bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Table S1 from Multiple Alternative Splicing Markers for Ovarian Cancer
Authors: Klinck Roscoe , Bramard Anne , Inkel Lyna , Dufresne-Martin Geneviève , Gervais-Bird Julien , Madden Richard , Paquet Éric R. , Koh ChuShin , Venables Julian P. , Prinos Panagiotis , Jilaveanu-Pelmus Manuela , Wellinger Raymund , Rancourt Claudine , Chabot Benoit , Abou Elela Sherif
Published: March 2023

Supplementary Table S1 from Multiple Alternative Splicing Markers for Ovarian Cancer
Supplementary Figure 3, page 4 of 4 from Multiple Alternative Splicing Markers for Ovarian Cancer
Authors: Klinck Roscoe , Bramard Anne , Inkel Lyna , Dufresne-Martin Geneviève , Gervais-Bird Julien , Madden Richard , Paquet Éric R. , Koh ChuShin , Venables Julian P. , Prinos Panagiotis , Jilaveanu-Pelmus Manuela , Wellinger Raymund , Rancourt Claudine , Chabot Benoit , Abou Elela Sherif
Published: March 2023

Supplementary Figure 3, page 4 of 4 from Multiple Alternative Splicing Markers for Ovarian Cancer
Supplementary Figure 7 from Nutlin-3a Activates p53 to Both Down-regulate Inhibitor of Growth 2 and Up-regulate mir-34a, mir-34b, and mir-34c Expression, and Induce Senescence
Authors: Kumamoto Kensuke , Spillare Elisa A. , Fujita Kaori , Horikawa Izumi , Yamashita Taro , Appella Ettore , Nagashima Makoto , Takenoshita Seiichi , Yokota Jun , Harris Curtis C.
Published: March 2023

Supplementary Figure 7 from Nutlin-3a Activates p53 to Both Down-regulate Inhibitor of Growth 2 and Up-regulate mir-34a, mir-34b, and mir-34c Expression, and Induce Senescence
Supplementary Figure 3, page 2 of 4 from Multiple Alternative Splicing Markers for Ovarian Cancer
Authors: Klinck Roscoe , Bramard Anne , Inkel Lyna , Dufresne-Martin Geneviève , Gervais-Bird Julien , Madden Richard , Paquet Éric R. , Koh ChuShin , Venables Julian P. , Prinos Panagiotis , Jilaveanu-Pelmus Manuela , Wellinger Raymund , Rancourt Claudine , Chabot Benoit , Abou Elela Sherif
Published: March 2023

Supplementary Figure 3, page 2 of 4 from Multiple Alternative Splicing Markers for Ovarian Cancer
Supplementary Figure 6 from Nutlin-3a Activates p53 to Both Down-regulate Inhibitor of Growth 2 and Up-regulate mir-34a, mir-34b, and mir-34c Expression, and Induce Senescence
Authors: Kumamoto Kensuke , Spillare Elisa A. , Fujita Kaori , Horikawa Izumi , Yamashita Taro , Appella Ettore , Nagashima Makoto , Takenoshita Seiichi , Yokota Jun , Harris Curtis C.
Published: March 2023

Supplementary Figure 6 from Nutlin-3a Activates p53 to Both Down-regulate Inhibitor of Growth 2 and Up-regulate mir-34a, mir-34b, and mir-34c Expression, and Induce Senescence
Supplementary Figure 4 from Nutlin-3a Activates p53 to Both Down-regulate Inhibitor of Growth 2 and Up-regulate mir-34a, mir-34b, and mir-34c Expression, and Induce Senescence
Authors: Kumamoto Kensuke , Spillare Elisa A. , Fujita Kaori , Horikawa Izumi , Yamashita Taro , Appella Ettore , Nagashima Makoto , Takenoshita Seiichi , Yokota Jun , Harris Curtis C.
Published: March 2023

Supplementary Figure 4 from Nutlin-3a Activates p53 to Both Down-regulate Inhibitor of Growth 2 and Up-regulate mir-34a, mir-34b, and mir-34c Expression, and Induce Senescence
Supplementary Figure 1 from CCN3/Nephroblastoma Overexpressed Matricellular Protein Regulates Integrin Expression, Adhesion, and Dissemination in Melanoma
Authors: Vallacchi Viviana , Daniotti Maria , Ratti Francesca , Di Stasi Delia , Deho Paola , De Filippo Annamaria , Tragni Gabrina , Balsari Andrea , Carbone Antonino , Rivoltini Licia , Parmiani Giorgio , Lazar Noureddine , Perbal Bernard , Rodolfo Monica
Published: March 2023

Supplementary Figure 1 from CCN3/Nephroblastoma Overexpressed Matricellular Protein Regulates Integrin Expression, Adhesion, and Dissemination in Melanoma
Supplementary Materials and Methods from Glioma Pathogenesis-Related Protein 1 Exerts Tumor Suppressor Activities through Proapoptotic Reactive Oxygen Species–c-Jun–NH2 Kinase Signaling
Authors: Li Likun , Abdel Fattah ElMoataz , Cao Guangwen , Ren Chengzhen , Yang Guang , Goltsov Alexei A. , Chinault A. Craig , Cai Wei-Wen , Timme Terry L. , Thompson Timothy C.
Published: March 2023

Supplementary Materials and Methods from Glioma Pathogenesis-Related Protein 1 Exerts Tumor Suppressor Activities through Proapoptotic Reactive Oxygen Species–c-Jun–NH2 Kinase Signaling
Supplementary Figure Legends 1-2 from Revealing Targeted Therapy for Human Cancer by Gene Module Maps
Authors: Wong David J. , Nuyten Dimitry S.A. , Regev Aviv , Lin Meihong , Adler Adam S. , Segal Eran , van de Vijver Marc J. , Chang Howard Y.
Published: March 2023

Supplementary Figure Legends 1-2 from Revealing Targeted Therapy for Human Cancer by Gene Module Maps
Supplementary Figure 2 from Revealing Targeted Therapy for Human Cancer by Gene Module Maps
Authors: Wong David J. , Nuyten Dimitry S.A. , Regev Aviv , Lin Meihong , Adler Adam S. , Segal Eran , van de Vijver Marc J. , Chang Howard Y.
Published: March 2023

Supplementary Figure 2 from Revealing Targeted Therapy for Human Cancer by Gene Module Maps
Supplementary Figure Legends 1-5 from Glioma Pathogenesis-Related Protein 1 Exerts Tumor Suppressor Activities through Proapoptotic Reactive Oxygen Species–c-Jun–NH2 Kinase Signaling
Authors: Li Likun , Abdel Fattah ElMoataz , Cao Guangwen , Ren Chengzhen , Yang Guang , Goltsov Alexei A. , Chinault A. Craig , Cai Wei-Wen , Timme Terry L. , Thompson Timothy C.
Published: March 2023

