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1. RAF1 contributes to cell proliferation and STAT3 activation in colorectal cancer independently of microsatellite and KRAS status

Author

Coralie Dorard, Claire Madry, Olivier Buhard, Stefanie Toifl, Sebastian Didusch, Toky Ratovomanana, Quentin Letourneur, Helmut Dolznig, Mathew J. Garnett, Alex Duval, and Manuela Baccarini

Subjects
Cancer Research, Genetics, Molecular Biology
Abstract

More than 30% of all human cancers are driven by RAS mutations and activating KRAS mutations are present in 40% of colorectal cancer (CRC) in the two main CRC subgroups, MSS (Microsatellite Stable) and MSI (Microsatellite Instable). Studies in RAS-driven tumors have shown essential roles of the RAS effectors RAF and specifically of RAF1, which can be dependent or independent of RAF’s ability to activate the MEK/ERK module. In this study, we demonstrate that RAF1, but not its kinase activity, plays a crucial role in the proliferation of both MSI and MSS CRC cell line-derived spheroids and patient-derived organoids, and independently of KRAS mutation status. Moreover, we could define a RAF1 transcriptomic signature which includes genes that contribute to STAT3 activation, and could demonstrate that RAF1 ablation decreases STAT3 phosphorylation in all CRC spheroids tested. The genes involved in STAT3 activation as well as STAT3 targets promoting angiogenesis were also downregulated in human primary tumors expressing low levels of RAF1. These results indicate that RAF1 could be an attractive therapeutic target in both MSI and MSS CRC regardless of their KRAS status and support the development of selective RAF1 degraders rather than RAF1 inhibitors for clinical use in combination therapies.

Published
2023

2. Primary vs patch‐based skin closure for in‐utero spina bifida repair

Author

M. Fishel Bartal, E. P. Bergh, K. Tsao, M. T. Austin, K. J. Moise, S. A. Fletcher, J. Garnett, L. Mann, E. Hernandez‐Andrade, A. Johnson, and R. Papanna

Subjects
Meningomyelocele, Radiological and Ultrasound Technology, Infant, Obstetrics and Gynecology, Gestational Age, General Medicine, Ventriculoperitoneal Shunt, Spina Bifida Cystica, Reproductive Medicine, Pregnancy, Humans, Animals, Female, Cattle, Radiology, Nuclear Medicine and imaging, Prospective Studies, Child
Abstract

During in-utero spina bifida (SB) repair, closure of large defects is often challenging, requiring tissue graft for watertight skin closure. No prior studies have compared primary skin closure vs patch-based repair. Our objective was to compare neonatal and 1-year outcomes associated with these two types of skin closure for in-utero SB repair.This was a prospective cohort study of 102 patients undergoing open prenatal SB repair from September 2011 to August 2021 at a single institution. All patients met the inclusion criteria of the Management of Myelomeningocele Study (MOMS), and the surgical procedure for in-utero SB repair was similar to that described in the MOMS trial. During the surgery, if primary skin approximation was not feasible due to the large size of the defect, the decision was at the discretion of the pediatric neurosurgeon to utilize a patch for closure. Neonatal outcomes at birth and 1-year outcomes were compared between the primary skin and patch-based closure groups.Of 102 patients included in the study, 70 (68.6%) underwent primary skin closure and 32 (31.4%) patch-based closure. The patch type included acellular bovine skin matrix (Durepair®; n = 31) and human acellular dermal matrix (Alloderm®; n = 1). Fetuses with myeloschisis were more likely to require patch-based repair than those with myelomeningocele. The median time of fetal repair was 4 min longer for patch-based compared with primary skin closure (37 vs 33 min; P = 0.001). Following patch-based repair, neonates had a longer length of stay in the neonatal intensive care unit (NICU) by 24 days (adjusted risk ratio, 2.40 (95% CI, 1.41-4.29)) compared to those that underwent primary skin closure. There was no difference between the two groups in the other neonatal outcomes, including the need for ventriculoperitoneal shunt placement and cerebrospinal fluid leakage. Outcome at 1 year of age was available for 90 infants. Need for wound revision within their first year after birth was more common in infants who underwent patch-based vs those with primary skin closure (19.4% vs 5.1%; P = 0.05). There was no difference between the two groups in other 1-year outcomes, including the need for ventriculoperitoneal shunt placement by 1 year of age and surgery for tethered cord.Patch-based closure during SB repair is often needed in fetuses with myeloschisis and is associated with prolonged fetal surgery time, long NICU stay and need for wound revision within the first year after birth. Further studies are required to identify optimal patches for SB repair or alternative methods to improve outcome. © 2022 International Society of Ultrasound in Obstetrics and Gynecology.

Published
2022

3. High-throughput phenotyping of single nucleotide variants by linking transcriptomes to genotypes in single cells

Author

Sarah E. Cooper, Matthew A. Coelho, Magdalena E. Strauss, Aleksander M. Gontarczyk, Qianxin Wu, Mathew J. Garnett, John C. Marioni, and Andrew R. Bassett

Abstract

CRISPR screens with single-cell transcriptomic readouts are a valuable tool to understand the effect of genetic perturbations, but are currently limited because genotypes are inferred from the guide RNA identity. We have developed a technique that couples single-cell genotyping to transcriptomics of the same cells to enable screening for the effects of single nucleotide variants. Analysis of variants tiling across theJAK1gene demonstrates the importance of determining the precise genetic perturbation and classifies missense variants into three functional categories.

Published
2023

5. Cell Model Network-UK from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

Author

Mathew J. Garnett, Alberto Bardelli, Emile E. Voest, Sabrina Arena, Salvatore Siena, Andrea Sartore-Bianchi, Federica Di Nicolantonio, Fengtang Yang, Martin Michaelis, Jindrich Cinatl, Krijn K. Dijkstra, Daniele Oddo, Luuk J. Schipper, Ruby Banerjee, Carlotta Cancelliere, Iñigo Sánchez Rodríguez, Sara F. Vieira, Sarah Consonni, Giuseppe Rospo, Giovanni Crisafulli, Esmée J. van Vliet, Chiara M. Cattaneo, and Gabriele Picco

