bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Figure S7 from Mesothelin CAR T Cells Secreting Anti-FAP/Anti-CD3 Molecules Efficiently Target Pancreatic Adenocarcinoma and its Stroma
Authors: Wehrli Marc , Guinn Samantha , Birocchi Filippo , Kuo Adam , Sun Yi , Larson Rebecca C. , Almazan Antonio J. , Scarfò Irene , Bouffard Amanda A. , Bailey Stefanie R. , Anekal Praju Vikas , Montero Llopis Paula , Nieman Linda T. , Song Yuhui , Xu Katherine H. , Berger Trisha R. , Kann Michael C. , Leick Mark B. , Silva Harrison , Salas-Benito Diego , Kienka Tamina , Grauwet Korneel , Armstrong Todd D. , Zhang Rui , Zhu Qingfeng , Fu Juan , Schmidts Andrea , Korell Felix , Jan Max , Choi Bryan D. , Liss Andrew S. , Boland Genevieve M. , Ting David T. , Burkhart Richard A. , Jenkins Russell W. , Zheng Lei , Jaffee Elizabeth M. , Zimmerman Jacquelyn W. , Maus Marcela V.
Published: May 2024

Supplementary Figure S7. Superior anti-tumor effect of meso^FAP compared to the combination of meso-CAR and FAP-CAR or meso^CD19.
Supplementary Figure S5 from Mesothelin CAR T Cells Secreting Anti-FAP/Anti-CD3 Molecules Efficiently Target Pancreatic Adenocarcinoma and its Stroma
Authors: Wehrli Marc , Guinn Samantha , Birocchi Filippo , Kuo Adam , Sun Yi , Larson Rebecca C. , Almazan Antonio J. , Scarfò Irene , Bouffard Amanda A. , Bailey Stefanie R. , Anekal Praju Vikas , Montero Llopis Paula , Nieman Linda T. , Song Yuhui , Xu Katherine H. , Berger Trisha R. , Kann Michael C. , Leick Mark B. , Silva Harrison , Salas-Benito Diego , Kienka Tamina , Grauwet Korneel , Armstrong Todd D. , Zhang Rui , Zhu Qingfeng , Fu Juan , Schmidts Andrea , Korell Felix , Jan Max , Choi Bryan D. , Liss Andrew S. , Boland Genevieve M. , Ting David T. , Burkhart Richard A. , Jenkins Russell W. , Zheng Lei , Jaffee Elizabeth M. , Zimmerman Jacquelyn W. , Maus Marcela V.
Published: May 2024

Supplementary Figure S5. Intratumoral multiplex RNA-ISH IF imaging and analysis of CAR-TEAM treated mice.
Supplementary Figure S2 from Mesothelin CAR T Cells Secreting Anti-FAP/Anti-CD3 Molecules Efficiently Target Pancreatic Adenocarcinoma and its Stroma
Authors: Wehrli Marc , Guinn Samantha , Birocchi Filippo , Kuo Adam , Sun Yi , Larson Rebecca C. , Almazan Antonio J. , Scarfò Irene , Bouffard Amanda A. , Bailey Stefanie R. , Anekal Praju Vikas , Montero Llopis Paula , Nieman Linda T. , Song Yuhui , Xu Katherine H. , Berger Trisha R. , Kann Michael C. , Leick Mark B. , Silva Harrison , Salas-Benito Diego , Kienka Tamina , Grauwet Korneel , Armstrong Todd D. , Zhang Rui , Zhu Qingfeng , Fu Juan , Schmidts Andrea , Korell Felix , Jan Max , Choi Bryan D. , Liss Andrew S. , Boland Genevieve M. , Ting David T. , Burkhart Richard A. , Jenkins Russell W. , Zheng Lei , Jaffee Elizabeth M. , Zimmerman Jacquelyn W. , Maus Marcela V.
Published: May 2024

Supplementary Figure S2. In vitro setup of CARTEAM to CAF:AsPC-1 with different ratios showing superiority of mesoFAP compared to CARs targeting mesothelin only.
Data from Molecular and Pathologic Characterization of YAP1-Expressing Small Cell Lung Cancer Cell Lines Leads to Reclassification as SMARCA4-Deficient Malignancies
Authors: Ng Jin , Cai Ling , Girard Luc , Prall Owen W.J. , Rajan Neeha , Khoo Christine , Batrouney Ahida , Byrne David J. , Boyd Danielle K. , Kersbergen Ariena J. , Christie Michael , Minna John D. , Burr Marian L. , Sutherland Kate D.
Published: May 2024

AbstractPurpose:
The classification of small cell lung cancer (SCLC) into distinct molecular subtypes defined by ASCL1, NEUROD1, POU2F3, or YAP1 (SCLC-A, -N, -P, or -Y) expression, paves the way for a personalized treatment approach. However, the existence of a distinct YAP1-expressing SCLC subtype remains controversial.
Experimental Design:
To better understand YAP1-expressing SCLC, the mutational landscape of human SCLC cell lines was interrogated to identify pathogenic alterations unique to SCLC-Y. Xenograft tumors, generated from cell lines representing the four SCLC molecular subtypes, were evaluated by a panel of pathologists who routinely diagnose thoracic malignancies. Diagnoses were complemented by transcriptomic analysis of primary tumors and human cell line datasets. Protein expression profiles were validated in patient tumor tissue.
Results:
Unexpectedly, pathogenic mutations in SMARCA4 were identified in six of eight SCLC-Y cell lines and correlated with reduced SMARCA4 mRNA and protein expression. Pathologist evaluations revealed that SMARCA4-deficient SCLC-Y tumors exhibited features consistent with thoracic SMARCA4-deficient undifferentiated tumors (SMARCA4-UT). Similarly, the transcriptional profile SMARCA4-mutant SCLC-Y lines more closely resembled primary SMARCA4-UT, or SMARCA4-deficient non–small cell carcinoma, than SCLC. Furthermore, SMARCA4-UT patient samples were associated with a YAP1 transcriptional signature and exhibited strong YAP1 protein expression. Together, we found little evidence to support a diagnosis of SCLC for any of the YAP1-expressing cell lines originally used to define the SCLC-Y subtype.
Conclusions:
SMARCA4-mutant SCLC-Y cell lines exhibit characteristics consistent with SMARCA4-deficient malignancies rather than SCLC. Our findings suggest that, unlike ASCL1, NEUROD1, and POU2F3, YAP1 is not a subtype defining transcription factor in SCLC.

