Cancer Biology

S100a4+ alveolar macrophages accelerate the progression of precancerous atypical adenomatous hyperplasia by promoting the angiogenic function regulated by fatty acid metabolism

1. Hong Huang
2. Ying Yang
3. Qiuju Zhang
4. Yongfeng Yang
5. Zhenqi Xiong
6. Shengqiang Mao
7. Tingting Song
8. Yilong Wang
9. Zhiqiang Liu
10. Hong Bu
11. Li Zhang
12. Le Zhang

• Curated by eLife

  eLife Assessment

  This is an important study demonstrating the importance of S100A4+ alveolar macrophages in the earlier stages of tumour development and suggesting a role in angiogenesis. As such this convincing study is of interest to cancer biologists focused on early tumour development and those interested in the development of therapeutics that may specifically target early cancers.

Reviewed by eLife

Loss function of tumor suppressor FRMD8 confers resistance to tamoxifen therapy via a dual mechanism

1. Weijie Wu
2. Miao Yu
3. Qianchen Li
4. Yiqian Zhao
5. Lei Zhang
6. Yi Sun
7. Zhenbin Wang
8. Yuqing Gong
9. Wenjing Wang
10. Chenying Liu
11. Jing Zhang
12. Yan Tang
13. Xiaojie Xu
14. Xiaojing Guo
15. Jun Zhan
16. Hongquan Zhang

• Curated by eLife

  eLife Assessment

  The research presents valuable findings on the impact of FRMD8 loss on tumor progression and resistance to tamoxifen therapy. Through a series of convincing and systematic experiments, the author thoroughly investigates the role of FRMD8 in breast cancer and its underlying regulatory mechanisms. The study confirms that FRMD8 holds potential as a therapeutic target for reversing tamoxifen resistance, offering helpful insights for future treatment strategies.

Reviewed by eLife

Ezh2 Delays Activation of Differentiation Genes During Normal Cerebellar Granule Neuron Development and in Medulloblastoma

1. James Purzner
2. Alexander S Brown
3. Teresa Purzner
4. Lauren Ellis
5. Sara Broski
6. Ulrike Litzenburger
7. Kaytlin Andrews
8. Aryaman Sharma
9. Xin Wang
10. Michael D Taylor
11. Yoon-Jae Cho
12. Margaret T Fuller
13. Matthew P Scott

• Curated by eLife

  eLife Assessment

  Using an unbiased approach, this important study discovered a role of Ezh2 in the differentiation of granule neuron precursors, the cell of origin for Shh group of medulloblastoma. Furthermore, the authors also provided solid evidence that combined inhibition of Ezh2 and CDK4/6 likely represents a promising strategy for the treatment of this subgroup of MB. Validation of these findings using the FDA-approved Ezh2 inhibitor is needed to further strengthen this preclinical study.

Reviewed by eLife

In vivo targeted and deterministic single-cell malignant transformation

1. Pierluigi Scerbo
2. Benjamin Tisserand
3. Marine Delagrange
4. Héloise Debare
5. David Bensimon
6. Bertrand Ducos

• Curated by eLife

  eLife Assessment

  This important study employs an optogenetics approach aimed at activating oncogene (KRASG12V) expression in a single somatic cell, with a focus on following the progression of activated cell to examine tumourigenesis probabilities under altered tissue environments. Although the description of the methodologies applied is incomplete, the authors propose a mechanism whereby reactivation of re-programming factors correlates with the increased likelihood of a mutant cell undergoing malignant transformation. This work will be of interest to developmental and cancer biologists, especially in relation to the genetic tools described.

Reviewed by eLife

Notch signaling maintains a progenitor-like subclass of hepatocellular carcinoma

1. Kerstin Seidel
2. Robert Piskol
3. Thi Thu Thao Nguyen
4. Amy Shelton
5. Charisa Cottonham
6. Cecile C de la Cruz
7. Joseph Castillo
8. Jesse Garcia
9. Udi Segal
10. Mark Merchant
11. Yeqing Angela Yang
12. Jasmine Chen
13. Musa Ahmed
14. Alexis Scherl
15. Rajesh Vij
16. Lluc Mosteiro
17. Yan Wu
18. Zora Modrusan
19. Ciara Metcalfe
20. Chris Siebel

• Curated by eLife

  eLife Assessment

  In this valuable study, Seidel et al. identify and characterize a novel subset of hepatocellular carcinoma patient-derived xenograft models defined by active Jagged 1-Notch2 signaling and a distinctive progenitor-like gene expression profile. Within the limitations of the PDX system they used, their methods are state-of-the-art, their data are strong and believable, and their conclusions are convincing. However, the ability to identify HCC patients that might respond is limited, and the mechanistic assessment downstream of JAG1/NOTCH2 is relatively descriptive. Some additional clarifications and experiments would strengthen the paper.

Reviewed by eLife

STAMBPL1 activates the GRHL3/HIF1A/VEGFA axis through interaction with FOXO1 to promote angiogenesis in triple-negative breast cancer

1. Huan Fang
2. Huichun Liang
3. Chuanyu Yang
4. Dewei Jiang
5. Qianmei Luo
6. Wen-Ming Cao
7. Huifeng Zhang
8. Ceshi Chen

• Curated by eLife

  eLife Assessment

  The study conducted by Fang et al. offers significant and fundamental insights, notably enhancing our understanding of angiogenesis. While some of the claims are supported by convincing experimental approaches, others lack sufficient validation. Additionally, there are instances where critical experimental controls appear to be absent.

Reviewed by eLife

Propionyl-CoA carboxylase subunit B regulates anti-tumor T cells in a pancreatic cancer mouse model

1. Han V Han
2. Richard Efem
3. Barbara Rosati
4. Kevin Lu
5. Sara Maimouni
6. Ya-Ping Jiang
7. Valeria Montoya
8. Ando Van Der Velden
9. Wei-Xing Zong
10. Richard Z Lin

• Curated by eLife

  eLife assessment

  The significance of the findings is valuable, with implications for immunotherapy design in pancreatic ductal adenocarcinoma. The evidence was considered incomplete and partially supportive of the major claims.

Reviewed by eLife

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

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