Cancer Biology

Spatial multi-omics defines a shared glioblastoma infiltrative signature at the resection margin

1. Balagopal Pai
2. Susana Isabel Ramos
3. Wan Sze Cheng
4. Tanvi Joshi
5. Gabrielle Price
6. Jessica Tome-Garcia
7. German Nudelman
8. Sanjana Shroff
9. Kristin Beaumont
10. Yong Raymund
11. Robert Sebra
12. Elena Zaslavsky
13. Nadejda Mincheva Tsankova

Reviewed by PREreview

Tks5 interactome reveals ER-associated machinery translation in invadosomes

1. Léa Normand
2. Benjamin Bonnard
3. Margaux Sala
4. Sylvaine Di-Tommaso
5. Cyril Dourthe
6. Anne-Aurélie Raymond
7. Jean-William Dupuy
8. Luc Mercier
9. Jacky G. Goetz
10. Violaine Moreau
11. Elodie Henriet
12. Frédéric Saltel

Reviewed by Review Commons

Interplay of YEATS2 and GCDH regulates histone crotonylation and drives EMT in head and neck cancer

1. Deepak Pant
2. Parik Kakani
3. Rushikesh Joshi
4. Abin Sabu
5. Shruti Agrawal
6. Atul Samaiya
7. Sanjeev Shukla

• Curated by eLife

  eLife Assessment

  These useful findings assigned a novel functional implication of histone acylation, crotonylation. Although the mechanistic insights have been provided in great detail regarding the role of the YEATS2-GCDH axis in modulating EMT in HNC, the strength of evidence for the manuscript is incomplete. The patient cohort is very small, with just 10 patients; to establish a significant result the cohort size should be increased. Furthermore, the functional implication of p300 is also to be looked into.

Reviewed by eLife

Loss of ZNRF3/RNF43 Unleashes EGFR in Cancer

1. Fei Yue
2. Amy T Ku
3. Payton D Stevens
4. Megan N Michalski
5. Weiyu Jiang
6. Jianghua Tu
7. Zhongcheng Shi
8. Yongchao Dou
9. Yi Wang
10. Xin-Hua Feng
11. Galen Hostetter
12. Xiangwei Wu
13. Shixia Huang
14. Noah F Shroyer
15. Bing Zhang
16. Bart O Williams
17. Qingyun Liu
18. Xia Lin
19. Yi Li

• Curated by eLife

  eLife Assessment

  This manuscript presents solid evidence suggesting that the loss of ZNRF3 and RNF43, two E3 ubiquitin ligases, leads to dysregulation of EGFR signaling in cancer. The authors propose that EGFR is a direct substrate of ZNRF3/RNF43. While the authors provide immunoprecipitation data showing increased detection of ubiquitinated species, this evidence does not definitively establish that EGFR itself is ubiquitinated by RNF43/ZNRF3. The absence of direct evidence for EGFR ubiquitination is a major limitation, although the findings are useful as they may provide novel insights into the mechanisms underlying EGFR-driven cancers and open new therapeutic avenues.

Reviewed by eLife

Systemic and local chronic inflammation and hormone disposition promote a tumor-permissive environment for breast cancer in older women

1. Neil Carleton
2. Sanghoon Lee
3. Ruxuan Li
4. Jian Zou
5. Daniel D Brown
6. Jagmohan Hooda
7. Alexander Chang
8. Rahul Kumar
9. Linda R Klei
10. Lora H Rigatti
11. Joseph Newsome
12. Dixcy Jaba Sheeba John Mary
13. Jennifer M Atkinson
14. Raymond E West
15. Thomas D Nolin
16. Patrick J Oberly
17. Ziyu Huang
18. Donald Poirier
19. Emilia J Diego
20. Peter C Lucas
21. George Tseng
22. Michael T Lotze
23. Priscilla F McAuliffe
24. Ioannis K Zervantonakis
25. Steffi Oesterreich
26. Adrian V Lee

Reviewed by PREreview

Intrinsic bioenergetic adaptations compensate for reduced mitochondrial content in HER2-driven mammary tumors

1. Sara M Frangos
2. Henver S Brunetta
3. Dongdong Wang
4. Maria Joy Therese Jabile
5. David WL Ma
6. William J Muller
7. Cezar M Khursigara
8. Kelsey H Fisher-Wellman
9. Gregory R Steinberg
10. Graham P Holloway

• Curated by eLife

  eLife Assessment

  This useful study uses the MMTV-Neu-YD5 mouse model for HER2-dependent breast cancer to generate transcriptomic and proteomic datasets from extracted primary tumour samples. The data sets generated appear to be solid and will be of interest to the community. However, mechanistic studies to support the conclusion that mitochondrial function is increased in the tumours remain incomplete and would benefit from experiments that would directly interrogate aspects such as cellular heterogeneity, and signalling.