See related commentary by Rekhtman, p. 1708
Data from Platinum-Based Chemotherapy Attenuates the Effector Response of CD8 T Cells to Concomitant PD-1 Blockade
Authors: Mariniello Annapaola , Nasti Tahseen H. , Chang Daniel Y. , Hashimoto Masao , Malik Sakshi , McManus Daniel T. , Lee Judong , McGuire Donald J. , Cardenas Maria A. , Umana Pablo , Nicolini Valeria , Antia Rustom , Saha Ananya , Buchwald Zachary , Kissick Hayden , Ghorani Ehsan , Novello Silvia , Sangiolo Dario , Scagliotti Giorgio V. , Ramalingam Suresh S. , Ahmed Rafi
Published: May 2024

AbstractPurpose:
Combination of chemotherapy with programmed cell death 1 (PD-1) blockade is a front-line treatment for lung cancer. However, it remains unknown whether and how chemotherapy affects the response of exhausted CD8 T cells to PD-1 blockade.
Experimental Design:
We used the well-established mouse model of T-cell exhaustion with chronic lymphocytic choriomeningitis virus (LCMV) infection to assess the effect of chemotherapy (cisplatin+pemetrexed) on T-cell response to PD-1 blockade, in the absence of the impact of chemotherapy on antigen release and presentation observed in tumor models.
Results:
When concomitantly administered with PD-1 blockade, chemotherapy affected the differentiation path of LCMV-specific CD8 T cells from stem-like to transitory effector cells, thereby reducing their expansion and production of IFNγ. After combination treatment, these restrained effector responses resulted in impaired viral control, compared with PD-1 blockade alone. The sequential combination strategy, where PD-1 blockade followed chemotherapy, proved to be superior to the concomitant combination, preserving the proliferative response of exhausted CD8 T cells to PD-1 blockade. Our findings suggest that the stem-like CD8 T cells themselves are relatively unaffected by chemotherapy partly because they are quiescent and maintained by slow self-renewal at the steady state. However, upon the proliferative burst mediated by PD-1 blockade, the accelerated differentiation and self-renewal of stem-like cells may be curbed by concomitant chemotherapy, ultimately resulting in impaired overall CD8 T-cell effector functions.
Conclusions:
In a translational context, we provide a proof-of-concept to consider optimizing the timing of chemo-immunotherapy strategies for improved CD8 T-cell functions.

See related commentary by Vignali and Luke, p. 1705
Data from Broad Next-Generation Integrated Sequencing of Myelofibrosis Identifies Disease-Specific and Age-Related Genomic Alterations
Authors: Kandarpa Malathi , Robinson Dan , Wu Yi-Mi , Qin Tingting , Pettit Kristen , Li Qing , Luker Gary , Sartor Maureen , Chinnaiyan Arul , Talpaz Moshe
Published: May 2024

AbstractPurpose:
Myeloproliferative neoplasms (MPN) are characterized by the overproduction of differentiated myeloid cells. Mutations in JAK2, CALR, and MPL are considered drivers of Bcr-Abl−ve MPN, including essential thrombocythemia (ET), polycythemia vera (PV), prefibrotic primary myelofibrosis (prePMF), and overt myelofibrosis (MF). However, how these driver mutations lead to phenotypically distinct and/or overlapping diseases is unclear.
Experimental Design:
To compare the genetic landscape of MF to ET/PV/PrePMF, we sequenced 1,711 genes for mutations along with whole transcriptome RNA sequencing of 137 patients with MPN.
Results:
In addition to driver mutations, 234 and 74 genes were found to be mutated in overt MF (N = 106) and ET/PV/PrePMF (N = 31), respectively. Overt MF had more mutations compared with ET/PV/prePMF (5 vs. 4 per subject, P = 0.006). Genes frequently mutated in MF included high-risk genes (ASXL1, SRSF2, EZH2, IDH1/2, and U2AF1) and Ras pathway genes. Mutations in NRAS, KRAS, SRSF2, EZH2, IDH2, and NF1 were exclusive to MF. Advancing age, higher DIPSS, and poor overall survival (OS) correlated with increased variants in MF. Ras mutations were associated with higher leukocytes and platelets and poor OS. The comparison of gene expression showed upregulation of proliferation and inflammatory pathways in MF. Notably, ADGRL4, DNASE1L3, PLEKHGB4, HSPG2, MAMDC2, and DPYSL3 were differentially expressed in hematopoietic stem and differentiated cells.
Conclusions:
Our results illustrate that evolution of MF from ET/PV/PrePMF likely advances with age, accumulation of mutations, and activation of proliferative pathways. The genes and pathways identified by integrated genomics approach provide insight into disease transformation and progression and potential targets for therapeutic intervention.
Data from Mesothelin CAR T Cells Secreting Anti-FAP/Anti-CD3 Molecules Efficiently Target Pancreatic Adenocarcinoma and its Stroma
Authors: Wehrli Marc , Guinn Samantha , Birocchi Filippo , Kuo Adam , Sun Yi , Larson Rebecca C. , Almazan Antonio J. , Scarfò Irene , Bouffard Amanda A. , Bailey Stefanie R. , Anekal Praju Vikas , Montero Llopis Paula , Nieman Linda T. , Song Yuhui , Xu Katherine H. , Berger Trisha R. , Kann Michael C. , Leick Mark B. , Silva Harrison , Salas-Benito Diego , Kienka Tamina , Grauwet Korneel , Armstrong Todd D. , Zhang Rui , Zhu Qingfeng , Fu Juan , Schmidts Andrea , Korell Felix , Jan Max , Choi Bryan D. , Liss Andrew S. , Boland Genevieve M. , Ting David T. , Burkhart Richard A. , Jenkins Russell W. , Zheng Lei , Jaffee Elizabeth M. , Zimmerman Jacquelyn W. , Maus Marcela V.
Published: May 2024