Abstract

The Cell Model Network-UK group author list

Published
2023

6. Supplementary Table 1 from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

Author

Mathew J. Garnett, Alberto Bardelli, Emile E. Voest, Sabrina Arena, Salvatore Siena, Andrea Sartore-Bianchi, Federica Di Nicolantonio, Fengtang Yang, Martin Michaelis, Jindrich Cinatl, Krijn K. Dijkstra, Daniele Oddo, Luuk J. Schipper, Ruby Banerjee, Carlotta Cancelliere, Iñigo Sánchez Rodríguez, Sara F. Vieira, Sarah Consonni, Giuseppe Rospo, Giovanni Crisafulli, Esmée J. van Vliet, Chiara M. Cattaneo, and Gabriele Picco

Abstract

Supplementary Table 1

Published
2023

7. Supplementary Table S5 from Isocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic Cholangiocarcinoma

Author

Nabeel Bardeesy, Cyril H. Benes, Kevan M. Shokat, J. Keith Joung, Andrew X. Zhu, Cristina R. Ferrone, Lipika Goyal, Yusuke Mizukami, Andrew S. Liss, Aram F. Hezel, Travis B. Sullivan, Kimberly M. Rieger-Christ, Roger L. Jenkins, Mathew J. Garnett, Ultan McDermott, Patricia Greninger, Regina K. Egan, Leah J. Damon, James T. Webber, Rebecca S. Levin, Yasutaka Kato, Lei Shi, Jia-Chi Yeo, Mortada S. Najem, Phuong Vu, Benjamin P. Kleinstiver, John D. Gordan, and Supriya K. Saha

Abstract

Source and cell culture information for cell lines.

Published
2023

8. Supplementary Figure Legends, Figures S1 - S6 from Isocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic Cholangiocarcinoma

Author

Nabeel Bardeesy, Cyril H. Benes, Kevan M. Shokat, J. Keith Joung, Andrew X. Zhu, Cristina R. Ferrone, Lipika Goyal, Yusuke Mizukami, Andrew S. Liss, Aram F. Hezel, Travis B. Sullivan, Kimberly M. Rieger-Christ, Roger L. Jenkins, Mathew J. Garnett, Ultan McDermott, Patricia Greninger, Regina K. Egan, Leah J. Damon, James T. Webber, Rebecca S. Levin, Yasutaka Kato, Lei Shi, Jia-Chi Yeo, Mortada S. Najem, Phuong Vu, Benjamin P. Kleinstiver, John D. Gordan, and Supriya K. Saha

Abstract

Supplementary Figure S1. IDHm ICC are insensitive to IDH inhibition. Supplementary Figure S2. Similarity matrix for drug response of BTC cell lines. Supplementary Figure S3. Hypersensitivity of ICC cells harboring endogenous IDH mutations to dasatinib. Supplementary Figure S4. Torin 1 inhibits growth of ICC cell lines. Supplementary Figure S5. Critical role for SRC in IDHm ICC cells. Supplementary Figure S6. Ectopic expression of mutant IDH has only a modest effect on dasatinib sensitivity.

Published
2023

9. Supplementary Figure 4 from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

Author

Mathew J. Garnett, Alberto Bardelli, Emile E. Voest, Sabrina Arena, Salvatore Siena, Andrea Sartore-Bianchi, Federica Di Nicolantonio, Fengtang Yang, Martin Michaelis, Jindrich Cinatl, Krijn K. Dijkstra, Daniele Oddo, Luuk J. Schipper, Ruby Banerjee, Carlotta Cancelliere, Iñigo Sánchez Rodríguez, Sara F. Vieira, Sarah Consonni, Giuseppe Rospo, Giovanni Crisafulli, Esmée J. van Vliet, Chiara M. Cattaneo, and Gabriele Picco

Abstract

Supplementary Figure 4

Published
2023

10. Supplementary Table 1 from AZD0364 Is a Potent and Selective ERK1/2 Inhibitor That Enhances Antitumor Activity in KRAS-Mutant Tumor Models when Combined with the MEK Inhibitor, Selumetinib

Author

Paul D. Smith, J. Elizabeth Pease, Sabina C. Cosulich, Iain Simpson, Richard A. Ward, Clifford D. Jones, Stephen E. Fawell, Mathew J. Garnett, Patricia Jaaks, Elizabeth A. Coker, Claire Rooney, Martine P. Roudier, Sophie E. Willis, Philip Hopcroft, Michael Tonge, Karen Roberts, Joanne Wilson, Aaron Smith, Nicola Lindsay, Francis D. Gibbons, Katarzyna Falenta, Sigourney Bell, Paul Farrington, Lyndsey Hanson, Pei Zhang, Oona Delpuech, Linda C. Sandin, David Robinson, Emma J. Davies, and Vikki Flemington

Abstract

Primers used for targeted gene profiling on selected RAS/MAPK pathway genes either on Fluidigm or by qRT-PCR on Roche Lightcycler 480

Published
2023

11. Supplementary Figure 3 from AZD0364 Is a Potent and Selective ERK1/2 Inhibitor That Enhances Antitumor Activity in KRAS-Mutant Tumor Models when Combined with the MEK Inhibitor, Selumetinib

Author

Paul D. Smith, J. Elizabeth Pease, Sabina C. Cosulich, Iain Simpson, Richard A. Ward, Clifford D. Jones, Stephen E. Fawell, Mathew J. Garnett, Patricia Jaaks, Elizabeth A. Coker, Claire Rooney, Martine P. Roudier, Sophie E. Willis, Philip Hopcroft, Michael Tonge, Karen Roberts, Joanne Wilson, Aaron Smith, Nicola Lindsay, Francis D. Gibbons, Katarzyna Falenta, Sigourney Bell, Paul Farrington, Lyndsey Hanson, Pei Zhang, Oona Delpuech, Linda C. Sandin, David Robinson, Emma J. Davies, and Vikki Flemington

Abstract

Supplementary Figure 3

Published
2023

12. Supplementary Figure 2 from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

Author

Mathew J. Garnett, Alberto Bardelli, Emile E. Voest, Sabrina Arena, Salvatore Siena, Andrea Sartore-Bianchi, Federica Di Nicolantonio, Fengtang Yang, Martin Michaelis, Jindrich Cinatl, Krijn K. Dijkstra, Daniele Oddo, Luuk J. Schipper, Ruby Banerjee, Carlotta Cancelliere, Iñigo Sánchez Rodríguez, Sara F. Vieira, Sarah Consonni, Giuseppe Rospo, Giovanni Crisafulli, Esmée J. van Vliet, Chiara M. Cattaneo, and Gabriele Picco

Abstract

Supplementary Figure 2

Published
2023

13. Supplementary Table S1 from Isocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic Cholangiocarcinoma

Author

Nabeel Bardeesy, Cyril H. Benes, Kevan M. Shokat, J. Keith Joung, Andrew X. Zhu, Cristina R. Ferrone, Lipika Goyal, Yusuke Mizukami, Andrew S. Liss, Aram F. Hezel, Travis B. Sullivan, Kimberly M. Rieger-Christ, Roger L. Jenkins, Mathew J. Garnett, Ultan McDermott, Patricia Greninger, Regina K. Egan, Leah J. Damon, James T. Webber, Rebecca S. Levin, Yasutaka Kato, Lei Shi, Jia-Chi Yeo, Mortada S. Najem, Phuong Vu, Benjamin P. Kleinstiver, John D. Gordan, and Supriya K. Saha

Abstract

Median centered Ln(IC50) values for 17 BTC cell lines screened against 122 drugs.