Supplementary Figure Legends 1-5 from Glioma Pathogenesis-Related Protein 1 Exerts Tumor Suppressor Activities through Proapoptotic Reactive Oxygen Species–c-Jun–NH2 Kinase Signaling
Supplementary Figure 1 from Revealing Targeted Therapy for Human Cancer by Gene Module Maps
Authors: Wong David J. , Nuyten Dimitry S.A. , Regev Aviv , Lin Meihong , Adler Adam S. , Segal Eran , van de Vijver Marc J. , Chang Howard Y.
Published: March 2023

Supplementary Figure 1 from Revealing Targeted Therapy for Human Cancer by Gene Module Maps
Supplementary Figure 6 from Transforming Growth Factor-β Activation Promotes Genetic Context–Dependent Invasion of Immortalized Melanocytes
Authors: Lo Roger S. , Witte Owen N.
Published: March 2023

Supplementary Figure 6 from Transforming Growth Factor-β Activation Promotes Genetic Context–Dependent Invasion of Immortalized Melanocytes
Supplementary Figure 5 from Transforming Growth Factor-β Activation Promotes Genetic Context–Dependent Invasion of Immortalized Melanocytes
Authors: Lo Roger S. , Witte Owen N.
Published: March 2023

Supplementary Figure 5 from Transforming Growth Factor-β Activation Promotes Genetic Context–Dependent Invasion of Immortalized Melanocytes
Supplementary Figure 4 from Transforming Growth Factor-β Activation Promotes Genetic Context–Dependent Invasion of Immortalized Melanocytes
Authors: Lo Roger S. , Witte Owen N.
Published: March 2023

Supplementary Figure 4 from Transforming Growth Factor-β Activation Promotes Genetic Context–Dependent Invasion of Immortalized Melanocytes
Supplementary Figure 3 from Transforming Growth Factor-β Activation Promotes Genetic Context–Dependent Invasion of Immortalized Melanocytes
Authors: Lo Roger S. , Witte Owen N.
Published: March 2023

Supplementary Figure 3 from Transforming Growth Factor-β Activation Promotes Genetic Context–Dependent Invasion of Immortalized Melanocytes
Supplementary Figures 1-3 from Tumor-Associated MICA Is Shed by ADAM Proteases
Authors: Waldhauer Inja , Goehlsdorf Dennis , Gieseke Friederike , Weinschenk Toni , Wittenbrink Mareike , Ludwig Andreas , Stevanovic Stefan , Rammensee Hans-Georg , Steinle Alexander
Published: March 2023

Supplementary Figures 1-3 from Tumor-Associated MICA Is Shed by ADAM Proteases
Supplementary Figures 1-2 from p53-Dependent and p53-Independent Activation of Autophagy by ARF
Authors: Abida Wassim M. , Gu Wei
Published: March 2023

Supplementary Figures 1-2 from p53-Dependent and p53-Independent Activation of Autophagy by ARF
Supplementary Figures 1-3 from Inhibition of Glycogen Synthase Kinase 3β Attenuates Neurocognitive Dysfunction Resulting from Cranial Irradiation
Authors: Thotala Dinesh K. , Hallahan Dennis E. , Yazlovitskaya Eugenia M.
Published: March 2023

Supplementary Figures 1-3 from Inhibition of Glycogen Synthase Kinase 3β Attenuates Neurocognitive Dysfunction Resulting from Cranial Irradiation
Supplementary Video 2 from Role of the Polarity Determinant Crumbs in Suppressing Mammalian Epithelial Tumor Progression
Authors: Karp Cristina M. , Tan Ting Ting , Mathew Robin , Nelson Deidre , Mukherjee Chandreyee , Degenhardt Kurt , Karantza-Wadsworth Vassiliki , White Eileen
Published: March 2023

Supplementary Video 2 from Role of the Polarity Determinant Crumbs in Suppressing Mammalian Epithelial Tumor Progression
Supplementary Table 1 from P-Glycoprotein–Mediated Resistance to Hsp90-Directed Therapy Is Eclipsed by the Heat Shock Response
Authors: McCollum Andrea K. , TenEyck Cynthia J. , Stensgard Bridget , Morlan Bruce W. , Ballman Karla V. , Jenkins Robert B. , Toft David O. , Erlichman Charles
Published: March 2023

Supplementary Table 1 from P-Glycoprotein–Mediated Resistance to Hsp90-Directed Therapy Is Eclipsed by the Heat Shock Response
Supplementary Video 1 from Role of the Polarity Determinant Crumbs in Suppressing Mammalian Epithelial Tumor Progression
Authors: Karp Cristina M. , Tan Ting Ting , Mathew Robin , Nelson Deidre , Mukherjee Chandreyee , Degenhardt Kurt , Karantza-Wadsworth Vassiliki , White Eileen
Published: March 2023

Supplementary Video 1 from Role of the Polarity Determinant Crumbs in Suppressing Mammalian Epithelial Tumor Progression
Supplementary Figure 2 from P-Glycoprotein–Mediated Resistance to Hsp90-Directed Therapy Is Eclipsed by the Heat Shock Response
Authors: McCollum Andrea K. , TenEyck Cynthia J. , Stensgard Bridget , Morlan Bruce W. , Ballman Karla V. , Jenkins Robert B. , Toft David O. , Erlichman Charles
Published: March 2023

Supplementary Figure 2 from P-Glycoprotein–Mediated Resistance to Hsp90-Directed Therapy Is Eclipsed by the Heat Shock Response
Supplementary Figure 4 from Phosphoinositide 3-kinase/AKT Signaling Can Promote AIB1 Stability Independently of GSK3 Phosphorylation
Authors: Ferrero Macarena , Avivar Álvaro , García-Macías María Carmen , de Mora Jaime Font
Published: March 2023

Supplementary Figure 4 from Phosphoinositide 3-kinase/AKT Signaling Can Promote AIB1 Stability Independently of GSK3 Phosphorylation
Supplementary Figure 3 from Phosphoinositide 3-kinase/AKT Signaling Can Promote AIB1 Stability Independently of GSK3 Phosphorylation
Authors: Ferrero Macarena , Avivar Álvaro , García-Macías María Carmen , de Mora Jaime Font
Published: March 2023

Supplementary Figure 3 from Phosphoinositide 3-kinase/AKT Signaling Can Promote AIB1 Stability Independently of GSK3 Phosphorylation
Supplementary Legends of Tables 1-2, Figures 1-5 from Complement-Dependent Tumor Cell Lysis Triggered by Combinations of Epidermal Growth Factor Receptor Antibodies
Authors: Dechant Michael , Weisner Wencke , Berger Sven , Peipp Matthias , Beyer Thomas , Schneider-Merck Tanja , Lammerts van Bueren Jeroen J. , Bleeker Wim K. , Parren Paul W.H.I. , van de Winkel Jan G.J. , Valerius Thomas
Published: March 2023

