bims-netuvo Biomed News
on Nerves in tumours of visceral organs
Issue of 2025–02–23
thirteen papers selected by
Maksym V. Kopanitsa, Charles River Laboratories
  1. Characterization of single neurons reprogrammed by pancreatic cancer.
  2. [Impact of perineural invasion upon chemotherapy duration and survival benefit in stageⅢ colon cancer].
  3. Perineural Invasion in Cervical Cancer.
  4. GABA regulates metabolic reprogramming to mediate the development of brain metastasis in non-small cell lung cancer.
  5. Pinpointing neurons that hinder cancer treatment.
  6. GPR37 Activation Alleviates Bone Cancer Pain via the Inhibition of Osteoclastogenesis and Neuronal Hyperexcitability.
  7. Nociceptive neurons promote gastric tumour progression via a CGRP-RAMP1 axis.
  8. Malignant Tumors in Vagal-innervated Organs: Exploring Its Homeostatic Role.
  9. Development of a nomogram predicting perineural invasion risk and assessment of the prognostic value of perineural invasion in colon cancer: a population study based on the Surveillance, Epidemiology, and End Results database.
  10. Expression of stearoyl coenzyme a desaturase in neuronal cells facilitates pancreatic cancer progression.
  11. Global prevalence and determinant factors of pain, depression, and anxiety among cancer patients: an umbrella review of systematic reviews and meta-analyses.
  12. Schwann cells in regeneration and cancer.
  13. The neuroscience in breast cancer: Current insights and clinical opportunities.
  1. Nature. 2025 Feb 17.
    Characterization of single neurons reprogrammed by pancreatic cancer.
    Vera Thiel, Simon Renders, Jasper Panten, Nicolas Dross, Katharina Bauer, Daniel Azorin, Vanessa Henriques, Vanessa Vogel, Corinna Klein, Aino-Maija Leppä, Isabel Barriuso Ortega, Jonas Schwickert, Iordanis Ourailidis, Julian Mochayedi, Jan-Philipp Mallm, Carsten Müller-Tidow, Hannah Monyer, John Neoptolemos, Thilo Hackert, Oliver Stegle, Duncan T Odom, Rienk Offringa, Albrecht Stenzinger, Frank Winkler, Martin Sprick, Andreas Trumpp.
      The peripheral nervous system (PNS) orchestrates organ function in health and disease. Most cancers including pancreatic ductal adenocarcinoma (PDAC) are infiltrated by PNS neurons, contributing to the complex tumor microenvironment (TME)1,2. However, neuronal cell bodies reside in various PNS ganglia, far from the tumor mass. Thus, cancer or healthy organ-innervating neurons elude current tissue sequencing datasets. To molecularly characterize pancreas- and PDAC-innervating neurons at single cell resolution, we developed "Trace-n-seq". This method employs retrograde tracing of axons from tissues to their respective ganglia followed by single-cell isolation and transcriptomic analysis. By characterizing >5.000 individual sympathetic and sensory neurons with about 4.000 innervating PDAC or healthy pancreas we reveal novel neuronal cell types and unique molecular networks distinct to pancreas, pancreatitis, PDAC, or melanoma metastasis. We integrate single-cell datasets of innervating neurons and the TME to establish a neuro-cancer-microenvironment interactome, delineate cancer-driven neuronal reprogramming and generate a pancreatic cancer-nerve signature. Pharmacological denervation induces a proinflammatory TME and increases immune-checkpoint inhibitor effectiveness. Nab-Paclitaxel causes intra-tumor neuropathy which attenuated PDAC growth and in combination with sympathetic denervation results in synergistic tumor regression. Our multi-dimensional data reveal new insights into the networks and functions of PDAC-innervating neurons, supporting inclusion of denervation in future therapies.
    DOI:  https://doi.org/10.1038/s41586-025-08735-3
  2. Zhonghua Wei Chang Wai Ke Za Zhi. 2025 Jan 25. 28(1): 58-66
    [Impact of perineural invasion upon chemotherapy duration and survival benefit in stageⅢ colon cancer].
    J X Chen, W L Zhang, W F Wang, J B Li, X J Wu, Z H Lu, D B Xu, J Z Lin, J H Peng.