Published
2023

14. Supplementary Tables 1 - 9 from Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition

Author

Kimberly Stegmaier, James E. Bradner, William A. Weiss, Andrew L. Kung, Cyril H. Benes, Ultan McDermott, Matthew J. Garnett, Patricia Greninger, William Clay Gustafson, Rhamy Zeid, Erin A. Nekritz, Yvan H. Chanthery, Jun Qi, Christopher F. Bassil, Gabriela Alexe, Stacey M. Frumm, and Alexandre Puissant

Abstract

PDF file - 93K, This file contains 9 supplementary tables including the full primary screening data and secondary testing of BETi in neuroblastoma, supporting tables for the expression profiling analyses, and the list of Affymetrix probes (MYCN) and shRNA sequences for BRD4 and MYCN.

Published
2023

15. Supplementary Figure 2 from AZD0364 Is a Potent and Selective ERK1/2 Inhibitor That Enhances Antitumor Activity in KRAS-Mutant Tumor Models when Combined with the MEK Inhibitor, Selumetinib

Author

Paul D. Smith, J. Elizabeth Pease, Sabina C. Cosulich, Iain Simpson, Richard A. Ward, Clifford D. Jones, Stephen E. Fawell, Mathew J. Garnett, Patricia Jaaks, Elizabeth A. Coker, Claire Rooney, Martine P. Roudier, Sophie E. Willis, Philip Hopcroft, Michael Tonge, Karen Roberts, Joanne Wilson, Aaron Smith, Nicola Lindsay, Francis D. Gibbons, Katarzyna Falenta, Sigourney Bell, Paul Farrington, Lyndsey Hanson, Pei Zhang, Oona Delpuech, Linda C. Sandin, David Robinson, Emma J. Davies, and Vikki Flemington

Abstract

Supplementary Figure 2

Published
2023

16. Supplementary Figure 3 from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

Author

Mathew J. Garnett, Alberto Bardelli, Emile E. Voest, Sabrina Arena, Salvatore Siena, Andrea Sartore-Bianchi, Federica Di Nicolantonio, Fengtang Yang, Martin Michaelis, Jindrich Cinatl, Krijn K. Dijkstra, Daniele Oddo, Luuk J. Schipper, Ruby Banerjee, Carlotta Cancelliere, Iñigo Sánchez Rodríguez, Sara F. Vieira, Sarah Consonni, Giuseppe Rospo, Giovanni Crisafulli, Esmée J. van Vliet, Chiara M. Cattaneo, and Gabriele Picco

Abstract

Supplementary Figure 3

Published
2023

17. Supplementary Figure 5 from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

Author

Mathew J. Garnett, Alberto Bardelli, Emile E. Voest, Sabrina Arena, Salvatore Siena, Andrea Sartore-Bianchi, Federica Di Nicolantonio, Fengtang Yang, Martin Michaelis, Jindrich Cinatl, Krijn K. Dijkstra, Daniele Oddo, Luuk J. Schipper, Ruby Banerjee, Carlotta Cancelliere, Iñigo Sánchez Rodríguez, Sara F. Vieira, Sarah Consonni, Giuseppe Rospo, Giovanni Crisafulli, Esmée J. van Vliet, Chiara M. Cattaneo, and Gabriele Picco

Abstract

Supplementary Figure 5

Published
2023

18. Supplementary Figure 2 from Mcl-1 and FBW7 Control a Dominant Survival Pathway Underlying HDAC and Bcl-2 Inhibitor Synergy in Squamous Cell Carcinoma

Author

Leif W. Ellisen, Cyril H. Benes, Stephen M. Rothenberg, Ultan McDermott, Mathew J. Garnett, Patricia Greninger, Saranya Ramakrishnan, Nicole Forster, Kristine Torres-Lockhart, and Lei He

Abstract

Supplementary Figure 2 PDF file 74K, Mcl-1 is essential for cell survival in SCC cells and vorinostat induces redistribution of Bim from Mcl-1 to Bcl-2/Bcl-xl

Published
2023

19. Supplementary Table 4 from AZD0364 Is a Potent and Selective ERK1/2 Inhibitor That Enhances Antitumor Activity in KRAS-Mutant Tumor Models when Combined with the MEK Inhibitor, Selumetinib

Author

Paul D. Smith, J. Elizabeth Pease, Sabina C. Cosulich, Iain Simpson, Richard A. Ward, Clifford D. Jones, Stephen E. Fawell, Mathew J. Garnett, Patricia Jaaks, Elizabeth A. Coker, Claire Rooney, Martine P. Roudier, Sophie E. Willis, Philip Hopcroft, Michael Tonge, Karen Roberts, Joanne Wilson, Aaron Smith, Nicola Lindsay, Francis D. Gibbons, Katarzyna Falenta, Sigourney Bell, Paul Farrington, Lyndsey Hanson, Pei Zhang, Oona Delpuech, Linda C. Sandin, David Robinson, Emma J. Davies, and Vikki Flemington

Abstract

KRAS mutation status of cell lines included in in vitro combination screen

Published
2023

20. Supplementary Figure 1 from Mcl-1 and FBW7 Control a Dominant Survival Pathway Underlying HDAC and Bcl-2 Inhibitor Synergy in Squamous Cell Carcinoma

Author

Leif W. Ellisen, Cyril H. Benes, Stephen M. Rothenberg, Ultan McDermott, Mathew J. Garnett, Patricia Greninger, Saranya Ramakrishnan, Nicole Forster, Kristine Torres-Lockhart, and Lei He