Supplementary Legends of Tables 1-2, Figures 1-5 from Complement-Dependent Tumor Cell Lysis Triggered by Combinations of Epidermal Growth Factor Receptor Antibodies
Supplementary Figure 5 from Complement-Dependent Tumor Cell Lysis Triggered by Combinations of Epidermal Growth Factor Receptor Antibodies
Authors: Dechant Michael , Weisner Wencke , Berger Sven , Peipp Matthias , Beyer Thomas , Schneider-Merck Tanja , Lammerts van Bueren Jeroen J. , Bleeker Wim K. , Parren Paul W.H.I. , van de Winkel Jan G.J. , Valerius Thomas
Published: March 2023

Supplementary Figure 5 from Complement-Dependent Tumor Cell Lysis Triggered by Combinations of Epidermal Growth Factor Receptor Antibodies
Supplementary Figure Legends 1-2 from PC3 Human Prostate Carcinoma Cell Holoclones Contain Self-renewing Tumor-Initiating Cells
Authors: Li Hangwen , Chen Xin , Calhoun-Davis Tammy , Claypool Kent , Tang Dean G.
Published: March 2023

Supplementary Figure Legends 1-2 from PC3 Human Prostate Carcinoma Cell Holoclones Contain Self-renewing Tumor-Initiating Cells
Supplementary Video 1 from Abnormal Cytokinesis after X-Irradiation in Tumor Cells that Override the G2 DNA Damage Checkpoint
Authors: Huang Haomin , Fletcher Lynda , Beeharry Neil , Daniel Rene , Kao Gary , Yen Tim J. , Muschel Ruth J.
Published: March 2023

Supplementary Video 1 from Abnormal Cytokinesis after X-Irradiation in Tumor Cells that Override the G2 DNA Damage Checkpoint
Supplementary Figure Legends 1-4 from Bortezomib (Velcade) Induces p27Kip1 Expression through S-Phase Kinase Protein 2 Degradation in Colorectal Cancer
Authors: Uddin Shahab , Ahmed Maqbool , Bavi Prashant , El-Sayed Raafat , Al-Sanea Nasser , AbdulJabbar Alaa , Ashari Luai H. , Alhomoud Samar , Al-Dayel Fouad , Hussain Azhar R. , Al-Kuraya Khawla S.
Published: March 2023

Supplementary Figure Legends 1-4 from Bortezomib (Velcade) Induces p27Kip1 Expression through S-Phase Kinase Protein 2 Degradation in Colorectal Cancer
Supplementary Figure 4 from Abnormal Cytokinesis after X-Irradiation in Tumor Cells that Override the G2 DNA Damage Checkpoint
Authors: Huang Haomin , Fletcher Lynda , Beeharry Neil , Daniel Rene , Kao Gary , Yen Tim J. , Muschel Ruth J.
Published: March 2023

Supplementary Figure 4 from Abnormal Cytokinesis after X-Irradiation in Tumor Cells that Override the G2 DNA Damage Checkpoint
Supplementary Figure 4 from Bortezomib (Velcade) Induces p27Kip1 Expression through S-Phase Kinase Protein 2 Degradation in Colorectal Cancer
Authors: Uddin Shahab , Ahmed Maqbool , Bavi Prashant , El-Sayed Raafat , Al-Sanea Nasser , AbdulJabbar Alaa , Ashari Luai H. , Alhomoud Samar , Al-Dayel Fouad , Hussain Azhar R. , Al-Kuraya Khawla S.
Published: March 2023

Supplementary Figure 4 from Bortezomib (Velcade) Induces p27Kip1 Expression through S-Phase Kinase Protein 2 Degradation in Colorectal Cancer
Supplementary Figure 3 from Abnormal Cytokinesis after X-Irradiation in Tumor Cells that Override the G2 DNA Damage Checkpoint
Authors: Huang Haomin , Fletcher Lynda , Beeharry Neil , Daniel Rene , Kao Gary , Yen Tim J. , Muschel Ruth J.
Published: March 2023

Supplementary Figure 3 from Abnormal Cytokinesis after X-Irradiation in Tumor Cells that Override the G2 DNA Damage Checkpoint
Supplementary Figure 3 from Bortezomib (Velcade) Induces p27Kip1 Expression through S-Phase Kinase Protein 2 Degradation in Colorectal Cancer
Authors: Uddin Shahab , Ahmed Maqbool , Bavi Prashant , El-Sayed Raafat , Al-Sanea Nasser , AbdulJabbar Alaa , Ashari Luai H. , Alhomoud Samar , Al-Dayel Fouad , Hussain Azhar R. , Al-Kuraya Khawla S.
Published: March 2023

Supplementary Figure 3 from Bortezomib (Velcade) Induces p27Kip1 Expression through S-Phase Kinase Protein 2 Degradation in Colorectal Cancer
Supplementary Figure 6 from Aplidin, a Marine Organism–Derived Compound with Potent Antimyeloma Activity In vitro and In vivo
Authors: Mitsiades Constantine S. , Ocio Enrique M. , Pandiella Atanasio , Maiso Patricia , Gajate Consuelo , Garayoa Mercedes , Vilanova David , Montero Juan Carlos , Mitsiades Nicholas , McMullan Ciaran J. , Munshi Nikhil C. , Hideshima Teru , Chauhan Dharminder , Aviles Pablo , Otero Gabriel , Faircloth Glynn , Mateos M. Victoria , Richardson Paul G. , Mollinedo Faustino , San-Miguel Jesus F. , Anderson Kenneth C.
Published: March 2023

Supplementary Figure 6 from Aplidin, a Marine Organism–Derived Compound with Potent Antimyeloma Activity In vitro and In vivo
Supplementary Figure 3 from A Gene Signature Predicting for Survival in Suboptimally Debulked Patients with Ovarian Cancer
Authors: Bonome Tomas , Levine Douglas A. , Shih Joanna , Randonovich Mike , Pise-Masison Cindy A. , Bogomolniy Faina , Ozbun Laurent , Brady John , Barrett J. Carl , Boyd Jeff , Birrer Michael J.
Published: March 2023

Supplementary Figure 3 from A Gene Signature Predicting for Survival in Suboptimally Debulked Patients with Ovarian Cancer
Supplementary Figure 1 from A Gene Signature Predicting for Survival in Suboptimally Debulked Patients with Ovarian Cancer
Authors: Bonome Tomas , Levine Douglas A. , Shih Joanna , Randonovich Mike , Pise-Masison Cindy A. , Bogomolniy Faina , Ozbun Laurent , Brady John , Barrett J. Carl , Boyd Jeff , Birrer Michael J.
Published: March 2023

