Musculoskeletal adverse events associated with CDK4/6 inhibitors: a real-world study using FDA Adverse Event Reporting System (FAERS) database DOI Creative Commons
Zhenlin Chen, Zhiwen Fu,

Zhang Nu

et al.

BMC Pharmacology and Toxicology, Journal Year: 2025, Volume and Issue: 26(1)

Published: Jan. 29, 2025

Language: Английский

Tumor biomarkers for diagnosis, prognosis and targeted therapy DOI Creative Commons
Yue Zhou, Lei Tao, Jiahao Qiu

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)

Published: May 20, 2024

Abstract Tumor biomarkers, the substances which are produced by tumors or body’s responses to during tumorigenesis and progression, have been demonstrated possess critical encouraging value in screening early diagnosis, prognosis prediction, recurrence detection, therapeutic efficacy monitoring of cancers. Over past decades, continuous progress has made exploring discovering novel, sensitive, specific, accurate tumor significantly promoted personalized medicine improved outcomes cancer patients, especially advances molecular biology technologies developed for detection biomarkers. Herein, we summarize discovery development including history conventional innovative used biomarker classification biomarkers based on tissue origins, application clinical management. In particular, highlight recent advancements biomarker-based anticancer-targeted therapies emerging as breakthroughs promising strategies. We also discuss limitations challenges that need be addressed provide insights perspectives turn into opportunities this field. Collectively, multiple emphasized review may guidance precision medicine, broaden horizons future research directions, expedite patients according their rather than organs origin.

Language: Английский

Citations

148

Rapid adaptation to CDK2 inhibition exposes intrinsic cell-cycle plasticity DOI Creative Commons
Mansi Arora, Justin Moser, Timothy E. Hoffman

et al.

Cell, Journal Year: 2023, Volume and Issue: 186(12), P. 2628 - 2643.e21

Published: June 1, 2023

Language: Английский

Citations

72

Therapeutic resistance to anti-oestrogen therapy in breast cancer DOI
Marie Will, Jackson Liang, Ciara Metcalfe

et al.

Nature reviews. Cancer, Journal Year: 2023, Volume and Issue: 23(10), P. 673 - 685

Published: July 27, 2023

Language: Английский

Citations

62

Chemotherapeutic and targeted drugs-induced immunogenic cell death in cancer models and antitumor therapy: An update review DOI Creative Commons

Jiaqi Zhai,

Xi Gu, Yang Liu

et al.

Frontiers in Pharmacology, Journal Year: 2023, Volume and Issue: 14

Published: April 21, 2023

As traditional strategies for cancer treatment, some chemotherapy agents, such as doxorubicin, oxaliplatin, cyclophosphamide, bortezomib, and paclitaxel exert their anti-tumor effects by inducing immunogenic cell death (ICD) of tumor cells. ICD induces immunity through release of, or exposure to, damage-related molecular patterns (DAMPs), including high mobility group box 1 (HMGB1), calreticulin, adenosine triphosphate, heat shock proteins. This leads to activation tumor-specific immune responses, which can act in combination with the direct killing functions drugs on cells further improve curative effects. In this review, we highlight mechanisms underlying ICD, those several chemotherapeutic DAMPs exposed during activate system, well discussing prospects application potential role immunotherapy, aim providing valuable inspiration future development chemoimmunotherapy.

Language: Английский

Citations

58

CDK4/6 inhibitor-mediated cell overgrowth triggers osmotic and replication stress to promote senescence DOI Creative Commons
Lisa Crozier, Reece Foy, Rozita Adib

et al.

Molecular Cell, Journal Year: 2023, Volume and Issue: 83(22), P. 4062 - 4077.e5

Published: Nov. 1, 2023

Abnormal increases in cell size are associated with senescence and cycle exit. The mechanisms by which overgrowth primes cells to withdraw from the remain unknown. We address this question using CDK4/6 inhibitors, arrest G0/G1 licensed treat advanced HR+/HER2- breast cancer. demonstrate that CDK4/6-inhibited overgrow during G0/G1, causing p38/p53/p21-dependent withdrawal. Cell withdrawal is triggered biphasic p21 induction. first wave caused osmotic stress, leading p38- size-dependent accumulation of p21. inhibitor washout results some entering S-phase. Overgrown experience replication resulting a second promotes G2 or subsequent G1. propose levels integrate signals overgrowth-triggered stresses determine fate. This model explains how hypertrophy can drive why inhibitors have long-lasting effects patients.