AbstractPurpose:
Targeting solid tumors with chimeric antigen receptor (CAR) T cells remains challenging due to heterogenous target antigen expression, antigen escape, and the immunosuppressive tumor microenvironment (TME). Pancreatic cancer is characterized by a thick stroma generated by cancer-associated fibroblasts (CAF), which may contribute to the limited efficacy of mesothelin-directed CAR T cells in early-phase clinical trials. To provide a more favorable TME for CAR T cells to target pancreatic ductal adenocarcinoma (PDAC), we generated T cells with an antimesothelin CAR and a secreted T-cell–engaging molecule (TEAM) that targets CAF through fibroblast activation protein (FAP) and engages T cells through CD3 (termed mesoFAP CAR-TEAM cells).
Experimental Design:
Using a suite of in vitro, in vivo, and ex vivo patient-derived models containing cancer cells and CAF, we examined the ability of mesoFAP CAR-TEAM cells to target PDAC cells and CAF within the TME. We developed and used patient-derived ex vivo models, including patient-derived organoids with patient-matched CAF and patient-derived organotypic tumor spheroids.
Results:
We demonstrated specific and significant binding of the TEAM to its respective antigens (CD3 and FAP) when released from mesothelin-targeting CAR T cells, leading to T-cell activation and cytotoxicity of the target cell. MesoFAP CAR-TEAM cells were superior in eliminating PDAC and CAF compared with T cells engineered to target either antigen alone in our ex vivo patient-derived models and in mouse models of PDAC with primary or metastatic liver tumors.
Conclusions:
CAR-TEAM cells enable modification of tumor stroma, leading to increased elimination of PDAC tumors. This approach represents a promising treatment option for pancreatic cancer.
Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor
Authors: Moure Casey J. , Vara Brandon , Cheng Mangeng M. , Sondey Christopher , Muise Eric , Park Eunsil , Vela Ramirez Julia Eulalia , Su Dan , D’Souza Shanti , Yan Qingyun , Yeung Charles S. , Zhang Minjia , Mansueto My Sam , Linn Doug , Buchanan Mark , Foti Robert , DiMauro Erin , Long Brian , Simov Vladimir , Barry Evan R.
Published: May 2024

Many tumor types harbor alterations in the Hippo pathway, including mesothelioma, where a high percentage of cases are considered YAP1/TEAD dependent. Identification of autopalmitoylation sites in the hydrophobic palmitate pocket of TEADs, which may be necessary for YAP1 protein interactions, has enabled modern drug discovery platforms to generate compounds that allosterically inhibit YAP1/TEAD complex formation and transcriptional activity. We report the discovery and characterization of a novel YAP1/TEAD inhibitor MRK-A from an aryl ether chemical series demonstrating potent and specific inhibition of YAP1/TEAD activity. In vivo, MRK-A showed a favorable tolerability profile in mice and demonstrated pharmacokinetics suitable for twice daily oral dosing in preclinical efficacy studies. Importantly, monotherapeutic targeting of YAP1/TEAD in preclinical models generated regressions in a mesothelioma CDX model; however, rapid resistance to therapy was observed. RNA-sequencing of resistant tumors revealed mRNA expression changes correlated with the resistance state and a marked increase of hepatocyte growth factor (HGF) expression. In vitro, exogenous HGF was able to fully rescue cytostasis induced by MRK-A in mesothelioma cell lines. In addition, co-administration of small molecule inhibitors of the MET receptor tyrosine kinase suppressed the resistance generating effect of HGF on MRK-A induced growth inhibition. In this work, we report the structure and characterization of MRK-A, demonstrating potent and specific inhibition of YAP1/TAZ-TEAD–mediated transcriptional responses, with potential implications for treating malignancies driven by altered Hippo signaling, including factors resulting in acquired drug resistance.
Exploiting Metabolic Defects in Glioma with Nanoparticle-Encapsulated NAMPT Inhibitors
Authors: Murray Matthew A. , Noronha Katelyn J. , Wang Yazhe , Friedman Anna P. , Paradkar Sateja , Suh Hee-Won , Sundaram Ranjini K. , Brenner Charles , Saltzman W.M. , Bindra Ranjit S.
Published: May 2024

The treatment of primary central nervous system tumors is challenging due to the blood–brain barrier and complex mutational profiles, which is associated with low survival rates. However, recent studies have identified common mutations in gliomas [isocitrate dehydrogenase (IDH)-wild-type and mutant, WHO grades II–IV; with grade IV tumors referred to as glioblastomas (GBM)]. These mutations drive epigenetic changes, leading to promoter methylation at the nicotinic acid phosphoribosyl transferase (NAPRT) gene locus, which encodes an enzyme involved in generating NAD+. Importantly, NAPRT silencing introduces a therapeutic vulnerability to inhibitors targeting another NAD+ biogenesis enzyme, nicotinamide phosphoribosyl transferase (NAMPT), rationalizing a treatment for these malignancies. Multiple systemically administered NAMPT inhibitors (NAMPTi) have been developed and tested in clinical trials, but dose-limiting toxicities—including bone marrow suppression and retinal toxicity—have limited their efficacy. Here, we report a novel approach for the treatment of NAPRT-silenced GBMs using nanoparticle (NP)-encapsulated NAMPTis administered by convection-enhanced delivery (CED). We demonstrate that GMX1778 (a NAMPTi) can be formulated in degradable polymer NPs with retention of potency for NAMPT inhibition and anticancer activity in vitro, plus sustained drug release in vitro and in vivo. Direct injection of these drugs via CED into the brain is associated with reduced retinal toxicity compared with systemic administration. Finally, we show that CED of NP-encapsulated GMX1778 to NAPRT-silenced intracranial GBM xenografts in mice exhibit significant tumor growth delay and extends survival. These data support an approach to treat gliomas harboring defects in NAD+ metabolism using CED of NP-encapsulated NAMPTis to greatly improve the therapeutic index and treatment efficacy for this class of drugs.
A Senescence-Mimicking (Senomimetic) VEGFR TKI Side Effect Primes Tumor Immune Responses via IFN/STING Signaling
Authors: Dolan Melissa , Shi Yuhao , Mastri Michalis , Long Mark D. , McKenery Amber , Hill James W. , Vaghi Cristina , Benzekry Sebastien , Barbi Joseph , Ebos John M.L.
Published: May 2024