Supplementary Figure 1 from A Gene Signature Predicting for Survival in Suboptimally Debulked Patients with Ovarian Cancer
Supplementary Figures 1-2 from Cyclooxygenase-2 Expression during Immortalization and Breast Cancer Progression
Authors: Zhao Xiangshan , Goswami Monica , Pokhriyal Nidhi , Ma Hui , Du Hongyan , Yao Jun , Victor Thomas A. , Polyak Kornelia , Sturgis Charles D. , Band Hamid , Band Vimla
Published: March 2023

Supplementary Figures 1-2 from Cyclooxygenase-2 Expression during Immortalization and Breast Cancer Progression
Supplementary Text 1 from Cell Lineage Analysis of a Mouse Tumor
Authors: Frumkin Dan , Wasserstrom Adam , Itzkovitz Shalev , Stern Tomer , Harmelin Alon , Eilam Raya , Rechavi Gideon , Shapiro Ehud
Published: March 2023

Supplementary Text 1 from Cell Lineage Analysis of a Mouse Tumor
Supplementary Figure 1 from Two Distinct Molecular Mechanisms Underlying Cytarabine Resistance in Human Leukemic Cells
Authors: Cai Jie , Damaraju Vijaya L. , Groulx Normand , Mowles Delores , Peng Yunshan , Robins Morris J. , Cass Carol E. , Gros Philippe
Published: March 2023

Supplementary Figure 1 from Two Distinct Molecular Mechanisms Underlying Cytarabine Resistance in Human Leukemic Cells
Supplementary Figure 1 from Subtypes of Breast Cancer Show Preferential Site of Relapse
Authors: Smid Marcel , Wang Yixin , Zhang Yi , Sieuwerts Anieta M. , Yu Jack , Klijn Jan G.M. , Foekens John A. , Martens John W.M.
Published: March 2023

Supplementary Figure 1 from Subtypes of Breast Cancer Show Preferential Site of Relapse
Supplementary Figure 1 from The Nuclear Factor-κB Pathway Controls the Progression of Prostate Cancer to Androgen-Independent Growth
Authors: Jin Ren Jie , Lho Yongsoo , Connelly Linda , Wang Yongqing , Yu Xiuping , Saint Jean Leshana , Case Thomas C. , Ellwood-Yen Katharine , Sawyers Charles L. , Bhowmick Neil A. , Blackwell Timothy S. , Yull Fiona E. , Matusik Robert J.
Published: March 2023

Supplementary Figure 1 from The Nuclear Factor-κB Pathway Controls the Progression of Prostate Cancer to Androgen-Independent Growth
Supplementary Figure 1 Legend from The Nuclear Factor-κB Pathway Controls the Progression of Prostate Cancer to Androgen-Independent Growth
Authors: Jin Ren Jie , Lho Yongsoo , Connelly Linda , Wang Yongqing , Yu Xiuping , Saint Jean Leshana , Case Thomas C. , Ellwood-Yen Katharine , Sawyers Charles L. , Bhowmick Neil A. , Blackwell Timothy S. , Yull Fiona E. , Matusik Robert J.
Published: March 2023

Supplementary Figure 1 Legend from The Nuclear Factor-κB Pathway Controls the Progression of Prostate Cancer to Androgen-Independent Growth
Supplementary Figure 4 from Curcumin Blocks RON Tyrosine Kinase–Mediated Invasion of Breast Carcinoma Cells
Authors: Narasimhan Madhusudhanan , Ammanamanchi Sudhakar
Published: March 2023

Supplementary Figure 4 from Curcumin Blocks RON Tyrosine Kinase–Mediated Invasion of Breast Carcinoma Cells
Supplementary Movie 6 from The Anaplastic Lymphoma Kinase Controls Cell Shape and Growth of Anaplastic Large Cell Lymphoma through Cdc42 Activation
Authors: Ambrogio Chiara , Voena Claudia , Manazza Andrea D. , Martinengo Cinzia , Costa Carlotta , Kirchhausen Tomas , Hirsch Emilio , Inghirami Giorgio , Chiarle Roberto
Published: March 2023

Supplementary Movie 6 from The Anaplastic Lymphoma Kinase Controls Cell Shape and Growth of Anaplastic Large Cell Lymphoma through Cdc42 Activation
Supplementary Movie 5 from The Anaplastic Lymphoma Kinase Controls Cell Shape and Growth of Anaplastic Large Cell Lymphoma through Cdc42 Activation
Authors: Ambrogio Chiara , Voena Claudia , Manazza Andrea D. , Martinengo Cinzia , Costa Carlotta , Kirchhausen Tomas , Hirsch Emilio , Inghirami Giorgio , Chiarle Roberto
Published: March 2023

Supplementary Movie 5 from The Anaplastic Lymphoma Kinase Controls Cell Shape and Growth of Anaplastic Large Cell Lymphoma through Cdc42 Activation
Supplementary Methods, Tables 1-3, Figure Legends 1-3 from Microphthalmia-Associated Transcription Factor Is a Critical Transcriptional Regulator of Melanoma Inhibitor of Apoptosis in Melanomas
Authors: Dynek Jasmin N. , Chan Sara M. , Liu Jinfeng , Zha Jiping , Fairbrother Wayne J. , Vucic Domagoj
Published: March 2023

Supplementary Methods, Tables 1-3, Figure Legends 1-3 from Microphthalmia-Associated Transcription Factor Is a Critical Transcriptional Regulator of Melanoma Inhibitor of Apoptosis in Melanomas
Supplementary Movie 3 from The Anaplastic Lymphoma Kinase Controls Cell Shape and Growth of Anaplastic Large Cell Lymphoma through Cdc42 Activation
Authors: Ambrogio Chiara , Voena Claudia , Manazza Andrea D. , Martinengo Cinzia , Costa Carlotta , Kirchhausen Tomas , Hirsch Emilio , Inghirami Giorgio , Chiarle Roberto
Published: March 2023

Supplementary Movie 3 from The Anaplastic Lymphoma Kinase Controls Cell Shape and Growth of Anaplastic Large Cell Lymphoma through Cdc42 Activation
Supplementary Movie 2 from The Anaplastic Lymphoma Kinase Controls Cell Shape and Growth of Anaplastic Large Cell Lymphoma through Cdc42 Activation
Authors: Ambrogio Chiara , Voena Claudia , Manazza Andrea D. , Martinengo Cinzia , Costa Carlotta , Kirchhausen Tomas , Hirsch Emilio , Inghirami Giorgio , Chiarle Roberto
Published: March 2023

Supplementary Movie 2 from The Anaplastic Lymphoma Kinase Controls Cell Shape and Growth of Anaplastic Large Cell Lymphoma through Cdc42 Activation
Supplementary Movie 1 from The Anaplastic Lymphoma Kinase Controls Cell Shape and Growth of Anaplastic Large Cell Lymphoma through Cdc42 Activation
Authors: Ambrogio Chiara , Voena Claudia , Manazza Andrea D. , Martinengo Cinzia , Costa Carlotta , Kirchhausen Tomas , Hirsch Emilio , Inghirami Giorgio , Chiarle Roberto
Published: March 2023