Language: Английский

Citations

44

Recent progress of CDK4/6 inhibitors’ current practice in breast cancer DOI Creative Commons
Xueqing Wang, Shanshan Zhao,

Qinghan Xin

et al.

Cancer Gene Therapy, Journal Year: 2024, Volume and Issue: 31(9), P. 1283 - 1291

Published: Feb. 26, 2024

Dysregulated cellular proliferation represents a hallmark feature across all cancers. Aberrant activation of the cyclin-dependent kinase 4 and 6 (CDK4/6) pathway, independent mitogenic signaling, engenders uncontrolled breast cancer cell proliferation. Consequently, advent CDK4/6 inhibition has constituted pivotal milestone in realm targeted therapy. The combination inhibitors (CDK4/6i) with endocrine therapy (ET) emerged as foremost therapeutic modality for patients afflicted hormone receptor-positive (HR + )/HER2-negative (HER2-) advanced cancer. At present, Food Drug Administration (FDA) sanctioned various CDK4/6i employment primary treatment regimen HR /HER2- This approach demonstrated substantial extension progression-free survival (PFS), often amounting to several months, when administered alongside Within this comprehensive review, we systematically evaluate utilization strategies subpopulations explore potential avenues following disease progression during application

Language: Английский

Citations

42

The role of aberrant DNA methylation in cancer initiation and clinical impacts DOI Creative Commons
Franziska Geissler, Ksenija Nesic, Olga Kondrashova

et al.

Therapeutic Advances in Medical Oncology, Journal Year: 2024, Volume and Issue: 16

Published: Jan. 1, 2024

Epigenetic alterations, including aberrant DNA methylation, are now recognized as bone fide hallmarks of cancer, which can contribute to cancer initiation, progression, therapy responses and resistance. Methylation gene promoters have a range impacts on risk, clinical stratification therapeutic outcomes. We provide several important examples genes, be silenced or activated by promoter methylation highlight their implications. These include the mismatch repair genes MLH1 MSH2, homologous recombination BRCA1 RAD51C, TERT oncogene within P15/P16/RB1/E2F tumour suppressor axis. also discuss how these changes might occur in first place – whether context CpG island methylator phenotype constitutional methylation. The choice assay used measure significant impact interpretation states, some where this influence decision-making presented. Aberrant patterns circulating (ctDNA) showing great promise non-invasive detection monitoring using liquid biopsies; however, caution must taken interpreting results cases may present. Thus, review aims researchers clinicians with comprehensive summary broad, but subject, illustrating potentials pitfalls assessing cancer.

Language: Английский

Citations

20

Von Hippel–Lindau protein signalling in clear cell renal cell carcinoma DOI
Chengheng Liao, Lianxin Hu, Qing Zhang

et al.

Nature Reviews Urology, Journal Year: 2024, Volume and Issue: 21(11), P. 662 - 675

Published: May 2, 2024

Language: Английский

Citations

20

An alternative cell cycle coordinates multiciliated cell differentiation DOI
Semil P. Choksi, Lauren Byrnes, Mia J. Konjikusic

et al.

Nature, Journal Year: 2024, Volume and Issue: 630(8015), P. 214 - 221

Published: May 29, 2024

Language: Английский

Citations

19

A deep learning model of tumor cell architecture elucidates response and resistance to CDK4/6 inhibitors DOI Creative Commons
Sungjoon Park, Erica Silva, Akshat Singhal

et al.

Nature Cancer, Journal Year: 2024, Volume and Issue: 5(7), P. 996 - 1009

Published: March 5, 2024

Abstract Cyclin-dependent kinase 4 and 6 inhibitors (CDK4/6is) have revolutionized breast cancer therapy. However, <50% of patients an objective response, nearly all develop resistance during To elucidate the underlying mechanisms, we constructed interpretable deep learning model response to palbociclib, a CDK4/6i, based on reference map multiprotein assemblies in cancer. The identifies eight core that integrate rare common alterations across 90 genes stratify palbociclib-sensitive versus palbociclib-resistant cell lines. Predictions translate patient-derived xenografts, whereas single-gene biomarkers do not. Most predictive can be shown by CRISPR–Cas9 genetic disruption regulate CDK4/6i response. Validated relate cell-cycle control, growth factor signaling histone regulatory complex show promotes S-phase entry through activation modifiers KAT6A TBL1XR1 transcription RUNX1. This study enables integrated assessment how tumor’s profile modulates resistance.

Language: Английский

Citations

18