Tyrosine kinase inhibitors (TKIs) that block the vascular endothelial growth factor receptors (VEGFRs) not only disrupt tumor angiogenesis but also have many unexpected side effects that impact tumor cells directly. This includes the induction of molecular markers associated with senescence, a form of cellular aging that typically involves growth arrest. We have shown that VEGFR TKIs can hijack these aging programs by transiently inducting senescence markers (SMs) in tumor cells to activate senescence-associated secretory programs that fuel drug resistance. Here we show that these same senescence-mimicking (“senomimetic”) VEGFR TKI effects drive an enhanced immunogenic signaling that, in turn, can alter tumor response to immunotherapy. By using a live cell sorting method to detect β-galactosidase, a commonly used SM, we found that subpopulations of SM-expressing (SM+) tumor cells have heightened IFN signaling and increased expression of IFN-stimulated genes (ISGs). These ISGs increase under the control of the STimulator of the INterferon Gene (STING) signaling pathway, which we found could be directly activated by several VEGFR TKIs. TKI-induced SM+ cells could stimulate or suppress CD8 T-cell activation depending on host–tumor cell contact while tumors grown from SM+ cells were more sensitive to PDL1 inhibition in vivo, suggesting that offsetting immune-suppressive functions of SM+ cells can improve TKI efficacy overall. Our findings may explain why some (but not all) VEGFR TKIs improve outcomes when combined with immunotherapy and suggest that exploiting senomimetic drug side effects may help identify TKIs that uniquely “prime” tumors for enhanced sensitivity to PDL1-targeted agents.
Pediatric Chordoma: A Tale of Two Genomes
Authors: O’Halloran Katrina , Hakimjavadi Hesamedin , Bootwalla Moiz , Ostrow Dejerianne , Kerawala Rhea , Cotter Jennifer A. , Yellapantula Venkata , Kaneva Kristiyana , Wadhwani Nitin R. , Treece Amy , Foreman Nicholas K. , Alexandrescu Sanda , Velazquez Vega Jose , Biegel Jaclyn A. , Gai Xiaowu
Published: May 2024

Little is known about the genomic alterations in chordoma, with the exception of loss of SMARCB1, a core member of the SWI/SNF complex, in poorly differentiated chordomas. A TBXT duplication and rs2305089 polymorphism, located at 6q27, are known genetic susceptibility loci. A comprehensive genomic analysis of the nuclear and mitochondrial genomes in pediatric chordoma has not yet been reported. In this study, we performed WES and mtDNA genome sequencing on 29 chordomas from 23 pediatric patients. Findings were compared with that from whole-genome sequencing datasets of 80 adult patients with skull base chordoma. In the pediatric chordoma cohort, 81% of the somatic mtDNA mutations were observed in NADH complex genes, which is significantly enriched compared with the rest of the mtDNA genes (P = 0.001). In adult chordomas, mtDNA mutations were also enriched in the NADH complex genes (P < 0.0001). Furthermore, a progressive increase in heteroplasmy of nonsynonymous mtDNA mutations was noted in patients with multiple tumors (P = 0.0007). In the nuclear genome, rare likely germline in-frame indels in ARID1B, a member of the SWI/SNF complex located at 6q25.3, were observed in five pediatric patients (22%) and four patients in the adult cohort (5%). The frequency of rare ARID1B indels in the pediatric cohort is significantly higher than that in the adult cohort (P = 0.0236, Fisher’s exact test), but they were both significantly higher than that in the ethnicity-matched populations (P < 5.9e−07 and P < 0.0001174, respectively).

Implications: germline ARID1B indels and mtDNA aberrations seem important for chordoma genesis, especially in pediatric chordoma.
Supplementary Table S3 from Jak2V617F Reversible Activation Shows Its Essential Requirement in Myeloproliferative Neoplasms
Authors: Dunbar Andrew J. , Bowman Robert L. , Park Young C. , O'Connor Kavi , Izzo Franco , Myers Robert M. , Karzai Abdul , Zaroogian Zachary , Kim Won Jun , Fernández-Maestre Inés , Waarts Michael R. , Nazir Abbas , Xiao Wenbin , Codilupi Tamara , Brodsky Max , Farina Mirko , Cai Louise , Cai Sheng F. , Wang Benjamin , An Wenbin , Yang Julie L. , Mowla Shoron , Eisman Shira E. , Hanasoge Somasundara Amritha Varshini , Glass Jacob L. , Mishra Tanmay , Houston Remie , Guzzardi Emily , Martinez Benitez Anthony R. , Viny Aaron D. , Koche Richard P. , Meyer Sara C. , Landau Dan A. , Levine Ross L.
Published: May 2024