      Objective: To investigate the prognostic impact of perineural invasion in patients with stageⅢ colon cancer and to clarify its guidance value for the duration of postoperative adjuvant chemotherapy. Methods: This study employed a retrospective cohort study method. It analyzed 426 patients with stageⅢ colon cancer who underwent radical surgery at Sun Yat-sen University Cancer Center and Longyan First Affiliated Hospital of Fujian Medical University, between April 2008 and June 2020. Inclusion criteria: patients received at least 3 months of adjuvant CapeOX therapy post-surgery, had complete pathological data, and were followed up for at least 12 months after the last chemotherapy. Among these patients, 231 were male, the median age was 59 (50~67) years, and 263 tumors were located in the right-sided colon. Postoperative pathology indicated that 107 cases (25.12%) had neural invasion, and 131 patients (30.75%) had vascular tumor thrombus. All patients received at least 4 cycles of postoperative CapeOX adjuvant chemotherapy, with 193 patients receiving 8 cycles and 233 patients receiving 4 to 7 cycles of adjuvant chemotherapy. The study analyzed the impact of neural invasion status and the duration of adjuvant chemotherapy on disease-free survival (DFS). Furthermore, within subgroups stratified by different risk levels (referencing the criteria proposed by the IDEA study: high risk: T4, N2 or T4N2; low risk: T3N1) and different neural invasion statuses, the impact of the duration of adjuvant chemotherapy on prognosis was analyzed. Results: The median follow-up time for the entire cohort was 94.00 months (55.27-128.80 months). Multivariate Cox analysis indicated that pathological T stage T4 (HR = 2.457, 95%CI: 1.499-4.029, P<0.001) and postoperative pathological confirmation of perineural invasion (HR = 2.465, 95% CI: 1.519-4.000, P<0.001) were independent adverse prognostic factors for 5-year DFS. In the perineural invasion-positive group, the 5-year DFS for patients who received 8 cycles of postoperative adjuvant CapeOX chemotherapy was 86.90%, compared to 58.22% for those who received 4-7 cycles, with statistically significant differences (both P<0.05). In the perineural invasion-negative group, the 5-year DFS for patients who received 8 cycles was 88.66%, compared to 90.99% for those who received 4-7 cycles, with no statistically significant differences (P=0.929). Among IDEA high-risk patients with perineural invasion, the 5-year DFS was 91.81% for those who received 8 cycles versus 50.66% for those who received 4-7 cycles, showing a statistically significant difference (P=0.003). In IDEA high-risk patients without perineural invasion, the 5-year DFS for those who received 8 cycles was 82.28% compared to 87.32% for those who received 4-7 cycles, with no statistically significant difference (P=0.806). In the IDEA low-risk patients, no differences were observed in the 5-year DFS between patients receiving 8 cycles and those receiving 4-7 cycles of adjuvant CapeOX chemotherapy in both perineural invasion-positive and negative subgroups (both P>0.05). Conclusion: Perineural invasion serves as a significant prognostic factor for 5-year DFS in stage Ⅲ colon cancer patients who have undergone radical surgery and postoperative adjuvant chemotherapy. It can also be considered an important reference factor in deciding the duration of postoperative adjuvant chemotherapy.
    DOI:  https://doi.org/10.3760/cma.j.cn441530-20240508-00170
  3. Cancer Lett. 2025 Feb 14. pii: S0304-3835(25)00125-9. [Epub ahead of print] 217561
    Perineural Invasion in Cervical Cancer.
    Xiayi Li, Xiaojing Yang, Shuchen Lin, Hui Cong, Yawen Liu, Yudong Wang, Jie Fu.
      Perineural invasion (PNI), the neoplastic infiltration of peripheral nerves, is recognized as the fourth mode of tumor metastasis and invasion. PNI is defined as a critical pathological feature observed across a various of cancers and is associated with poor prognosis. Recent studies have demonstrated that PNI also occurs in cervical cancer. Nerve-sparing radical hysterectomy (NSRH) has been promoted as the preferred approach for radical surgical resection of cervical cancer, as it reduces postoperative complications such as bladder, rectal, and sexual dysfunction. However, the presence of PNI has become a contraindication for NSRH. Despite the increasing volume of studies on PNI, the underlying mechanisms of its pathogenesis remain largely unclear. In this review, we discuss the innervation, characteristics, preoperative prediction and diagnosis of PNI in cervical cancer, along with its underlying mechanism, paving the way for advancements in treatment strategies and improving the prognosis for cervical cancer patients.