Supplementary Movie 1 from The Anaplastic Lymphoma Kinase Controls Cell Shape and Growth of Anaplastic Large Cell Lymphoma through Cdc42 Activation
Supplementary Figure Legends 1-2 from Protein Phosphatase-2A Is a Target of Epigallocatechin-3-Gallate and Modulates p53-Bak Apoptotic Pathway
Authors: Qin Jichao , Chen He-Ge , Yan Qin , Deng Mi , Liu Jinping , Doerge Stephan , Ma Weiya , Dong Zigang , Wan-Cheng Li David
Published: March 2023

Supplementary Figure Legends 1-2 from Protein Phosphatase-2A Is a Target of Epigallocatechin-3-Gallate and Modulates p53-Bak Apoptotic Pathway
Supplementary Figure 2 from Protein Phosphatase-2A Is a Target of Epigallocatechin-3-Gallate and Modulates p53-Bak Apoptotic Pathway
Authors: Qin Jichao , Chen He-Ge , Yan Qin , Deng Mi , Liu Jinping , Doerge Stephan , Ma Weiya , Dong Zigang , Wan-Cheng Li David
Published: March 2023

Supplementary Figure 2 from Protein Phosphatase-2A Is a Target of Epigallocatechin-3-Gallate and Modulates p53-Bak Apoptotic Pathway
Supplementary Figures 1-7 from The Anaplastic Lymphoma Kinase Controls Cell Shape and Growth of Anaplastic Large Cell Lymphoma through Cdc42 Activation
Authors: Ambrogio Chiara , Voena Claudia , Manazza Andrea D. , Martinengo Cinzia , Costa Carlotta , Kirchhausen Tomas , Hirsch Emilio , Inghirami Giorgio , Chiarle Roberto
Published: March 2023

Supplementary Figures 1-7 from The Anaplastic Lymphoma Kinase Controls Cell Shape and Growth of Anaplastic Large Cell Lymphoma through Cdc42 Activation
Supplementary Figure 1 from Protein Phosphatase-2A Is a Target of Epigallocatechin-3-Gallate and Modulates p53-Bak Apoptotic Pathway
Authors: Qin Jichao , Chen He-Ge , Yan Qin , Deng Mi , Liu Jinping , Doerge Stephan , Ma Weiya , Dong Zigang , Wan-Cheng Li David
Published: March 2023

Supplementary Figure 1 from Protein Phosphatase-2A Is a Target of Epigallocatechin-3-Gallate and Modulates p53-Bak Apoptotic Pathway
Supplementary Table 3 from Quantitative Analysis of DNA Methylation Profiles in Lung Cancer Identifies Aberrant DNA Methylation of Specific Genes and Its Association with Gender and Cancer Risk Factors
Authors: Vaissière Thomas , Hung Rayjean J. , Zaridze David , Moukeria Anush , Cuenin Cyrille , Fasolo Virginie , Ferro Gilles , Paliwal Anupam , Hainaut Pierre , Brennan Paul , Tost Jörg , Boffetta Paolo , Herceg Zdenko
Published: March 2023

Supplementary Table 3 from Quantitative Analysis of DNA Methylation Profiles in Lung Cancer Identifies Aberrant DNA Methylation of Specific Genes and Its Association with Gender and Cancer Risk Factors
Supplementary Methods and Figures 1-12 from Different Roles of Estrogen Receptors α and β in the Regulation of E-Cadherin Protein Levels in a Mouse Mammary Epithelial Cell Line
Authors: Helguero Luisa A. , Lindberg Karolina , Gardmo Cissi , Schwend Thomas , Gustafsson Jan-Åke , Haldosén Lars-Arne
Published: March 2023

Supplementary Methods and Figures 1-12 from Different Roles of Estrogen Receptors α and β in the Regulation of E-Cadherin Protein Levels in a Mouse Mammary Epithelial Cell Line
Supplementary Table 1 from Quantitative Analysis of DNA Methylation Profiles in Lung Cancer Identifies Aberrant DNA Methylation of Specific Genes and Its Association with Gender and Cancer Risk Factors
Authors: Vaissière Thomas , Hung Rayjean J. , Zaridze David , Moukeria Anush , Cuenin Cyrille , Fasolo Virginie , Ferro Gilles , Paliwal Anupam , Hainaut Pierre , Brennan Paul , Tost Jörg , Boffetta Paolo , Herceg Zdenko
Published: March 2023

Supplementary Table 1 from Quantitative Analysis of DNA Methylation Profiles in Lung Cancer Identifies Aberrant DNA Methylation of Specific Genes and Its Association with Gender and Cancer Risk Factors
Supplementary Figure 4 from Quantitative Analysis of DNA Methylation Profiles in Lung Cancer Identifies Aberrant DNA Methylation of Specific Genes and Its Association with Gender and Cancer Risk Factors
Authors: Vaissière Thomas , Hung Rayjean J. , Zaridze David , Moukeria Anush , Cuenin Cyrille , Fasolo Virginie , Ferro Gilles , Paliwal Anupam , Hainaut Pierre , Brennan Paul , Tost Jörg , Boffetta Paolo , Herceg Zdenko
Published: March 2023

Supplementary Figure 4 from Quantitative Analysis of DNA Methylation Profiles in Lung Cancer Identifies Aberrant DNA Methylation of Specific Genes and Its Association with Gender and Cancer Risk Factors
Supplementary Table 1 from Evidence that Resistance to Nilotinib May Be Due to BCR-ABL, Pgp, or Src Kinase Overexpression
Authors: Mahon François-Xavier , Hayette Sandrine , Lagarde Valérie , Belloc Francis , Turcq Béatrice , Nicolini Franck , Belanger Coralie , Manley Paul W. , Leroy Cédric , Etienne Gabriel , Roche Serge , Pasquet Jean-Max
Published: March 2023

Supplementary Table 1 from Evidence that Resistance to Nilotinib May Be Due to BCR-ABL, Pgp, or Src Kinase Overexpression
Supplementary Figure 2 from Quantitative Analysis of DNA Methylation Profiles in Lung Cancer Identifies Aberrant DNA Methylation of Specific Genes and Its Association with Gender and Cancer Risk Factors
Authors: Vaissière Thomas , Hung Rayjean J. , Zaridze David , Moukeria Anush , Cuenin Cyrille , Fasolo Virginie , Ferro Gilles , Paliwal Anupam , Hainaut Pierre , Brennan Paul , Tost Jörg , Boffetta Paolo , Herceg Zdenko
Published: March 2023