RNA-Seq analysis - MPN vs. RUX
Supplementary Table S2 from Jak2V617F Reversible Activation Shows Its Essential Requirement in Myeloproliferative Neoplasms
Authors: Dunbar Andrew J. , Bowman Robert L. , Park Young C. , O'Connor Kavi , Izzo Franco , Myers Robert M. , Karzai Abdul , Zaroogian Zachary , Kim Won Jun , Fernández-Maestre Inés , Waarts Michael R. , Nazir Abbas , Xiao Wenbin , Codilupi Tamara , Brodsky Max , Farina Mirko , Cai Louise , Cai Sheng F. , Wang Benjamin , An Wenbin , Yang Julie L. , Mowla Shoron , Eisman Shira E. , Hanasoge Somasundara Amritha Varshini , Glass Jacob L. , Mishra Tanmay , Houston Remie , Guzzardi Emily , Martinez Benitez Anthony R. , Viny Aaron D. , Koche Richard P. , Meyer Sara C. , Landau Dan A. , Levine Ross L.
Published: May 2024

ATAC-Seq analysis - MPN vs. TAM
Supplementary Figure S8 from Jak2V617F Reversible Activation Shows Its Essential Requirement in Myeloproliferative Neoplasms
Authors: Dunbar Andrew J. , Bowman Robert L. , Park Young C. , O'Connor Kavi , Izzo Franco , Myers Robert M. , Karzai Abdul , Zaroogian Zachary , Kim Won Jun , Fernández-Maestre Inés , Waarts Michael R. , Nazir Abbas , Xiao Wenbin , Codilupi Tamara , Brodsky Max , Farina Mirko , Cai Louise , Cai Sheng F. , Wang Benjamin , An Wenbin , Yang Julie L. , Mowla Shoron , Eisman Shira E. , Hanasoge Somasundara Amritha Varshini , Glass Jacob L. , Mishra Tanmay , Houston Remie , Guzzardi Emily , Martinez Benitez Anthony R. , Viny Aaron D. , Koche Richard P. , Meyer Sara C. , Landau Dan A. , Levine Ross L.
Published: May 2024

Differential responses of Jak2V617F deletion compared to JAK inhibitor therapy in vivo
Table S8 from Early Immune Remodeling Steers Clinical Response to First-Line Chemoimmunotherapy in Advanced Gastric Cancer
Authors: An Minae , Mehta Arnav , Min Byung Hoon , Heo You Jeong , Wright Samuel J. , Parikh Milan , Bi Lynn , Lee Hyuk , Kim Tae Jun , Lee Song-Yi , Moon Jeonghyeon , Park Ryan J. , Strickland Matthew R. , Park Woong-Yang , Kang Won Ki , Kim Kyoung-Mee , Kim Seung Tae , Klempner Samuel J. , Lee Jeeyun
Published: May 2024

Representativeness of study participants
Table S6 from Early Immune Remodeling Steers Clinical Response to First-Line Chemoimmunotherapy in Advanced Gastric Cancer
Authors: An Minae , Mehta Arnav , Min Byung Hoon , Heo You Jeong , Wright Samuel J. , Parikh Milan , Bi Lynn , Lee Hyuk , Kim Tae Jun , Lee Song-Yi , Moon Jeonghyeon , Park Ryan J. , Strickland Matthew R. , Park Woong-Yang , Kang Won Ki , Kim Kyoung-Mee , Kim Seung Tae , Klempner Samuel J. , Lee Jeeyun
Published: May 2024

CellPhoneDB significant ligand-receptor interactions
Figure S5 from Early Immune Remodeling Steers Clinical Response to First-Line Chemoimmunotherapy in Advanced Gastric Cancer
Authors: An Minae , Mehta Arnav , Min Byung Hoon , Heo You Jeong , Wright Samuel J. , Parikh Milan , Bi Lynn , Lee Hyuk , Kim Tae Jun , Lee Song-Yi , Moon Jeonghyeon , Park Ryan J. , Strickland Matthew R. , Park Woong-Yang , Kang Won Ki , Kim Kyoung-Mee , Kim Seung Tae , Klempner Samuel J. , Lee Jeeyun
Published: May 2024

Figure S5. Proportion of cells expression each of the 16 markers used for multiplex
immunohistochemistry (mIHC) split by timepoint and fast vs slow progressor status.
Figure S25 from Early Immune Remodeling Steers Clinical Response to First-Line Chemoimmunotherapy in Advanced Gastric Cancer
Authors: An Minae , Mehta Arnav , Min Byung Hoon , Heo You Jeong , Wright Samuel J. , Parikh Milan , Bi Lynn , Lee Hyuk , Kim Tae Jun , Lee Song-Yi , Moon Jeonghyeon , Park Ryan J. , Strickland Matthew R. , Park Woong-Yang , Kang Won Ki , Kim Kyoung-Mee , Kim Seung Tae , Klempner Samuel J. , Lee Jeeyun
Published: May 2024

Figure S25. (A) UMAP embedding of single cell transcriptomes of all T cells
obtained from all samples in this trial. Labeled are granular T cell subsets
separated by tumor v.s. normal tissue, and by timepoint. (B) UMAP embeddings
showing marker gene expression for T cell subsets in (A).
Figure S24 from Early Immune Remodeling Steers Clinical Response to First-Line Chemoimmunotherapy in Advanced Gastric Cancer
Authors: An Minae , Mehta Arnav , Min Byung Hoon , Heo You Jeong , Wright Samuel J. , Parikh Milan , Bi Lynn , Lee Hyuk , Kim Tae Jun , Lee Song-Yi , Moon Jeonghyeon , Park Ryan J. , Strickland Matthew R. , Park Woong-Yang , Kang Won Ki , Kim Kyoung-Mee , Kim Seung Tae , Klempner Samuel J. , Lee Jeeyun
Published: May 2024