    Keywords:  cervical cancer; diagnosis; nerve-sparing radical hysterectomy; perineural invasion; prediction
    DOI:  https://doi.org/10.1016/j.canlet.2025.217561
  4. J Exp Clin Cancer Res. 2025 Feb 19. 44(1): 61
    GABA regulates metabolic reprogramming to mediate the development of brain metastasis in non-small cell lung cancer.
    Mengqing Xie, Hao Qin, Li Liu, Jing Wu, Zhikai Zhao, Yaodong Zhao, Yujia Fang, Xin Yu, Chunxia Su.
       BACKGROUND: Brain metastasis (BrM) poses a significant challenge to the prognosis and quality of life for patients with non-small cell lung cancer (NSCLC). Gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter in the central nervous system (CNS), has been implicated in the progression of various tumors. However, its potential role in BrM of NSCLC and the underlying mechanisms remain largely unexplored.
    METHODS: A multi-omics approach combined with in vivo and in vitro experiments identified GABA as a key target in BrM of NSCLC. Functional and mechanistic studies were conducted to investigate how GABA mediates brain metastasis through the activation of the NF-κB pathway.
    RESULTS: GABA levels were significantly elevated in both cells and serum of patients with NSCLC who had BrM. GABA markedly enhanced the brain metastatic capabilities and malignancy of NSCLC cells. Mechanistically, tumor cells with a tendency for brain metastasis can inhibit 4-aminobutyrate aminotransferase (ABAT) by downregulating forkhead box A2 (FOXA2) expression, leading to increased GABA accumulation. GABA subsequently activates the NF-κB pathway and the astrocytes, thus facilitating the brain metastasis of NSCLC.
    CONCLUSIONS: Our findings indicate that GABA plays a crucial role in the development of NSCLC brain metastasis by activating the NF-κB pathway through the FOXA2/ABAT/GABA axis. Additionally, the interaction between NSCLC and astrocytes creates an inhibitory microenvironment that promotes tumor colonization.
    Keywords:  Astrocyte; Brain metastasis; GABA; Metabolic reprogramming; NSCLC
    DOI:  https://doi.org/10.1186/s13046-025-03315-9
  5. Nature. 2025 Feb 18.
    Pinpointing neurons that hinder cancer treatment.
    Ihsan Ekin Demir, Elke Demir.
      
    Keywords:  Cancer; Immunology; Medical research
    DOI:  https://doi.org/10.1038/d41586-025-00501-9
  6. Adv Sci (Weinh). 2025 Feb 18. e2417367
    GPR37 Activation Alleviates Bone Cancer Pain via the Inhibition of Osteoclastogenesis and Neuronal Hyperexcitability.
    Kaiyuan Wang, Yongfang Zhang, Ruichen Shu, Limei Yuan, Huifang Tu, Shengran Wang, Bo Ni, Yi-Fan Zhang, Changyu Jiang, Yuhui Luo, Yiqing Yin.
      Osteolytic bone cancer pain is a primary concern for cancer patients with bone metastasis, and current therapies offer inadequate pain relief. The present study demonstrates that activation of the G protein-coupled receptor 37 (GPR37) by neuroprotectin D1 (NPD1) or artesunate (ARU) alleviates both acute and persistent pain in multiple mouse models of bone cancer. GPR37 agonists also protect against cancer-induced bone destruction. Mechanistically, NPD1 or ARU binding to GPR37 in macrophages promotes the release of IL-10, which further inhibits cancer-induced osteoclastogenesis. Moreover, direct activation of GPR37 in dorsal root ganglion (DRG) neurons and the spinal dorsal horn reduces action potential firing and the frequency of spontaneous excitatory postsynaptic currents (sEPSCs), thereby suppressing cancer-induced neuronal hyperexcitability. Importantly, the analgesic and protective effects of NPD1 and ARU are abolished in Gpr37-/- mice, and β-arrestin 2 is identified as a key mediator in IL-10 release and neuronal inhibition. In patients with bone metastases, plasma levels of endogenous NPD1 are negatively correlated with both pain intensity and the bone resorption marker CTX-I. Collectively, these findings highlight GPR37 activation as a potential therapeutic strategy for alleviating bone cancer pain through direct and synergistic inhibition of osteoclastogenesis and neuronal hyperexcitability.
    Keywords:  cancer pain, GPR37; neuroimmune modulation; neuroprotectin D1; osteoclastogenesis
    DOI:  https://doi.org/10.1002/advs.202417367
  7. Nature. 2025 Feb 19.
    Nociceptive neurons promote gastric tumour progression via a CGRP-RAMP1 axis.