Abstract

Supplementary Figure 1 PDF file 140K, Vorinostat induces apoptosis and alters gene expression of Bcl-2 family members in different SCC cell lines

Published
2023

21. Data from AZD0364 Is a Potent and Selective ERK1/2 Inhibitor That Enhances Antitumor Activity in KRAS-Mutant Tumor Models when Combined with the MEK Inhibitor, Selumetinib

Author

Paul D. Smith, J. Elizabeth Pease, Sabina C. Cosulich, Iain Simpson, Richard A. Ward, Clifford D. Jones, Stephen E. Fawell, Mathew J. Garnett, Patricia Jaaks, Elizabeth A. Coker, Claire Rooney, Martine P. Roudier, Sophie E. Willis, Philip Hopcroft, Michael Tonge, Karen Roberts, Joanne Wilson, Aaron Smith, Nicola Lindsay, Francis D. Gibbons, Katarzyna Falenta, Sigourney Bell, Paul Farrington, Lyndsey Hanson, Pei Zhang, Oona Delpuech, Linda C. Sandin, David Robinson, Emma J. Davies, and Vikki Flemington

Abstract

The RAS-regulated RAF–MEK1/2–ERK1/2 (RAS/MAPK) signaling pathway is a major driver in oncogenesis and is frequently dysregulated in human cancers, primarily by mutations in BRAF or RAS genes. The clinical benefit of inhibitors of this pathway as single agents has only been realized in BRAF-mutant melanoma, with limited effect of single-agent pathway inhibitors in KRAS-mutant tumors. Combined inhibition of multiple nodes within this pathway, such as MEK1/2 and ERK1/2, may be necessary to effectively suppress pathway signaling in KRAS-mutant tumors and achieve meaningful clinical benefit. Here, we report the discovery and characterization of AZD0364, a novel, reversible, ATP-competitive ERK1/2 inhibitor with high potency and kinase selectivity. In vitro, AZD0364 treatment resulted in inhibition of proximal and distal biomarkers and reduced proliferation in sensitive BRAF-mutant and KRAS-mutant cell lines. In multiple in vivo xenograft models, AZD0364 showed dose- and time-dependent modulation of ERK1/2-dependent signaling biomarkers resulting in tumor regression in sensitive BRAF- and KRAS-mutant xenografts. We demonstrate that AZD0364 in combination with the MEK1/2 inhibitor, selumetinib (AZD6244 and ARRY142886), enhances efficacy in KRAS-mutant preclinical models that are moderately sensitive or resistant to MEK1/2 inhibition. This combination results in deeper and more durable suppression of the RAS/MAPK signaling pathway that is not achievable with single-agent treatment. The AZD0364 and selumetinib combination also results in significant tumor regressions in multiple KRAS-mutant xenograft models. The combination of ERK1/2 and MEK1/2 inhibition thereby represents a viable clinical approach to target KRAS-mutant tumors.

Published
2023

22. Supplementary Figure 6 from AZD0364 Is a Potent and Selective ERK1/2 Inhibitor That Enhances Antitumor Activity in KRAS-Mutant Tumor Models when Combined with the MEK Inhibitor, Selumetinib

Author

Paul D. Smith, J. Elizabeth Pease, Sabina C. Cosulich, Iain Simpson, Richard A. Ward, Clifford D. Jones, Stephen E. Fawell, Mathew J. Garnett, Patricia Jaaks, Elizabeth A. Coker, Claire Rooney, Martine P. Roudier, Sophie E. Willis, Philip Hopcroft, Michael Tonge, Karen Roberts, Joanne Wilson, Aaron Smith, Nicola Lindsay, Francis D. Gibbons, Katarzyna Falenta, Sigourney Bell, Paul Farrington, Lyndsey Hanson, Pei Zhang, Oona Delpuech, Linda C. Sandin, David Robinson, Emma J. Davies, and Vikki Flemington

Abstract

Supplementary Figure 6

Published
2023

23. Data from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

Author

Mathew J. Garnett, Alberto Bardelli, Emile E. Voest, Sabrina Arena, Salvatore Siena, Andrea Sartore-Bianchi, Federica Di Nicolantonio, Fengtang Yang, Martin Michaelis, Jindrich Cinatl, Krijn K. Dijkstra, Daniele Oddo, Luuk J. Schipper, Ruby Banerjee, Carlotta Cancelliere, Iñigo Sánchez Rodríguez, Sara F. Vieira, Sarah Consonni, Giuseppe Rospo, Giovanni Crisafulli, Esmée J. van Vliet, Chiara M. Cattaneo, and Gabriele Picco

Abstract

Targeted therapies, chemotherapy, and immunotherapy are used to treat patients with mismatch repair–deficient (dMMR)/microsatellite instability-high (MSI-H) colorectal cancer. The clinical effectiveness of targeted therapy and chemotherapy is limited by resistance and drug toxicities, and about half of patients receiving immunotherapy have disease that is refractory to immune checkpoint inhibitors. Loss of Werner syndrome ATP-dependent helicase (WRN) is a synthetic lethality in dMMR/MSI-H cells. To inform the development of WRN as a therapeutic target, we performed WRN knockout or knockdown in 60 heterogeneous dMMR colorectal cancer preclinical models, demonstrating that WRN dependency is an almost universal feature and a robust marker for patient selection. Furthermore, models of resistance to clinically relevant targeted therapy, chemotherapy, and immunotherapy retain WRN dependency. These data show the potential of therapeutically targeting WRN in patients with dMMR/MSI-H colorectal cancer and support WRN as a therapeutic option for patients with dMMR/MSI-H cancers refractory to current treatment strategies.Significance:We found that a large, diverse set of dMMR/MSI-H colorectal cancer preclinical models, including models of treatment-refractory disease, are WRN-dependent. Our results support WRN as a promising synthetic-lethal target in dMMR/MSI-H colorectal cancer tumors as a monotherapy or in combination with targeted agents, chemotherapy, or immunotherapy.This article is highlighted in the In This Issue feature, p. 1861

Published
2023

24. Supplementary Table S3 from Isocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic Cholangiocarcinoma

Author

Nabeel Bardeesy, Cyril H. Benes, Kevan M. Shokat, J. Keith Joung, Andrew X. Zhu, Cristina R. Ferrone, Lipika Goyal, Yusuke Mizukami, Andrew S. Liss, Aram F. Hezel, Travis B. Sullivan, Kimberly M. Rieger-Christ, Roger L. Jenkins, Mathew J. Garnett, Ultan McDermott, Patricia Greninger, Regina K. Egan, Leah J. Damon, James T. Webber, Rebecca S. Levin, Yasutaka Kato, Lei Shi, Jia-Chi Yeo, Mortada S. Najem, Phuong Vu, Benjamin P. Kleinstiver, John D. Gordan, and Supriya K. Saha

Abstract

IC50 values for dasatinib in nM of nine ICC cell lines and the immortalized human cholangiocyte cell line MMNK-1.