Figure S24. (A) Immune gene expression program signature scored from bulk
RNA-seq profiles across all samples separated by timepoint. (B) Immunogenic
cell death signatures scored from bulk RNA-seq profiles split by fast and slow
progressing patients and by timepoint.
Figure S22 from Early Immune Remodeling Steers Clinical Response to First-Line Chemoimmunotherapy in Advanced Gastric Cancer
Authors: An Minae , Mehta Arnav , Min Byung Hoon , Heo You Jeong , Wright Samuel J. , Parikh Milan , Bi Lynn , Lee Hyuk , Kim Tae Jun , Lee Song-Yi , Moon Jeonghyeon , Park Ryan J. , Strickland Matthew R. , Park Woong-Yang , Kang Won Ki , Kim Kyoung-Mee , Kim Seung Tae , Klempner Samuel J. , Lee Jeeyun
Published: May 2024

Figure S22. Phagocytosis, angiogenesis and PDGF pathway gene module scores
in different M2 macrophage subsets from scRNAseq data.
Supplementary figure S3 from TREX1 Inactivation Unleashes Cancer Cell STING–Interferon Signaling and Promotes Antitumor Immunity
Authors: Tani Tetsuo , Mathsyaraja Haritha , Campisi Marco , Li Ze-Hua , Haratani Koji , Fahey Caroline G. , Ota Keiichi , Mahadevan Navin R. , Shi Yingxiao , Saito Shin , Mizuno Kei , Thai Tran C. , Sasaki Nobunari , Homme Mizuki , Yusuf Choudhury Fabliha B. , Kashishian Adam , Panchal Jipsa , Wang Min , Wolf Benjamin J. , Barbie Thanh U. , Paweletz Cloud P. , Gokhale Prafulla C. , Liu David , Uppaluri Ravindra , Kitajima Shunsuke , Cain Jennifer , Barbie David A.
Published: May 2024

Supplementary figureS3 shows the figures related to Figure 3.
Supplementary figure S2 from TREX1 Inactivation Unleashes Cancer Cell STING–Interferon Signaling and Promotes Antitumor Immunity
Authors: Tani Tetsuo , Mathsyaraja Haritha , Campisi Marco , Li Ze-Hua , Haratani Koji , Fahey Caroline G. , Ota Keiichi , Mahadevan Navin R. , Shi Yingxiao , Saito Shin , Mizuno Kei , Thai Tran C. , Sasaki Nobunari , Homme Mizuki , Yusuf Choudhury Fabliha B. , Kashishian Adam , Panchal Jipsa , Wang Min , Wolf Benjamin J. , Barbie Thanh U. , Paweletz Cloud P. , Gokhale Prafulla C. , Liu David , Uppaluri Ravindra , Kitajima Shunsuke , Cain Jennifer , Barbie David A.
Published: May 2024

Supplementary figureS2 shows the figures related to Figure 2.
Supplementary Table S9 from Pan-Cancer Comparative and Integrative Analyses of Driver Alterations Using Japanese and International Genomic Databases
Authors: Horie Sara , Saito Yuki , Kogure Yasunori , Mizuno Kota , Ito Yuta , Tabata Mariko , Kanai Takanori , Murakami Koichi , Koya Junji , Kataoka Keisuke
Published: May 2024

GSEA analyses comparing samples with and without driver mutations in epigenetic regulators in 6 cancer types/subtypes
Supplementary Table S8 from Pan-Cancer Comparative and Integrative Analyses of Driver Alterations Using Japanese and International Genomic Databases
Authors: Horie Sara , Saito Yuki , Kogure Yasunori , Mizuno Kota , Ito Yuta , Tabata Mariko , Kanai Takanori , Murakami Koichi , Koya Junji , Kataoka Keisuke
Published: May 2024

Analysis of co-occurring and mutually exclusive relationships
Supplementary Table S5 from Pan-Cancer Comparative and Integrative Analyses of Driver Alterations Using Japanese and International Genomic Databases
Authors: Horie Sara , Saito Yuki , Kogure Yasunori , Mizuno Kota , Ito Yuta , Tabata Mariko , Kanai Takanori , Murakami Koichi , Koya Junji , Kataoka Keisuke
Published: May 2024

Details of driver CNAs in C-CAT
Supplementary Table S3 from Pan-Cancer Comparative and Integrative Analyses of Driver Alterations Using Japanese and International Genomic Databases
Authors: Horie Sara , Saito Yuki , Kogure Yasunori , Mizuno Kota , Ito Yuta , Tabata Mariko , Kanai Takanori , Murakami Koichi , Koya Junji , Kataoka Keisuke
Published: May 2024

Details of 69 driver genes
Supplementary Table S1 from Pan-Cancer Comparative and Integrative Analyses of Driver Alterations Using Japanese and International Genomic Databases
Authors: Horie Sara , Saito Yuki , Kogure Yasunori , Mizuno Kota , Ito Yuta , Tabata Mariko , Kanai Takanori , Murakami Koichi , Koya Junji , Kataoka Keisuke
Published: May 2024

Number of samples in 26 principal cancer types/subtypes
Supplementary Figures S1-S9 from Pan-Cancer Comparative and Integrative Analyses of Driver Alterations Using Japanese and International Genomic Databases
Authors: Horie Sara , Saito Yuki , Kogure Yasunori , Mizuno Kota , Ito Yuta , Tabata Mariko , Kanai Takanori , Murakami Koichi , Koya Junji , Kataoka Keisuke
Published: May 2024

Supplementary Figure S1. Analytical workflow for the C-CAT, GENIE, and TCGA cohorts.

Supplementary Figure S2. Comparison of targeted gene panels.

Supplementary Figure S3. Comparison of genetic alterations in C-CAT and GENIE cohorts.

Supplementary Figure S4. Comparison of mutation frequency, type, and position in C-CAT and GENIE cohorts.

Supplementary Figure S5. Co-occurring and mutually exclusive relationships across cohorts.

Supplementary Figure S6. Co-occurring and mutually exclusive relationships across cancer types/subtypes.

Supplementary Figure S7. Co-occurring and mutually exclusive relationships using a permutation approach.