    Xiaofei Zhi, Feijing Wu, Jin Qian, Yosuke Ochiai, Guodong Lian, Ermanno Malagola, Biyun Zheng, Ruhong Tu, Yi Zeng, Hiroki Kobayashi, Zhangchuan Xia, Ruizhi Wang, Yueqing Peng, Qiongyu Shi, Duan Chen, Sandra W Ryeom, Timothy C Wang.
      Cancer cells have been shown to exploit neurons to modulate their survival and growth, including through the establishment of neural circuits within the central nervous system1-3. Here we report a distinct pattern of cancer-nerve interactions between the peripheral nervous system and gastric cancer. In multiple mouse models of gastric cancer, nociceptive nerves demonstrated the greatest degree of nerve expansion in an NGF-dependent manner. Neural tracing identified CGRP+ peptidergic neurons as the primary gastric sensory neurons. Three-dimensional co-culture models showed that sensory neurons directly connect with gastric cancer spheroids. Chemogenetic activation of sensory neurons induced the release of calcium into the cytoplasm of cancer cells, promoting tumour growth and metastasis. Pharmacological ablation of sensory neurons or treatment with CGRP inhibitors suppressed tumour growth and extended survival. Depolarization of gastric tumour membranes through in vivo optogenetic activation led to enhanced calcium flux in jugular nucleus complex and CGRP release, defining a cancer cell-peptidergic neuronal circuit. Together, these findings establish the functional connectivity between cancer and sensory neurons, identifying this pathway as a potential therapeutic target.
    DOI:  https://doi.org/10.1038/s41586-025-08591-1
  8. Cancer Lett. 2025 Feb 13. pii: S0304-3835(25)00103-X. [Epub ahead of print] 217539
    Malignant Tumors in Vagal-innervated Organs: Exploring Its Homeostatic Role.
    Pierrick Martinez, Jean-Marc Sabatier.
      Cancer remains a significant global health challenge, with its progression shaped by complex and multifactorial mechanisms. Recent research suggests that the vagus nerve could play a critical role in mediating communication between the tumor microenvironment and the central nervous system (CNS). This review highlights the diversity of vagal afferent receptors, which could position the vagus nerve as a unique pathway for transmitting immune, metabolic, mechanical, and chemical signals from tumors to the CNS. Such signaling could influence systemic disease progression and tumor-related responses. Additionally, the vagus nerve's interactions with the microbiome and the renin-angiotensin system (RAS)-both implicated in cancer biology-further underscore its potential central role in modulating tumor-related processes. Contradictions in the literature, particularly concerning vagal fibers, illustrate the complexity of its involvement in tumor progression, with both tumor-promoting and tumor-suppressive effects reported depending on cancer type and context. These contradictions often overlook certain experimental biases, such as the failure to distinguish between vagal afferent and efferent fibers during vagotomies or the localized parasympathetic effects that cannot always be extrapolated to the systemic level. By focusing on the homeostatic role of the vagus nerve, understanding these mechanisms could open the door to new perspectives in cancer research related to the vagus nerve and lead to potential therapeutic innovations.
    Keywords:  Autonomic nervous system; Microbiome; Neural addiction; Renin-angiotensin-system; Tumor neurobiology; Vagus nerve
    DOI:  https://doi.org/10.1016/j.canlet.2025.217539
  9. Transl Cancer Res. 2025 Jan 31. 14(1): 141-158
    Development of a nomogram predicting perineural invasion risk and assessment of the prognostic value of perineural invasion in colon cancer: a population study based on the Surveillance, Epidemiology, and End Results database.
    Zhongqiang Zheng, Xuanzi Sun.
       Background: Perineural invasion (PNI) in colon cancer (CC) is widely associated with poor prognosis. In this study, we aimed to develop a predictive model for PNI and to assess its prognostic value in CC patients.
    Methods: Data for CC patients with or without PNI were obtained from the Surveillance, Epidemiology, and End Results (SEER) database from 2010 to 2015. Potential features were selected by stepwise logistic regression, and multivariate logistic regression was used to develop the nomogram. Nomogram performance was assessed based on its calibration curve, discrimination ability and clinical utility. The prognostic value of PNI was assessed using Kaplan-Meier analysis, a competing risk model, and a Fine-Gray multivariable regression model.