Published
2023

25. Supplementary materials and methods from AZD0364 Is a Potent and Selective ERK1/2 Inhibitor That Enhances Antitumor Activity in KRAS-Mutant Tumor Models when Combined with the MEK Inhibitor, Selumetinib

Author

Paul D. Smith, J. Elizabeth Pease, Sabina C. Cosulich, Iain Simpson, Richard A. Ward, Clifford D. Jones, Stephen E. Fawell, Mathew J. Garnett, Patricia Jaaks, Elizabeth A. Coker, Claire Rooney, Martine P. Roudier, Sophie E. Willis, Philip Hopcroft, Michael Tonge, Karen Roberts, Joanne Wilson, Aaron Smith, Nicola Lindsay, Francis D. Gibbons, Katarzyna Falenta, Sigourney Bell, Paul Farrington, Lyndsey Hanson, Pei Zhang, Oona Delpuech, Linda C. Sandin, David Robinson, Emma J. Davies, and Vikki Flemington

Abstract

Supplementary materials and methods

Published
2023

26. Supplementary Table S2 from Isocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic Cholangiocarcinoma

Author

Nabeel Bardeesy, Cyril H. Benes, Kevan M. Shokat, J. Keith Joung, Andrew X. Zhu, Cristina R. Ferrone, Lipika Goyal, Yusuke Mizukami, Andrew S. Liss, Aram F. Hezel, Travis B. Sullivan, Kimberly M. Rieger-Christ, Roger L. Jenkins, Mathew J. Garnett, Ultan McDermott, Patricia Greninger, Regina K. Egan, Leah J. Damon, James T. Webber, Rebecca S. Levin, Yasutaka Kato, Lei Shi, Jia-Chi Yeo, Mortada S. Najem, Phuong Vu, Benjamin P. Kleinstiver, John D. Gordan, and Supriya K. Saha

Abstract

Cell viability and Ln(IC50) for 885 cancer cell lines treated with dasatinib and saracatinib over nine doses.

Published
2023

27. Supplementary Figure 1 from AZD0364 Is a Potent and Selective ERK1/2 Inhibitor That Enhances Antitumor Activity in KRAS-Mutant Tumor Models when Combined with the MEK Inhibitor, Selumetinib

Author

Paul D. Smith, J. Elizabeth Pease, Sabina C. Cosulich, Iain Simpson, Richard A. Ward, Clifford D. Jones, Stephen E. Fawell, Mathew J. Garnett, Patricia Jaaks, Elizabeth A. Coker, Claire Rooney, Martine P. Roudier, Sophie E. Willis, Philip Hopcroft, Michael Tonge, Karen Roberts, Joanne Wilson, Aaron Smith, Nicola Lindsay, Francis D. Gibbons, Katarzyna Falenta, Sigourney Bell, Paul Farrington, Lyndsey Hanson, Pei Zhang, Oona Delpuech, Linda C. Sandin, David Robinson, Emma J. Davies, and Vikki Flemington

Abstract

Supplementary Figure 1

Published
2023

28. Supplementary Table S4 from Isocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic Cholangiocarcinoma

Author

Nabeel Bardeesy, Cyril H. Benes, Kevan M. Shokat, J. Keith Joung, Andrew X. Zhu, Cristina R. Ferrone, Lipika Goyal, Yusuke Mizukami, Andrew S. Liss, Aram F. Hezel, Travis B. Sullivan, Kimberly M. Rieger-Christ, Roger L. Jenkins, Mathew J. Garnett, Ultan McDermott, Patricia Greninger, Regina K. Egan, Leah J. Damon, James T. Webber, Rebecca S. Levin, Yasutaka Kato, Lei Shi, Jia-Chi Yeo, Mortada S. Najem, Phuong Vu, Benjamin P. Kleinstiver, John D. Gordan, and Supriya K. Saha

Abstract

Peptide quantification from MIB column isolation of the active kinome in DMSO- versus dasatinib-treated HuCCT1, RBE, and SNU-1079 cells.

Published
2023

30. Supplementary Table S6 from Isocitrate Dehydrogenase Mutations Confer Dasatinib Hypersensitivity and SRC Dependence in Intrahepatic Cholangiocarcinoma

Author

Nabeel Bardeesy, Cyril H. Benes, Kevan M. Shokat, J. Keith Joung, Andrew X. Zhu, Cristina R. Ferrone, Lipika Goyal, Yusuke Mizukami, Andrew S. Liss, Aram F. Hezel, Travis B. Sullivan, Kimberly M. Rieger-Christ, Roger L. Jenkins, Mathew J. Garnett, Ultan McDermott, Patricia Greninger, Regina K. Egan, Leah J. Damon, James T. Webber, Rebecca S. Levin, Yasutaka Kato, Lei Shi, Jia-Chi Yeo, Mortada S. Najem, Phuong Vu, Benjamin P. Kleinstiver, John D. Gordan, and Supriya K. Saha

Abstract

Cas9 and sgRNA expression plasmids.