Supplementary Figure S8. Co-occurring and mutually exclusive relationships across driver mutations in epigenetic regulators.

Supplementary Figure S9. Functional and prognostic relevance of driver mutations in epigenetic regulators.
Supplementary Table 8 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Mass spectrometry analysis for MCF7 and T47D
Supplementary Table 7 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Expression matrix for dormancy associated genes
Supplementary Table 1 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Annotation of coding mutations from the patient cohorts and cell lines
Supplementary Figure S6 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Spatially resolved changes in the transcriptional profile of tumour-associated immune cells and stroma (Patient 1-3, rare cohort treated with long-term ET until progression)
Supplementary Figure S4 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Spatial transcriptomics of patient 1 (rare cohort treated with long-term ET until progression)
Supplementary Figure S2 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of MYC Paralogs
Authors: Pal Choudhuri Shreoshi , Girard Luc , Lim Jun Yi Stanley , Wise Jillian F. , Freitas Braeden , Yang Di , Wong Edmond , Hamilton Seth , Chien Victor D. , Kim Yoon Jung , Gilbreath Collin , Zhong Jun , Phat Sarah , Myers David T. , Christensen Camilla L. , Mazloom-Farsibaf Hanieh , Stanzione Marcello , Wong Kwok-Kin , Hung Yin P. , Farago Anna F. , Meador Catherine B. , Dyson Nicholas J. , Lawrence Michael S. , Wu Sihan , Drapkin Benjamin J.
Published: May 2024

Comparison gene expression and H3K27ac between MGH1518 serial models
Supplementary Figure S13 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of MYC Paralogs
Authors: Pal Choudhuri Shreoshi , Girard Luc , Lim Jun Yi Stanley , Wise Jillian F. , Freitas Braeden , Yang Di , Wong Edmond , Hamilton Seth , Chien Victor D. , Kim Yoon Jung , Gilbreath Collin , Zhong Jun , Phat Sarah , Myers David T. , Christensen Camilla L. , Mazloom-Farsibaf Hanieh , Stanzione Marcello , Wong Kwok-Kin , Hung Yin P. , Farago Anna F. , Meador Catherine B. , Dyson Nicholas J. , Lawrence Michael S. , Wu Sihan , Drapkin Benjamin J.
Published: May 2024

MYC paralog copy number and ecDNA status in SCLC cell lines, PDX models and biopsy samples derived before treatment or after relapse.
Supplementary Figure S12 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of MYC Paralogs
Authors: Pal Choudhuri Shreoshi , Girard Luc , Lim Jun Yi Stanley , Wise Jillian F. , Freitas Braeden , Yang Di , Wong Edmond , Hamilton Seth , Chien Victor D. , Kim Yoon Jung , Gilbreath Collin , Zhong Jun , Phat Sarah , Myers David T. , Christensen Camilla L. , Mazloom-Farsibaf Hanieh , Stanzione Marcello , Wong Kwok-Kin , Hung Yin P. , Farago Anna F. , Meador Catherine B. , Dyson Nicholas J. , Lawrence Michael S. , Wu Sihan , Drapkin Benjamin J.
Published: May 2024

Acquired ecMYCN amplification in MGH1578 serial models and lineage oncogene expression compared with ecDNA status across the PDX panel.
Supplementary Figure S26 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Validation of mass spectrometry and inhibitors’ activity
Supplementary Figure S11 from Acquired Cross-Resistance in Small Cell Lung Cancer due to Extrachromosomal DNA Amplification of MYC Paralogs
Authors: Pal Choudhuri Shreoshi , Girard Luc , Lim Jun Yi Stanley , Wise Jillian F. , Freitas Braeden , Yang Di , Wong Edmond , Hamilton Seth , Chien Victor D. , Kim Yoon Jung , Gilbreath Collin , Zhong Jun , Phat Sarah , Myers David T. , Christensen Camilla L. , Mazloom-Farsibaf Hanieh , Stanzione Marcello , Wong Kwok-Kin , Hung Yin P. , Farago Anna F. , Meador Catherine B. , Dyson Nicholas J. , Lawrence Michael S. , Wu Sihan , Drapkin Benjamin J.
Published: May 2024

Frequency of amplified oncogenes across PDX panel, similarity of ecMYC/L/N structures, and regression analysis of average drug response versus MYC paralog copy number, expression and amplicon type.
Supplementary Figure S23 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

High frequency barcode occupancy of scRNA-seq clusters
Supplementary Figure S20 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

TRADITIOM MCF7 LSC barcode analysis
Supplementary Figure S19 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

TRADITIOM LSC awakening dynamics
Supplementary Figure S18 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Traditiom LSC barcode statistics at single cell level and quality checks
Table S6 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations
Authors: Bashi Azadeh C. , Coker Elizabeth A. , Bulusu Krishna C. , Jaaks Patricia , Crafter Claire , Lightfoot Howard , Milo Marta , McCarten Katrina , Jenkins David F. , van der Meer Dieudonne , Lynch James T. , Barthorpe Syd , Andersen Courtney L. , Barry Simon T. , Beck Alexandra , Cidado Justin , Gordon Jacob A. , Hall Caitlin , Hall James , Mali Iman , Mironenko Tatiana , Mongeon Kevin , Morris James , Richardson Laura , Smith Paul D. , Tavana Omid , Tolley Charlotte , Thomas Frances , Willis Brandon S. , Yang Wanjuan , O'Connor Mark J. , McDermott Ultan , Critchlow Susan E. , Drew Lisa , Fawell Stephen E. , Mettetal Jerome T. , Garnett Mathew J.
Published: May 2024