Reviewed by eLife

NAB2-STAT6 drives an EGR1-dependent neuroendocrine program in Solitary Fibrous Tumors

1. Connor M Hill
2. Alexandra Indeglia
3. Francis Picone
4. Maureen E Murphy
5. Cara Cipriano
6. Robert G Maki
7. Alessandro Gardini

• Curated by eLife

  eLife Assessment

  This study provides compelling data regarding the molecular characterization of a rare tumor type with few treatment options. This fundamental work significantly advances our mechanistic understanding of solitary fibrous tumours, a critical first step towards targeted precision medicine approaches. The results of this study will be of broad interest to cancer biologists and experimental oncologists.

Reviewed by eLife

Deuterium metabolic imaging phenotypes mouse glioblastoma heterogeneity through glucose turnover kinetics

1. Rui Vasco Simoes
2. Rafael Neto Henriques
3. Jonas L Olesen
4. Beatriz M Cardoso
5. Francisca F Fernandes
6. Mariana AV Monteiro
7. Sune N Jespersen
8. Tânia Carvalho
9. Noam Shemesh

• Curated by eLife

  eLife Assessment

  This study provides a valuable approach to image and analyze in vivo metabolic flux through glucose turnover kinetics in glioblastoma tumor microenvironments. The evidence for the method's validity is convincing, which establishes the dynamic Deuterium Metabolic Imaging technique as an effective tool enabling non-invasive exploration of various tumors.

Reviewed by eLife

Combinatorial CRISPR screen reveals FYN and KDM4 as targets for synergistic drug combination for treating triple negative breast cancer

1. Tackhoon Kim
2. Byung-Sun Park
3. Soobeen Heo
4. Heeju Jeon
5. Jaeyeal Kim
6. Donghwa Kim
7. Sang Kook Lee
8. So-Youn Jung
9. Sun-Young Kong
10. Timothy Lu

• Curated by eLife

  eLife Assessment

  This study presents a valuable finding that synthetically lethal kinase genes FYN and KDM4 may play a role in drug resistance to kinase inhibitors in TNBC. The evidence supporting the claims of the authors is solid, although the exploration of the upstream mechanisms regulating KDM4A or the downstream pathways through which FYN upregulation confers drug resistance would have strengthened the study. The work will be of interest to medical biologists working in the field of breast cancer.

Reviewed by eLife

Citalopram exhibits immune-dependent anti-tumor effects by modulating C5aR1+ TAMs and CD8+ T cells

1. Fangyuan Dong
2. Shan Zhang
3. Kaiyuan Song
4. Luju Jiang
5. Li-Peng Hu
6. Qing Li
7. Xue-Li Zhang
8. Jun Li
9. Mingxuan Feng
10. Zhi-Wei Cai
11. Hong-Fei Yao
12. Rong-Kun Li
13. Hui Li
14. Jie Chen
15. Xiaona Hu
16. Jiaofeng Wang
17. Chongyi Jiang
18. Helen He Zhu
19. Cun Wang
20. Lin-Tai Da
21. Zhi-Gang Zhang
22. Zhijun Bao
23. Xu Wang
24. Shu-Heng Jiang

• Curated by eLife

  eLife Assessment

  This important study provides solid evidence to support the anti-tumor potential of citalopram, originally an anti-depression drug, in hepatocellular carcinoma (HCC). In addition to their previous report on directly targeting tumor cells via glucose transporter 1 (GLUT1), they tried to uncover additional working mechanisms of citalopram in HCC treatment in the current study. The data here suggested that citalopram may regulate the phagocytotic function of TAM via C5aR1 or CD8+T cell function to suppress HCC growth in vivo.

Reviewed by eLife