues the ability of tumor cells to invade. Overall, our results suggest that stromal cell expression of DDR2 is an important mediator of ovarian cancer metastasis.

Implications: DDR2 is highly expressed by stromal cells in ovarian cancer that can mediate metastasis and is a potential therapeutic target in ovarian cancer.
Data from FBXO24 suppresses breast cancer tumorigenesis by targeting LSD1 for Ubiquitination
Authors: Dong Bo , Song Xiang , Wang Xinzhao , Dai Tao , Wang Jianlin , Yu Zhiyong , Deng Jiong , Evers B. Mark , Wu Yadi
Published: September 2024

Abstract
LSD1, a critical chromatin modulator, functions as an oncogene by demethylation of H3K4me1/2. The stability of LSD1 is governed by a complex and intricate process involving ubiquitination and deubiquitination. Several deubiquitinases preserve LSD1 protein levels. However, the precise mechanism underlying the degradation of LSD1, which could mitigate its oncogenic function remains unknown. To gain a better understanding of LSD1 degradation, we conducted an unbiased siRNA screening targeting all the human SCF family E3 ligases. Our screening identified FBXO24 as a genuine E3 ligase that ubiquitinates and degrades LSD1. As a result, FBXO24 inhibits LSD1-induced tumorigenesis and functions as a tumor suppressor in breast cancer cells. Moreover, FBXO24 exhibits an inverse correlation with LSD1 and is associated with a favorable prognosis in breast cancer patient samples. Taken together, our study uncovers the significant role of FBXO24 in impeding breast tumor progression by targeting LSD1 for degradation.
Implications: Our study provides comprehensive characterization of the significant role of FBXO24 in impeding breast tumor progression by targeting LSD1 for degradation.
Data from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Authors: Cismas Sonia , Pasca Sylvya , Crudden Caitrin , Troccoli Drakensjo Iara , Suleymanova Naida , Zhang Simin , Gebhard Benjamin , Song Dawei , Neo Shiyong , Shibano Takashi , Smith Terry J. , Calin George A. , Girnita Ada , Girnita Leonard
Published: September 2024

Abstract
Constraints on the p53 tumour suppressor pathway have long been associated with the progression, therapeutic resistance, and poor prognosis of melanoma, the most aggressive form of skin cancer. Likewise, the insulin-like growth factor type 1 receptor (IGF1R) is recognized as an essential coordinator of transformation, proliferation, survival, and migration of melanoma cells.
Given that β-arrestin (β-arr) system critically governs the anti/pro-tumorigenic p53/IGF1R signaling pathways through their common E3 ubiquitin-protein ligase MDM2, we explore whether unbalancing this system downstream of IGF1R can enhance the response of melanoma cells to chemotherapy.
Altering β-arr expression demonstrated that both β-arr1-silencing and β-arr2-overexpression (-β-arr1/+β-arr2) facilitated nuclear-to-cytosolic MDM2 translocation accompanied by decreased IGF1R expression, while increasing p53 levels, resulting in reduced cell proliferation/survival. Imbalance towards β-arr2 (-β-arr1/+β-arr2) synergizes with the chemotherapeutic agent, dacarbazine, in promoting melanoma cell toxicity. In both 3D spheroid models and in vivo in zebrafish models, this combination strategy, through dual IGF1R downregulation/p53 activation, limits melanoma cell growth, survival and metastatic spread. In clinical settings, analysis of the TCGA-SKCM patient cohort confirms β-arr1-/β-arr2+ imbalance as a metastatic melanoma vulnerability that may enhance therapeutic benefit. Our findings suggest that under steady-state conditions, IGF1R/p53-tumor promotion/suppression status-quo is preserved by β-arr1/2 homeostasis. Biasing this balance towards β-arr2 can limit the pro-tumorigenic IGF1R activities while enhancing p53 activity, thus reducing multiple cancer-sustaining mechanisms. Combined with other therapeutics, this strategy improves patient responses and outcomes to therapies relying on p53 or IGF1R pathways.
Implications: Altogether, β-arrestin system bias downstream IGF1R is an important metastatic melanoma vulnerability that may be conductive for therapeutic benefit.
Supplementary Figure S3 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: September 2024

Supplementary Figure S3: The calibration plot of the simple risk prediction model for a composite endpoint of high-risk high-risk serrated polyps (SPs) and high-risk conventional adenoma (HRAs) across deciles of predicted risk in women and men.
Supplementary Table S3 from Precision cut lung slices as a preclinical model for non-small cell lung cancer chemoprevention
Authors: Sompel Kayla , Smith Alex J. , Hauer Caroline , Elango Alamelu P. , Clambey Eric T. , Keith Robert L. , Tennis Meredith A.
Published: September 2024

Supplementary Table S3 lists antibody combinations used for immune cell detection in Figure 5.
Supplementary Figure S4 from Precision cut lung slices as a preclinical model for non-small cell lung cancer chemoprevention
Authors: Sompel Kayla , Smith Alex J. , Hauer Caroline , Elango Alamelu P. , Clambey Eric T. , Keith Robert L. , Tennis Meredith A.
Published: September 2024