Published
2023

31. Supplementary Figure 5 from AZD0364 Is a Potent and Selective ERK1/2 Inhibitor That Enhances Antitumor Activity in KRAS-Mutant Tumor Models when Combined with the MEK Inhibitor, Selumetinib

Author

Paul D. Smith, J. Elizabeth Pease, Sabina C. Cosulich, Iain Simpson, Richard A. Ward, Clifford D. Jones, Stephen E. Fawell, Mathew J. Garnett, Patricia Jaaks, Elizabeth A. Coker, Claire Rooney, Martine P. Roudier, Sophie E. Willis, Philip Hopcroft, Michael Tonge, Karen Roberts, Joanne Wilson, Aaron Smith, Nicola Lindsay, Francis D. Gibbons, Katarzyna Falenta, Sigourney Bell, Paul Farrington, Lyndsey Hanson, Pei Zhang, Oona Delpuech, Linda C. Sandin, David Robinson, Emma J. Davies, and Vikki Flemington

Abstract

Supplementary Figure 5

Published
2023

32. Supplementary Figure 1 from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

Author

Mathew J. Garnett, Alberto Bardelli, Emile E. Voest, Sabrina Arena, Salvatore Siena, Andrea Sartore-Bianchi, Federica Di Nicolantonio, Fengtang Yang, Martin Michaelis, Jindrich Cinatl, Krijn K. Dijkstra, Daniele Oddo, Luuk J. Schipper, Ruby Banerjee, Carlotta Cancelliere, Iñigo Sánchez Rodríguez, Sara F. Vieira, Sarah Consonni, Giuseppe Rospo, Giovanni Crisafulli, Esmée J. van Vliet, Chiara M. Cattaneo, and Gabriele Picco

Abstract

Supplementary Figure 1

Published
2023

33. Supplementary Figures 1 -11 from Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition

Author

Kimberly Stegmaier, James E. Bradner, William A. Weiss, Andrew L. Kung, Cyril H. Benes, Ultan McDermott, Matthew J. Garnett, Patricia Greninger, William Clay Gustafson, Rhamy Zeid, Erin A. Nekritz, Yvan H. Chanthery, Jun Qi, Christopher F. Bassil, Gabriela Alexe, Stacey M. Frumm, and Alexandre Puissant

Abstract

PDF file - 326K, This file contains 11 supplementary figures with biochemistry, computational analysis, in vitro and in vivo studies to support the role of targeting MYCN in neuroblastoma with BETi.

Published
2023

34. Supplementary Table 3 from AZD0364 Is a Potent and Selective ERK1/2 Inhibitor That Enhances Antitumor Activity in KRAS-Mutant Tumor Models when Combined with the MEK Inhibitor, Selumetinib

Author

Paul D. Smith, J. Elizabeth Pease, Sabina C. Cosulich, Iain Simpson, Richard A. Ward, Clifford D. Jones, Stephen E. Fawell, Mathew J. Garnett, Patricia Jaaks, Elizabeth A. Coker, Claire Rooney, Martine P. Roudier, Sophie E. Willis, Philip Hopcroft, Michael Tonge, Karen Roberts, Joanne Wilson, Aaron Smith, Nicola Lindsay, Francis D. Gibbons, Katarzyna Falenta, Sigourney Bell, Paul Farrington, Lyndsey Hanson, Pei Zhang, Oona Delpuech, Linda C. Sandin, David Robinson, Emma J. Davies, and Vikki Flemington

Abstract

Cell lines defined as sensitive to AZD0364 from 747 cell panel screen

Published
2023

35. Supplementary Table 2 from AZD0364 Is a Potent and Selective ERK1/2 Inhibitor That Enhances Antitumor Activity in KRAS-Mutant Tumor Models when Combined with the MEK Inhibitor, Selumetinib

Author

Paul D. Smith, J. Elizabeth Pease, Sabina C. Cosulich, Iain Simpson, Richard A. Ward, Clifford D. Jones, Stephen E. Fawell, Mathew J. Garnett, Patricia Jaaks, Elizabeth A. Coker, Claire Rooney, Martine P. Roudier, Sophie E. Willis, Philip Hopcroft, Michael Tonge, Karen Roberts, Joanne Wilson, Aaron Smith, Nicola Lindsay, Francis D. Gibbons, Katarzyna Falenta, Sigourney Bell, Paul Farrington, Lyndsey Hanson, Pei Zhang, Oona Delpuech, Linda C. Sandin, David Robinson, Emma J. Davies, and Vikki Flemington

Abstract

Response of 747 cell lines to treatment with AZD0364 for 72 hours.

Published
2023

37. Supplementary Figure Legends from AZD0364 Is a Potent and Selective ERK1/2 Inhibitor That Enhances Antitumor Activity in KRAS-Mutant Tumor Models when Combined with the MEK Inhibitor, Selumetinib

Author

Paul D. Smith, J. Elizabeth Pease, Sabina C. Cosulich, Iain Simpson, Richard A. Ward, Clifford D. Jones, Stephen E. Fawell, Mathew J. Garnett, Patricia Jaaks, Elizabeth A. Coker, Claire Rooney, Martine P. Roudier, Sophie E. Willis, Philip Hopcroft, Michael Tonge, Karen Roberts, Joanne Wilson, Aaron Smith, Nicola Lindsay, Francis D. Gibbons, Katarzyna Falenta, Sigourney Bell, Paul Farrington, Lyndsey Hanson, Pei Zhang, Oona Delpuech, Linda C. Sandin, David Robinson, Emma J. Davies, and Vikki Flemington

Abstract

Supplementary Figure Legends

Published
2023

39. Supplementary Data from MTH1 Inhibitor TH1579 Induces Oxidative DNA Damage and Mitotic Arrest in Acute Myeloid Leukemia

Author

Ulrika Warpman Berglund, Thomas Helleday, Julian Walfridsson, Päivi Östling, Mathew J. Garnett, Kim Theilgaard-Mönch, Sören Lehmann, Teresa Sandvall, Olov Wallner, Martin Henriksson, Tobias Koolmeister, Martin Scobie, Torkild Visnes, Nona Struyf, Thea Kristin Våtsveen, Montserrat Estruch, Anders Centio, Stefanie Friedrich, Azita Rasti, Camilla Göktürk, Elisee Wiita, Helge Gad, Akhilesh Nagesh Danda, Brinton Seashore-Ludlow, Yaser Heshmati, Andreas Höglund, Ingrid Almlöf, Viktoriia Tsuber, Tom Erkers, Therese M. Pham, José Manuel Calderón-Montaño, and Kumar Sanjiv

Abstract

Supplementary figures and tables and material and methods

Published
2023

40. Data from MTH1 Inhibitor TH1579 Induces Oxidative DNA Damage and Mitotic Arrest in Acute Myeloid Leukemia

Author

Ulrika Warpman Berglund, Thomas Helleday, Julian Walfridsson, Päivi Östling, Mathew J. Garnett, Kim Theilgaard-Mönch, Sören Lehmann, Teresa Sandvall, Olov Wallner, Martin Henriksson, Tobias Koolmeister, Martin Scobie, Torkild Visnes, Nona Struyf, Thea Kristin Våtsveen, Montserrat Estruch, Anders Centio, Stefanie Friedrich, Azita Rasti, Camilla Göktürk, Elisee Wiita, Helge Gad, Akhilesh Nagesh Danda, Brinton Seashore-Ludlow, Yaser Heshmati, Andreas Höglund, Ingrid Almlöf, Viktoriia Tsuber, Tom Erkers, Therese M. Pham, José Manuel Calderón-Montaño, and Kumar Sanjiv