Supplementary Figure 2 from Quantitative Analysis of DNA Methylation Profiles in Lung Cancer Identifies Aberrant DNA Methylation of Specific Genes and Its Association with Gender and Cancer Risk Factors
Supplementary Data 1 from Involvement of the Leptin Receptor in the Immune Response in Intestinal Cancer
Authors: Aloulou Nijez , Bastuji-Garin Sylvie , Le Gouvello Sabine , Abolhassani Mohammad , Chaumette Marie Thérèse , Charachon Antoine , Leroy Karen , Sobhani Iradj
Published: March 2023

Supplementary Data 1 from Involvement of the Leptin Receptor in the Immune Response in Intestinal Cancer
Supplementary Figures 2-3 from Signal Transducers and Activators of Transcription Mediate Fibroblast Growth Factor–Induced Vascular Endothelial Morphogenesis
Authors: Yang Xinhai , Qiao Dianhua , Meyer Kristy , Friedl Andreas
Published: March 2023

Supplementary Figures 2-3 from Signal Transducers and Activators of Transcription Mediate Fibroblast Growth Factor–Induced Vascular Endothelial Morphogenesis
Supplementary Annex 2 from Involvement of the Leptin Receptor in the Immune Response in Intestinal Cancer
Authors: Aloulou Nijez , Bastuji-Garin Sylvie , Le Gouvello Sabine , Abolhassani Mohammad , Chaumette Marie Thérèse , Charachon Antoine , Leroy Karen , Sobhani Iradj
Published: March 2023

Supplementary Annex 2 from Involvement of the Leptin Receptor in the Immune Response in Intestinal Cancer
Supplementary Figure Legends 1-4 from Signal Transducers and Activators of Transcription Mediate Fibroblast Growth Factor–Induced Vascular Endothelial Morphogenesis
Authors: Yang Xinhai , Qiao Dianhua , Meyer Kristy , Friedl Andreas
Published: March 2023

Supplementary Figure Legends 1-4 from Signal Transducers and Activators of Transcription Mediate Fibroblast Growth Factor–Induced Vascular Endothelial Morphogenesis
Data from Perifosine Inhibits Multiple Signaling Pathways in Glial Progenitors and Cooperates With Temozolomide to Arrest Cell Proliferation in Gliomas In vivo
Authors: Momota Hiroyuki , Nerio Edward , Holland Eric C.
Published: March 2023

Abstract
Perifosine is an oral Akt inhibitor which exerts a marked cytotoxic effect on human tumor cell lines, and is currently being tested in several phase II trials for treatment of major human cancers. However, the efficacy of perifosine in human gliomas has not been established. As Akt is activated in ∼70% of human glioblastomas, we investigated the impact of perifosine on glia in culture and on a mouse glioma model in vivo. Here we show that perifosine strongly reduces phosphorylation levels of Akt and extracellular signal-regulated kinase (Erk) 1/2, induces cell cycle arrest in G1 and G2, and causes dose-dependent growth inhibition of mouse glial progenitors in which Akt and/or Ras-Erk 1/2 pathways are activated. Furthermore, because temozolomide is a common oral alkylating agent used in the treatment of gliomas, we investigated the effect of perifosine in combination with temozolomide. We observed an enhanced effect when both were used in culture. With these results, we combined perifosine and temozolomide as treatment of platelet-derived growth factor B–driven gliomas in mice. Animal studies showed that perifosine and temozolomide combination therapy was more effective than temozolomide treatment alone (P < 0.01). These results indicate that perifosine is an effective drug in gliomas in which Akt and Ras-Erk 1/2 pathways are frequently activated, and may be a new candidate for glioma treatment in the clinic.
Data from Identification and Testing of a Gene Expression Signature of Invasive Carcinoma Cells within Primary Mammary Tumors
Authors: Wang Weigang , Goswami Sumanta , Lapidus Kyle , Wells Amber L. , Wyckoff Jeffrey B. , Sahai Erik , Singer Robert H. , Segall Jeffrey E. , Condeelis John S.
Published: March 2023

Abstract
We subjected cells collected using an in vivo invasion assay to cDNA microarray analysis to identify the gene expression profile of invasive carcinoma cells in primary mammary tumors. Expression of genes involved in cell division, survival, and cell motility were most dramatically changed in invasive cells indicating a population that is neither dividing nor apoptotic but intensely motile. In particular, the genes coding for the minimum motility machine that regulates β-actin polymerization at the leading edge and, therefore, the motility and chemotaxis of carcinoma cells, were dramatically up-regulated. However, ZBP1, which restricts the localization of β-actin, the substrate for the minimum motility machine, was down-regulated. This pattern of expression implicated ZBP1 as a suppressor of invasion. Reexpression of ZBP1 in metastatic cells with otherwise low levels of ZBP1 reestablished normal patterns of β-actin mRNA targeting and suppressed chemotaxis and invasion in primary tumors. ZBP1 reexpression also inhibited metastasis from tumors. These experiments support the involvement in metastasis of the pathways identified in invasive cells, which are regulated by ZBP1.
Data from Induction of Centrosome Amplification and Chromosome Instability in Human Bladder Cancer Cells by p53 Mutation and Cyclin E Overexpression
Authors: Kawamura Kenji , Izumi Hideki , Ma Zhiyong , Ikeda Ryosuke , Moriyama Manabu , Tanaka Tatsuro , Nojima Takayuki , Levin Linda S. , Fujikawa-Yamamoto Kohzaburo , Suzuki Koji , Fukasawa Kenji
Published: March 2023

Abstract
Centrosome amplification frequently occurs in human cancers and is a major cause of chromosome instability (CIN). In mouse cells, centrosome amplification can be readily induced by loss or mutational inactivation of p53. In human cells, however, silencing of endogenous p53 alone does not induce centrosome amplification or CIN, although high degrees of correlation between p53 mutation and CIN/centrosome amplification in human cancer can be detected, suggesting the presence of additional regulatory mechanism(s) in human cells that ensures the numeral integrity of centrosomes and genomic integrity. Cyclin E, a regulatory subunit for CDK2 that plays a key role in centrosome duplication, frequently is overexpressed in human cancers. We found that cyclin E overexpression, together with loss of p53, efficiently induces centrosome amplification and CIN in human bladder cancer cells but not by either cyclin E overexpression or loss of p53 alone. We extended these findings to bladder cancer specimens and found that centrosome amplification is strongly correlated with concomitant occurrence of cyclin E overexpression and p53 inactivation but not with either cyclin E overexpression or p53 inactivation alone. Because cyclin E expression is strictly controlled in human cells compared with mouse cells, our findings suggest that this stringent regulation of cyclin E expression plays an additional role underlying numeral homeostasis of centrosomes in human cells and that deregulation of cyclin E expression, together with inactivation of p53, results in centrosome amplification.
Data from Stepwise Neoplastic Transformation of a Telomerase Immortalized Fibroblast Cell Line
Authors: Zongaro Samantha , de Stanchina Elisa , Colombo Tina , D'Incalci Maurizio , Giulotto Elena , Mondello Chiara
Published: March 2023