Supplementary Figure S4 shows a representative immunofluorescence image for Figure 5.
Supplementary Table S3 from Reallocating Cervical Cancer Preventive Service Spending from Low to High-Value Clinical Scenarios
Authors: Rockwell Michelle S. , Armbruster Shannon D. , Capucao Jillian C. , Russell Kyle B. , Rockwell John A. , Perkins Karen E. , Huffstetler Alison N. , Mafi John N. , Fendrick A Mark.
Published: September 2024

Supplementary Table S3 shows CPT codes used in the analysis of colposcopy and related cervical services.
Supplementary Table S2 from Reallocating Cervical Cancer Preventive Service Spending from Low to High-Value Clinical Scenarios
Authors: Rockwell Michelle S. , Armbruster Shannon D. , Capucao Jillian C. , Russell Kyle B. , Rockwell John A. , Perkins Karen E. , Huffstetler Alison N. , Mafi John N. , Fendrick A Mark.
Published: September 2024

Supplementary Table S2 displays specifications for high and low-value cervical cancer screening as specified by the Milliman Medinsight Health Waste Calculator.
Supplementary Table S1 from Reallocating Cervical Cancer Preventive Service Spending from Low to High-Value Clinical Scenarios
Authors: Rockwell Michelle S. , Armbruster Shannon D. , Capucao Jillian C. , Russell Kyle B. , Rockwell John A. , Perkins Karen E. , Huffstetler Alison N. , Mafi John N. , Fendrick A Mark.
Published: September 2024

Supplementary Table S1 includes codes used to identify cervical cancer screening tests within claims data.
Supplementary Table 6 from Associations between physical activity and incidence of cancer among overweight adults in Korea: Results from the Health Examinees-G study
Authors: Choi Jaesung , Park JooYong , Kim Ji-Eun , Lee Miyoung , Kang Daehee , Shin Aesun , Choi Ji-Yeob
Published: September 2024

Supplementary Table 6 shows the association of physical activity with overall cancer incidence in the normal population, defined as those with body mass index between 18.5 and 25.0
Supplementary Table 5 from Associations between physical activity and incidence of cancer among overweight adults in Korea: Results from the Health Examinees-G study
Authors: Choi Jaesung , Park JooYong , Kim Ji-Eun , Lee Miyoung , Kang Daehee , Shin Aesun , Choi Ji-Yeob
Published: September 2024

Supplementary Table 5 shows the association of physical activity with overall cancer incidence stratified by obesity status
Supplementary Table 3 from Associations between physical activity and incidence of cancer among overweight adults in Korea: Results from the Health Examinees-G study
Authors: Choi Jaesung , Park JooYong , Kim Ji-Eun , Lee Miyoung , Kang Daehee , Shin Aesun , Choi Ji-Yeob
Published: September 2024

Supplementary Table 3 shows the association of physical activity with overall cancer incidence after excluding those diagnosed with thyroid cancer
Supplementary Table 17 from Associations between physical activity and incidence of cancer among overweight adults in Korea: Results from the Health Examinees-G study
Authors: Choi Jaesung , Park JooYong , Kim Ji-Eun , Lee Miyoung , Kang Daehee , Shin Aesun , Choi Ji-Yeob
Published: September 2024

Supplementary Table 17 shows the association of physical activity with 13 obesity-related cancers incidence
Supplemental Table 2 from Polymorphisms in the non-homologous end-joining DNA repair pathway are associated with HPV integration in cervical dysplasia
Authors: Geris Jennifer M. , Amirian E. Susan. , Marquez-Do Deborah A. , Guillaud Martial , Dillon Laura M. , Follen Michele , Scheurer Michael E.
Published: September 2024

Supplemental Table 2: Integration assay primer and probe sequences
Supplementary Table S2 from EXAMINING THE BARRIERS AND OPPORTUNITIES FOR HUMAN PAPILLOMAVIRUS VACCINE DELIVERY IN CANCER CARE SETTINGS: A MIXED-METHODS STUDY
Authors: Garcia Melany A. , Schlecht Nicolas F. , Rokitka Denise A. , Attwood Kristopher M. , Rodriguez Elisa M.
Published: September 2024

Supplementary Table S2 presents the qualitative findings from the survey questionnaire item pertaining to perceived roles in HPV vaccine delivery among PAYA cancer care providers.
Supplementary Figure S3 from Progressive spreading of DNA methylation in the GSTP1 promoter CpG island across transitions from precursors to invasive prostate cancer
Authors: Gupta Harshath , Inoue Hitoshi , Nakai Yasutomo , Nakayama Masashi , Jones Tracy , Hicks Jessica L. , Kumar Balasubramanian , Gurel Meltem , Nelson William G. , De Marzo Angelo M. , Yegnasubramanian Srinivasan
Published: September 2024

Supplementary Figure S3 shows the GSTP1 promoter methylation and its corresponding GSTP1 immunohistochemistry expression for PIA and PIN lesions within an individual patient, and notably the heterogeneity of the PIA lesions.