    Results: A total of 51,826 subjects were included in the study. The nomogram consisted of 11 features was constructed, which provided good calibration and discrimination with area under the curve values of 0.787 vs. 0.781 (development cohort vs. validation cohort). Patients with PNI had worse CC-specific survival (P<0.001) and a higher CC-specific death rate (Gray's test, P<0.001) than patients without PNI. Fine-Gray multivariable regression analysis showed that patients with PNI had a higher CC-specific death rate than patients without PNI [hazard ratio (HR) =1.243; 95% confidence interval (CI): 1.183-1.305; P<0.001]. Pathologic stage T4 (pT4) CC patients without PNI treated with chemotherapy (ChemT) plus radiotherapy (RT) had a lower CC-specific death rate than ChemT-treated or non-therapy patients.
    Conclusions: The nomogram developed herein has certain clinical application value for predicting PNI risk in CC patients. PNI is a survival predictor for CC patients. pT4 patients without PNI might benefit from combined ChemT and RT.
    Keywords:  Colon cancer (CC); Surveillance, Epidemiology, and End Results (SEER); competing risk model; nomogram; perineural invasion (PNI)
    DOI:  https://doi.org/10.21037/tcr-24-1030
  10. Cancer Cell Int. 2025 Feb 20. 25(1): 57
    Expression of stearoyl coenzyme a desaturase in neuronal cells facilitates pancreatic cancer progression.
    Xue Zhang, Ling-Xiao Zhao, Si-Qi Cheng, Ye-Fu Liu.
       BACKGROUND: Pancreatic adenocarcinoma (PDAC) is the most fatal malignant tumor that focuses on men and the elderly (40-85 years) and is aggressive. Its surgical resection rate is only 10-44%, and the rate of local recurrence in the retroperitoneum 1 year after surgery is as high as about 60%. The main reason for local recurrence in the majority of patients is that PDAC is perineural invasion (PNI) and the cancer cells infiltrate and grow along the peripancreatic nerve bundles. The identification of biomarkers associated with the diagnosis of PDAC may help to improve the current difficulty in early diagnosis of pancreatic cancer and guide clinical treatment. We constructed a co-culture model system of Schwann and PDCA cells to determined that Stearoyl Coenzyme A Desaturase (SCD) is a key gene driving the progress of PDAC.
    METHODS: Single-cell data files for PDAC were analyzed to compare cellular composition and subpopulation-specific gene expression between control (n = 4) and pancreatic cancer (n = 6). Among 36,277 cells, we obtained a total of 16 subpopulations, including a Neurons subpopulation, by UMAP analysis. Further screening by Mendelian randomization analysis yielded three pairs of key genes corresponding to eQTL-positive outcome causally, the corresponding genes were, in order: the three genes COL18A1, RASSF4, and SCD. Among them, SCD was significantly positively correlated with with the malignant progression of pancreatic cancer, and enriched in signaling pathways such as MTORC1_SIGNALING and P53-PATHWAY. In this study, We further applied CRISPR-Cas9 technology to knock out SCD expression in Schwann cells under co culture system to detect the growth status of PDAC cells.
    RESULTS: Three genes (COL18A1, RASSF4, SCD) showed significant correlation with PDAC. The identified SCD genes were positively correlated with the development of PDAC. We further demonstrated through experiments that SCD is overexpressed in PDAC tissues, and knocking down SCD in neuronal cells reduces the PDAC cells growth rate and migration ability.
    CONCLUSION: In this article, we demonstrated that the upregulation of SCD expression level in neuronal cells is related to the PDAC, and SCD may be a promising candidate for PDAC therapy.
    Keywords:  Mendelian randomization; Pancreatic ductal adenocarcinoma; Peripheral nerves
    DOI:  https://doi.org/10.1186/s12935-025-03682-5
  11. BMC Psychiatry. 2025 Feb 19. 25(1): 156
    Global prevalence and determinant factors of pain, depression, and anxiety among cancer patients: an umbrella review of systematic reviews and meta-analyses.
    Addisu Getie, Manay Ayalneh, Melaku Bimerew.
       INTRODUCTION: Depression and anxiety are prevalent psychological disorders that significantly affect physical, emotional, and social well-being, reducing quality of life and increasing medical costs. These issues are especially challenging for cancer survivors, complicating treatment management, affecting adherence, and potentially impacting survival rates. Thus, this umbrella review aimed to evaluate the global prevalence of pain, depression, and anxiety, as well as their determinants among cancer patients.