Abstract

Acute myeloid leukemia (AML) is an aggressive hematologic malignancy, exhibiting high levels of reactive oxygen species (ROS). ROS levels have been suggested to drive leukemogenesis and is thus a potential novel target for treating AML. MTH1 prevents incorporation of oxidized nucleotides into the DNA to maintain genome integrity and is upregulated in many cancers. Here we demonstrate that hematologic cancers are highly sensitive to MTH1 inhibitor TH1579 (karonudib). A functional precision medicine ex vivo screen in primary AML bone marrow samples demonstrated a broad response profile of TH1579, independent of the genomic alteration of AML, resembling the response profile of the standard-of-care treatments cytarabine and doxorubicin. Furthermore, TH1579 killed primary human AML blast cells (CD45+) as well as chemotherapy resistance leukemic stem cells (CD45+Lin−CD34+CD38−), which are often responsible for AML progression. TH1579 killed AML cells by causing mitotic arrest, elevating intracellular ROS levels, and enhancing oxidative DNA damage. TH1579 showed a significant therapeutic window, was well tolerated in animals, and could be combined with standard-of-care treatments to further improve efficacy. TH1579 significantly improved survival in two different AML disease models in vivo. In conclusion, the preclinical data presented here support that TH1579 is a promising novel anticancer agent for AML, providing a rationale to investigate the clinical usefulness of TH1579 in AML in an ongoing clinical phase I trial.Significance:The MTH1 inhibitor TH1579 is a potential novel AML treatment, targeting both blasts and the pivotal leukemic stem cells while sparing normal bone marrow cells.

Published
2023

41. Can Drug Repurposing Accelerate Precision Oncology?

Author

Luuk J. Schipper, Laurien J. Zeverijn, Mathew J. Garnett, and Emile E. Voest

Subjects
Oncology, Neoplasms, Drug Repositioning, Humans, Antineoplastic Agents, Precision Medicine, Medical Oncology
Abstract

Ongoing new insights in the field of cancer diagnostics, genomic profiling, and cancer behavior have raised the demand for novel, personalized cancer treatments. As the development of new cancer drugs is a challenging, costly, and time-consuming endeavor, drug repurposing is regarded as an attractive alternative to potentially accelerate this. In this review, we describe strategies for drug repurposing of anticancer agents, translation of preclinical findings in novel trial designs, and associated challenges. Furthermore, we provide suggestions to further utilize the potential of drug repurposing within precision oncology, with a focus on combinatorial approaches. Significance: Oncologic drug development is a timely and costly endeavor, with only few compounds progressing to meaningful therapy options. Although repurposing of existing agents for novel, oncologic indications provides an opportunity to accelerate this process, it is not without challenges.

Published
2022

42. Figure S6 from AZD4320, A Dual Inhibitor of Bcl-2 and Bcl-xL, Induces Tumor Regression in Hematologic Cancer Models without Dose-limiting Thrombocytopenia

Author

Francis D. Gibbons, Stephen E. Fawell, Barry R. Davies, J. Paul Secrist, Michael Zinda, Martin Wild, Eric Gangl, Ricky W. Johnstone, Andrea Newbold, Gareth P. Gregory, Elizabeth A. Coker, Patricia Jaaks, Mathew J. Garnett, Alwin Schuller, Nancy Su, Omid Tavana, Areya Tabatabai, Jamal C. Saeh, William McCoull, Edward J. Hennessy, Stephanos Ioannidis, Thomas Gero, R. Bruce Diebold, Jeffrey Varnes, Shannon K. McWeeney, Stephen E. Kurtz, Jeffrey W. Tyner, Tristan Lubinski, Kathleen Burke, Deborah Lawson, Shenghua Wen, Terry Macintyre, Paula Lewis, Ammar Adam, Justin Cidado, Kate F. Byth, Steven W. Criscione, and Srividya B. Balachander

Abstract

Figure S6

Published
2023

43. Supplementary Data_Clean from AZD4320, A Dual Inhibitor of Bcl-2 and Bcl-xL, Induces Tumor Regression in Hematologic Cancer Models without Dose-limiting Thrombocytopenia

Author

Francis D. Gibbons, Stephen E. Fawell, Barry R. Davies, J. Paul Secrist, Michael Zinda, Martin Wild, Eric Gangl, Ricky W. Johnstone, Andrea Newbold, Gareth P. Gregory, Elizabeth A. Coker, Patricia Jaaks, Mathew J. Garnett, Alwin Schuller, Nancy Su, Omid Tavana, Areya Tabatabai, Jamal C. Saeh, William McCoull, Edward J. Hennessy, Stephanos Ioannidis, Thomas Gero, R. Bruce Diebold, Jeffrey Varnes, Shannon K. McWeeney, Stephen E. Kurtz, Jeffrey W. Tyner, Tristan Lubinski, Kathleen Burke, Deborah Lawson, Shenghua Wen, Terry Macintyre, Paula Lewis, Ammar Adam, Justin Cidado, Kate F. Byth, Steven W. Criscione, and Srividya B. Balachander

Abstract

contains methods.

Published
2023

45. Supplemental Figures and Tables from Discovery of Potent and Selective MRCK Inhibitors with Therapeutic Effect on Skin Cancer

Author

Michael F. Olson, Mairi Sime, Alexander W. Schüttelkopf, Nicola Rath, Gregory Naylor, June Munro, Nicolas A. Morrice, Mokdad Mezna, Carol McMenemy, Heather McKinnon, Lynn McGarry, Laura McDonald, Patricia McConnell, Duncan McArthur, Sergio Lilla, Jennifer Konczal, James A.M. Hall, David A. Greenhalgh, Christopher Gray, Kathryn Gill, Mathew J. Garnett, Martin J. Drysdale, Daniel R. Croft, Diane Crighton, Jacqueline Cordes, Maeve Clarke, Justin Bower, Simone Belshaw, and Mathieu Unbekandt

Abstract

Supplemental Figure 1. Kinome selectivity profiles for BDP8900 and BDP9066. Supplemental Figure 2. Cancer cell line sensitivity to BDP8900 and BDP9066. Supplemental Figure 3. MRCKα phosphorylations compared with MRCKβ. Supplemental Figure 4. MRCKα, MRCKβ and MRCKα pS1003 antibody validation. Supplemental Figure 5. MRCK and DMPK expression in MDA MB 231 D3H2 LN human breast cancer cells, SCC12 human squamous cell carcinoma cells, and human skeletal muscle. Supplemental Table 1. Crystallographic data and model statistics. Supplemental Table 2: BDP8900 and BDP9066 selectivity in vitro (in-house determinations). Supplemental Table 3. Kinase selectivity screen for BDP8900 and BDP9066. Supplemental Table 4. BDP8900 selectivity in vitro (out-sourced determinations). Supplemental Table 5. BDP9066 selectivity in vitro (out-sourced determinations). Supplemental Table 6. Cancer cell line EC50 values for BDP8900 and BDP9066. Supplemental Table 7. MRCKα phosphorylation sites. Supplemental Table 8. MRCKα phosphorylation on S1003.