Abstract
We have described recently a human fibroblast cell line immortalized through ectopic telomerase expression (cen3tel), in which the extension of the life span was associated with the appearance of chromosomal aberrations and with the ability to grow in the absence of solid support. As reported in this article, on further propagation in culture, cen3tel cells became neoplastically transformed, being able to form tumors in nude mice. The analysis of the cells, during the gradual transition toward the tumorigenic phenotype, allowed us to trace cellular and molecular changes associated with different phases of transformation. At the stage in which they were able to grow in agar, cen3tel cells had lost contact growth inhibition but still retained the requirement of serum to proliferate and were not tumorigenic in immunocompromised mice. Moreover, they showed a down-regulation of the INK4A locus and were resistant to oncogenic Ras-induced senescence but still retained a functional p53. Subsequently, cen3tel cells became tumorigenic, lost p53 function because of a mutation in the DNA-binding motif, and overexpressed c-myc. Interestingly, tumorigenic cells did not carry activating mutations either in the ras proto-oncogenes (H-ras, N-ras, and K-ras) or in B-raf. Cen3tel cells gradually became hyperdiploid but did not display centrosome abnormalities. To our knowledge, cen3tel is the first telomerase immortalized fibroblast line, which became neoplastically transformed. In this system, we could associate a down-regulation of the INK4A locus with anchorage-independent growth and with resistance to Ras-induced senescence and link p53 mutations and c-myc overexpression with tumorigenicity. (Cancer Res 2005; 65(24): 11411-8)
Data from BRCA1 and c-Myc Associate to Transcriptionally Repress Psoriasin, a DNA Damage–Inducible Gene
Authors: Kennedy Richard D. , Gorski Julia J. , Quinn Jennifer E. , Stewart Gail E. , James Colin R. , Moore Stephen , Mulligan Karl , Emberley Ethan D. , Lioe Tong F. , Morrison Patrick J. , Mullan Paul B. , Reid George , Johnston Patrick G. , Watson Peter H. , Harkin D. Paul
Published: March 2023

Abstract
Evidence is accumulating to suggest that some of the diverse functions associated with BRCA1 may relate to its ability to transcriptionally regulate key downstream target genes. Here, we identify S100A7 (psoriasin), S100A8, and S100A9, members of the S100A family of calcium-binding proteins, as novel BRCA1-repressed targets. We show that functional BRCA1 is required for repression of these family members and that a BRCA1 disease–associated mutation abrogates BRCA1-mediated repression of psoriasin. Furthermore, we show that BRCA1 and c-Myc form a complex on the psoriasin promoter and that BRCA1-mediated repression of psoriasin is dependent on functional c-Myc. Finally, we show that psoriasin expression is induced by the topoisomerase IIα poison, etoposide, in the absence of functional BRCA1 and increased psoriasin expression enhances cellular sensitivity to this chemotherapeutic agent. Therefore, we identified a novel transcriptional mechanism that is likely to contribute to BRCA1-mediated resistance to etoposide.
Data from Autocrine/Paracrine Platelet-Derived Growth Factor Regulates Proliferation of Neural Progenitor Cells
Authors: Erlandsson Anna , Brännvall Karin , Gustafsdottir Sigrun , Westermark Bengt , Forsberg-Nilsson Karin
Published: March 2023

Abstract
Growth factors play an important role in regulating neural stem cell proliferation and differentiation. This study shows that platelet-derived growth factor (PDGF) induces a partial differentiation of neural stem/progenitor cells (NSPCs) in the absence of other mitogens in vitro. NSPCs thus acquire an immature morphology and display markers for both neurons and glia. In addition, these cells do not readily mature in the absence of further stimuli. When NSPC cultures treated with PDGF were exposed to additional differentiation factors, however, the differentiation proceeded into neurons, astrocytes, and oligodendrocytes. We find that NSPC cultures are endowed with an endogenous PDGF-BB production. The PDGF-BB expression peaks during early differentiation and is present both in cell lysates and in conditioned medium, allowing for autocrine as well as paracrine signaling. When the NSPC-derived PDGF was inhibited, progenitor cell numbers decreased, showing that PDGF is involved in NSPC expansion. Addition of a PDGF receptor (PDGFR) inhibitor resulted in a more rapid differentiation. Neurons and oligodendrocytes appeared earlier and had more elaborate processes than in control cultures where endogenous PDGFR signaling was not blocked. Our observations point to PDGF as an inducer of partial differentiation of NSPC that also sustains progenitor cell division. Such an intermediate stage in stem cell differentiation is of relevance for the understanding of brain tumor development because autocrine PDGF stimulation is believed to drive malignant conversion of central nervous system progenitor cells. (Cancer Res 2006; 66(16): 8042-8)
Data from Chemosensitization by Knockdown of Adenine Nucleotide Translocase-2
Authors: Le Bras Morgane , Borgne-Sanchez Annie , Touat Zahia , El Dein Ossama Sharaf , Deniaud Aurélien , Maillier Evelyne , Lecellier Gael , Rebouillat Dominique , Lemaire Christophe , Kroemer Guido , Jacotot Etienne , Brenner Catherine
Published: March 2023

Abstract
Mitochondrial membrane permeabilization (MMP) is a rate-limiting step of apoptosis, including in anticancer chemotherapy. Adenine nucleotide translocase (ANT) mediates the exchange of ADP and ATP on the inner mitochondrial membrane in healthy cells. In addition, ANT can cooperate with Bax to form a lethal pore during apoptosis. Humans possess four distinct ANT isoforms, encoded by four genes, whose transcription depends on the cell type, developmental stage, cell proliferation, and hormone status. Here, we show that the ANT2 gene is up-regulated in several hormone-dependent cancers. Knockdown of ANT2 by RNA interference induced no major changes in the aspect of the mitochondrial network or cell cycle but provoked minor increase in mitochondrial transmembrane potential and reactive oxygen species level and reduced intracellular ATP concentration without affecting glycolysis. At expression and functional levels, ANT2 depletion was not compensated by other ANT isoforms. Most importantly, ANT2, but not ANT1, silencing facilitated MMP induction by lonidamine, a mitochondrion-targeted antitumor compound already used in clinical studies for breast, ovarian, glioma, and lung cancer as well as prostate adenoma. The combination of ANT2 knockdown with lonidamine induced apoptosis irrespective of the Bcl-2 status. These data identify ANT2 as an endogenous inhibitor of MMP and suggest that its selective inhibition could constitute a promising strategy of chemosensitization. (Cancer Res 2006; 66(18): 9143-52)
Data from c-Abl Expression in Chronic Lymphocytic Leukemia Cells: Clinical and Therapeutic Implications
Authors: Lin Ke , Glenn Mark A. , Harris Robert J. , Duckworth Andrew D. , Dennett Sally , Cawley John C. , Zuzel Mirko , Slupsky Joseph R.
Published: March 2023