Supplementary Table 6 shows combination-cancer type pairs with selective activity
Supplementary Figure S11 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Barcode extinction dynamics of Traditiom samples
Supplementary Figure S1 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Genomic profiling and clinical history of late relapse patients.
Figure 5 from Long-term Multimodal Recording Reveals Epigenetic Adaptation Routes in Dormant Breast Cancer Cells
Authors: Rosano Dalia , Sofyali Emre , Dhiman Heena , Ghirardi Chiara , Ivanoiu Diana , Heide Timon , Vingiani Andrea , Bertolotti Alessia , Pruneri Giancarlo , Canale Eleonora , Dewhurst Hannah F. , Saha Debjani , Slaven Neil , Barozzi Iros , Li Tong , Zemlyanskiy Grigory , Phillips Henry , James Chela , Győrffy Balázs , Lynn Claire , Cresswell George D. , Rehman Farah , Noberini Roberta , Bonaldi Tiziana , Sottoriva Andrea , Magnani Luca
Published: May 2024

Failed awakenings. A, TRADITIOM Live awakening topography analysis depicting the awakening dynamics. Twelve carbon copies (cc; replicates) were seeded in a 48-well plate and imaged two times a week for 150 days using IncuCyte Zoom (9 scanning windows per well) to monitor awakening dynamics. Awakening was defined as wells reaching a confluency of 50% (FA: failed awakening; D: dormant; AW: awakening; GA: global awakening; LA: localized awakening; 1LA: 1 localized awakening; >1LA: more than 1 localized awakening). B, IncuCyte time-lapse images from a failed and a bona fide awakening are shown as an example. C, Proliferation dynamics of a representative MCF7 [AI (−E2) awakening 2] and T47D TRADITIOM LSC sample determined by weekly IncuCyte time-lapse imaging until awakening. Pink lines indicate failed awakenings. Magenta lines follow the growth dynamics of main awakening areas. D, MCF7 Geminin-mCherry NLS-GFP cells were treated with estrogen deprivation (−E2) for 3 months to establish a detailed understanding of long-term dormancy–awakening dynamics. Image sets were analyzed using Essenbio Sartorius software from daily imaging. 35% of replicates (n = 60) had dormant persister cells/small colonies until day 88. The proportion of Geminin-mCherry-positive (S/G2–M; pink lines) is indicated normalized to total count which was quantified by NLS-GFP (gray lines). E, Distribution of Ki-67 expression levels in winner and non-winner (others) lineages associated with either G1 or S/G2–M states across T0, dormancy, and awakening samples of MCF7 TRADITIOM LSC cell-cycle regressed data set. F, Cell-cycle regressed UMAPs of the subset of cells in S/G2–M state of TRADITIOM MCF7 LSC data set. G, Pathway enrichment analysis comparing failed awakenings (S/G2–M cells in dormancy: cluster 0, 3) to bona fide awakenings (S/G2–M cells of awakening winner lineages: cluster 4).
Table S15 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations
Authors: Bashi Azadeh C. , Coker Elizabeth A. , Bulusu Krishna C. , Jaaks Patricia , Crafter Claire , Lightfoot Howard , Milo Marta , McCarten Katrina , Jenkins David F. , van der Meer Dieudonne , Lynch James T. , Barthorpe Syd , Andersen Courtney L. , Barry Simon T. , Beck Alexandra , Cidado Justin , Gordon Jacob A. , Hall Caitlin , Hall James , Mali Iman , Mironenko Tatiana , Mongeon Kevin , Morris James , Richardson Laura , Smith Paul D. , Tavana Omid , Tolley Charlotte , Thomas Frances , Willis Brandon S. , Yang Wanjuan , O'Connor Mark J. , McDermott Ultan , Critchlow Susan E. , Drew Lisa , Fawell Stephen E. , Mettetal Jerome T. , Garnett Mathew J.
Published: May 2024

Supplementary Table 15 shows biomarkers associated with top 5 enriched pathways for each drug combination category used in this study (CD = cell death, CS = cell signaling)
Table S14 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations
Authors: Bashi Azadeh C. , Coker Elizabeth A. , Bulusu Krishna C. , Jaaks Patricia , Crafter Claire , Lightfoot Howard , Milo Marta , McCarten Katrina , Jenkins David F. , van der Meer Dieudonne , Lynch James T. , Barthorpe Syd , Andersen Courtney L. , Barry Simon T. , Beck Alexandra , Cidado Justin , Gordon Jacob A. , Hall Caitlin , Hall James , Mali Iman , Mironenko Tatiana , Mongeon Kevin , Morris James , Richardson Laura , Smith Paul D. , Tavana Omid , Tolley Charlotte , Thomas Frances , Willis Brandon S. , Yang Wanjuan , O'Connor Mark J. , McDermott Ultan , Critchlow Susan E. , Drew Lisa , Fawell Stephen E. , Mettetal Jerome T. , Garnett Mathew J.
Published: May 2024

Supplementary Table 14 shows the top 100 significant emergent biomarkers
Table S12 from Large-scale Pan-cancer Cell Line Screening Identifies Actionable and Effective Drug Combinations
Authors: Bashi Azadeh C. , Coker Elizabeth A. , Bulusu Krishna C. , Jaaks Patricia , Crafter Claire , Lightfoot Howard , Milo Marta , McCarten Katrina , Jenkins David F. , van der Meer Dieudonne , Lynch James T. , Barthorpe Syd , Andersen Courtney L. , Barry Simon T. , Beck Alexandra , Cidado Justin , Gordon Jacob A. , Hall Caitlin , Hall James , Mali Iman , Mironenko Tatiana , Mongeon Kevin , Morris James , Richardson Laura , Smith Paul D. , Tavana Omid , Tolley Charlotte , Thomas Frances , Willis Brandon S. , Yang Wanjuan , O'Connor Mark J. , McDermott Ultan , Critchlow Susan E. , Drew Lisa , Fawell Stephen E. , Mettetal Jerome T. , Garnett Mathew J.
Published: May 2024

Supplementary Table 12 shows the number of top combinations:cancer type pairs hits in each combination drug category