Published
2023

46. Data from NOTCH1 Represses MCL-1 Levels in GSI-resistant T-ALL, Making them Susceptible to ABT-263

Author

Cyril H. Benes, Anthony C. Faber, Michelle Kelliher, Jeffrey A. Engelman, Kathryn Rizzo, Steven Grant, Jorge Almenara, Mathew J. Garnett, Ultan McDermott, Jessica Boisvert, Neha U. Patel, Justine Roderick, Max Greenberg, Joseph McClanaghan, August Williams, Xunqin Yin, Carlotta Costa, AHyun Choi, and Anahita Dastur

Abstract

Purpose:Effective targeted therapies are lacking for refractory and relapsed T-cell acute lymphoblastic leukemia (T-ALL). Suppression of the NOTCH pathway using gamma-secretase inhibitors (GSI) is toxic and clinically not effective. The goal of this study was to identify alternative therapeutic strategies for T-ALL.Experimental Design:We performed a comprehensive analysis of our high-throughput drug screen across hundreds of human cell lines including 15 T-ALL models. We validated and further studied the top hit, navitoclax (ABT-263). We used multiple human T-ALL cell lines as well as primary patient samples, and performed both in vitro experiments and in vivo studies on patient-derived xenograft models.Results:We found that T-ALL are hypersensitive to navitoclax, an inhibitor of BCL2 family of antiapoptotic proteins. Importantly, GSI-resistant T-ALL are also susceptible to navitoclax. Sensitivity to navitoclax is due to low levels of MCL-1 in T-ALL. We identify an unsuspected regulation of mTORC1 by the NOTCH pathway, resulting in increased MCL-1 upon GSI treatment. Finally, we show that pharmacologic inhibition of mTORC1 lowers MCL-1 levels and further sensitizes cells to navitoclax in vitro and leads to tumor regressions in vivo.Conclusions:Our results support the development of navitoclax, as single agent and in combination with mTOR inhibitors, as a new therapeutic strategy for T-ALL, including in the setting of GSI resistance.

Published
2023

47. Supplementary Data from Patient-Derived Xenografts and Matched Cell Lines Identify Pharmacogenomic Vulnerabilities in Colorectal Cancer

Author

Sabrina Arena, Alberto Bardelli, Michael Linnebacher, Federica Di Nicolantonio, Livio Trusolino, Andrea Bertotti, Mathew J. Garnett, Salvatore Siena, Andrea Sartore-Bianchi, Enzo Medico, Carlotta Cancelliere, Andrea Cassingena, Fabiane Barbosa, Luca Novara, Eugenia R. Zanella, Erika Durinikova, Pamela Arcella, Monica Montone, Claudio Isella, Gabriele Picco, Giorgio Corti, and Luca Lazzari

Abstract

Supplementary Legends and Figures

Published
2023

48. Supplementary Table S1 from Patient-Derived Xenografts and Matched Cell Lines Identify Pharmacogenomic Vulnerabilities in Colorectal Cancer

Author

Sabrina Arena, Alberto Bardelli, Michael Linnebacher, Federica Di Nicolantonio, Livio Trusolino, Andrea Bertotti, Mathew J. Garnett, Salvatore Siena, Andrea Sartore-Bianchi, Enzo Medico, Carlotta Cancelliere, Andrea Cassingena, Fabiane Barbosa, Luca Novara, Eugenia R. Zanella, Erika Durinikova, Pamela Arcella, Monica Montone, Claudio Isella, Gabriele Picco, Giorgio Corti, and Luca Lazzari

Abstract

Supplementary Table S1

Published
2023

49. Figure S10 from AZD4320, A Dual Inhibitor of Bcl-2 and Bcl-xL, Induces Tumor Regression in Hematologic Cancer Models without Dose-limiting Thrombocytopenia

Author

Francis D. Gibbons, Stephen E. Fawell, Barry R. Davies, J. Paul Secrist, Michael Zinda, Martin Wild, Eric Gangl, Ricky W. Johnstone, Andrea Newbold, Gareth P. Gregory, Elizabeth A. Coker, Patricia Jaaks, Mathew J. Garnett, Alwin Schuller, Nancy Su, Omid Tavana, Areya Tabatabai, Jamal C. Saeh, William McCoull, Edward J. Hennessy, Stephanos Ioannidis, Thomas Gero, R. Bruce Diebold, Jeffrey Varnes, Shannon K. McWeeney, Stephen E. Kurtz, Jeffrey W. Tyner, Tristan Lubinski, Kathleen Burke, Deborah Lawson, Shenghua Wen, Terry Macintyre, Paula Lewis, Ammar Adam, Justin Cidado, Kate F. Byth, Steven W. Criscione, and Srividya B. Balachander

Abstract

Figure S10

Published
2023

50. Supplementary Table S3 from Patient-Derived Xenografts and Matched Cell Lines Identify Pharmacogenomic Vulnerabilities in Colorectal Cancer

Author

Sabrina Arena, Alberto Bardelli, Michael Linnebacher, Federica Di Nicolantonio, Livio Trusolino, Andrea Bertotti, Mathew J. Garnett, Salvatore Siena, Andrea Sartore-Bianchi, Enzo Medico, Carlotta Cancelliere, Andrea Cassingena, Fabiane Barbosa, Luca Novara, Eugenia R. Zanella, Erika Durinikova, Pamela Arcella, Monica Montone, Claudio Isella, Gabriele Picco, Giorgio Corti, and Luca Lazzari

Abstract

Supplementary Table S3

Published
2023

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