Abstract
c-Abl is important for normal B-cell development, but little is known about the function of this nonreceptor tyrosine kinase in chronic lymphocytic leukemia (CLL). Therefore, the aim of the present study was to examine the clinical, therapeutic, and pathogenetic importance of c-Abl in this disease. We show that the malignant cells of CLL predominantly express the type 1b splice variant of c-Abl and that the expression of c-Abl protein is higher in CLL cells than in normal peripheral blood B cells. Moreover, we show that the levels of c-Abl protein expression correlate positively with tumor burden and disease stage, and negatively with IgVH mutation. We also show that STI-571, an inhibitor of c-Abl kinase activity, induces apoptosis of CLL cells with high c-Abl expression levels through a mechanism involving inhibition of nuclear factor κB. We conclude that overexpression of c-Abl is likely to play a pathogenetic role in CLL and that STI-571 may be of potential use in the treatment of this disease. (Cancer Res 2006; 66(15): 7801-9)
Data from Uncoupling between Epidermal Growth Factor Receptor and Downstream Signals Defines Resistance to the Antiproliferative Effect of Gefitinib in Bladder Cancer Cells
Authors: Kassouf Wassim , Dinney Colin P.N. , Brown Gordon , McConkey David J. , Diehl Alan J. , Bar-Eli Menashe , Adam Liana
Published: March 2023

Abstract
Activation of the epidermal growth factor receptor (EGFR) and downstream signaling pathways, such as phosphatidylinositol-3 kinase/Akt and Ras/mitogen-activated protein kinase (MAPK), have been implicated in causing resistance to EGFR-targeted therapy in solid tumors, including the urogenital tumors. To investigate the mechanism of resistance to EGFR inhibition in bladder cancer, we compared EGFR tyrosine kinase inhibitor (Gefitinib, Iressa, ZD1839) with respect to its inhibitory effects on three kinases situated downstream of EGFR: MAPK, Akt, and glycogen synthase kinase-3β (GSK-3β). We found that the resistance to the antiproliferative effects of gefitinib, in vitro as well as in vivo in nude mice models, was associated with uncoupling between EGFR and MAPK inhibition, and that GSK-3β activation and degradation of its target cyclin D1 were indicators of a high cell sensitivity to gefitinib. Further analysis of one phenotypic sensitive (253J B-V) and resistant (UM-UC13) cell lines revealed that platelet-derived growth factor receptor-β (PDGFRβ) activation was responsible for short circuiting the EGFR/MAPK pathway for mitogenic stimuli. However, invasion as well as actin dynamics were efficiently reduced by EGFR inhibition in UM-UC13. Chemical disruption of signaling pathways or of PDGFR kinase activity significantly reduced the inactive pool of cellular GSK-3β in UM-UC13 cells. In conclusion, our data show that the uncoupling of EGFR with mitogenic pathways can cause resistance to EGFR inhibition in bladder cancer. Although this uncoupling may arise through different mechanisms, we suggest that the resistance of bladder cancer cells to EGFR blockade can be predicted early in the course of treatment by measuring the activation of GSK-3β and of nuclear cyclin D1.
Data from Selective Targeting of Antitumor Immune Responses with Engineered Live-Attenuated Listeria monocytogenes
Authors: Yoshimura Kiyoshi , Jain Ajay , Allen Heather E. , Laird Lindsay S. , Chia Christina Y. , Ravi Sowmya , Brockstedt Dirk G. , Giedlin Martin A. , Bahjat Keith S. , Leong Meredith L. , Slansky Jill E. , Cook David N. , Dubensky Thomas W. , Pardoll Drew M. , Schulick Richard D.
Published: March 2023

Abstract
Improved immunization and ex vivo T-cell culture strategies can generate larger numbers and more potent tumor-specific effector cells than previously possible. Nonetheless, the capacity of these cells to eliminate established tumors is limited by their ability to efficiently enter tumor-bearing organs and mediate their effector function. In the current study, we show that the administration of an engineered organ-homing microbe selectively targets tumor-specific immune responses to metastases within that organ. Specifically, an attenuated Listeria monocytogenes strain, which preferentially infects the liver following systemic administration, dramatically enhances the activity of a cancer vaccine against liver metastases but not metastases in the lung. This enhanced activity results from both local recruitment of innate immune effectors as well as concentration and increased activation of vaccine-induced antitumor T cells within the liver. These findings show a general approach to focus systemic cancer immunotherapies to specific organs bearing tumor metastases by taking advantage of differential tropisms and the proinflammatory nature of microbes. (Cancer Res 2006; 66(2): 1096-104)
Data from Gene Expression Profiles in Pancreatic Intraepithelial Neoplasia Reflect the Effects of Hedgehog Signaling on Pancreatic Ductal Epithelial Cells
Authors: Prasad Nijaguna B. , Biankin Andrew V. , Fukushima Noriyoshi , Maitra Anirban , Dhara Surajit , Elkahloun Abdel G. , Hruban Ralph H. , Goggins Michael , Leach Steven D.
Published: March 2023

Abstract
Invasive pancreatic cancer is thought to develop through a series of noninvasive duct lesions known as pancreatic intraepithelial neoplasia (PanIN). We used cDNA microarrays interrogating 15,000 transcripts to identify 49 genes that were differentially expressed in microdissected early PanIN lesions (PanIN-1B/2) compared with microdissected normal duct epithelium. In this analysis, a cluster of extrapancreatic foregut markers, including pepsinogen C, MUC6, KLF4, and TFF1, was found to be up-regulated in PanIN. Up-regulation of these genes was further validated using combinations of real-time reverse transcription-PCR, in situ hybridization, and immunohistochemistry in a total of 150 early PanIN lesions from 81 patients. Identification of these gastrointestinal transcripts in human PanIN prompted assessment of other foregut markers by both semiquantitative and real-time reverse transcription-PCR, revealing similar up-regulation of Sox-2, Gastrin, HoxA5, GATA4/5/6, Villin and Forkhead 6 (Foxl1). In contrast to frequent expression of multiple gastric epithelial markers, the intestinal markers intestinal fatty acid binding protein, CDX1 and CDX2 were rarely expressed either in PanIN lesions or in invasive pancreatic cancer. Hedgehog pathway activation induced by transfection of immortalized human pancreatic ductal epithelial cells with Gli1 resulted in up-regulation of the majority of foregut markers seen in early PanIN lesions. These data show frequent up-regulation of foregut markers in early PanIN lesions and suggest that PanIN development may involve Hedgehog-mediated conversion to a gastric epithelial differentiation program.