    METHOD: An exhaustive umbrella review was conducted to systematically assess the prevalence and determinants of pain, depression, and anxiety among cancer survivors worldwide by analyzing systematic reviews and meta-analyses. The review involved a thorough search of multiple databases and included studies published in English up to July 2024 that reported on these symptoms. The process involved screening and selecting studies based on specific criteria, assessing the risk of bias using the AMSTAR tool, and analyzing data with statistical methods to determine overall prevalence and identify predictors. This comprehensive approach aimed to provide a detailed understanding of these psychological issues in cancer survivors and guide future research and interventions.
    RESULT: The global summary prevalence of depression among cancer survivors was 33.16% (95% CI 27.59-38.74), while anxiety had a prevalence of 30.55% (95% CI 24.04-37.06). Pain prevalence after treatment was 39.77% (95% CI 31.84-47.70). Before treatment, 65.22% (95% CI 62.86-67.57) of cancer patients reported pain, which persisted in 51.34% (95% CI 40.01-62.67) during treatment. The analysis also found that during the COVID-19 pandemic, depression and anxiety rates among cancer patients were at their highest, with prevalences of 43.25% (95% CI 41.25-45.26) and 52.93% (95% CI 50.91-54.96), respectively.
    CONCLUSION: The umbrella review found that depression and anxiety prevalence among cancer survivors was 33.16% and 30.55%, respectively, with significantly higher rates during COVID-19 at 43.25% and 52.93%. Key factors contributing to depression included poor social support, advanced cancer stage, and inadequate sleep, while anxiety was significantly linked to advanced cancer stage and poor sleep quality.
    CLINICAL TRIAL NUMBER: Not applicable.
    Keywords:  Anxiety; Cancer; Cancer survivors; Depression; Meta-analysis; Oncology; Pain; Systematic review; Umbrella review
    DOI:  https://doi.org/10.1186/s12888-025-06599-5
  12. Front Pharmacol. 2025 ;16 1506552
    Schwann cells in regeneration and cancer.
    Lan Zhang, Jiale Xie, Wenyu Dai, Bing Lu, Sheng Yi.
      Schwann cells are specific peripheral glial cells with remarkable plasticity following peripheral nerve injury. Injury responses stimulate c-Jun activation in Schwann cells, drive epithelial-mesenchymal transition and cellular phenotypic changes, and induce the generation of reprogrammed repair Schwann cells to orchestrate peripheral nerve regeneration process. Schwann cells and/or Schwann cell-derived molecules are commonly used as supporting cells and/or neurotrophic factors to construct Schwann cell-based tissue-engineered nerve grafts for repairing severe peripheral nerve injury with long defects. Transplantation of Schwann cells and/or Schwann cell-derived molecules also serves as a helpful approach for the treatment of other injured tissues, such as the spinal cord, skin, digit tip, and bone. Schwann cells are not only associated with tissue regeneration but also involved in tumorigenesis and tumor progression. Schwann cells are the major cellular component of neurofibromatosis type 1 and the sole cell type in neurofibromatosis type 2 and schwannomatosis. In addition, Schwann cells also function as an important player in the tumor microenvironment and aid in the growth and invasiveness of many other solid cancers. In the present review, we outline the physiological and pathological activities of Schwann cells and discuss the functional roles of Schwann cells in homeostasis, regeneration, and cancer.
    Keywords:  Schwann cells; cell plasticity; tissue regeneration; tumor progression; tumorigenesis
    DOI:  https://doi.org/10.3389/fphar.2025.1506552
  13. Heliyon. 2025 Feb 15. 11(3): e42293
    The neuroscience in breast cancer: Current insights and clinical opportunities.
    Jia-Feng Wang, Meng-Chuan Wang, Lei-Lei Jiang, Neng-Ming Lin.
      The involvement of nerves in the development of breast cancer has emerged as a significant factor. Interaction between the nervous system and breast cancer can influence tumor initiation, growth, invasion, metastasis, reverse resistance to drugs, promote inflammation in tumors, and impair the immune system's ability to combat cancer. This review examined the intricate relationship linking the nervous system with breast cancer, emphasizing both central and peripheral aspects of the nervous system. Moreover, we reviewed neural cell factors and their impact on breast cancer progression, alongside the interactions between nerves and immunology, microbiota in breast cancer. Furthermore, the study discussed the potential of nerves as biomarkers for diagnosing and prognosticating breast cancer, and evaluated prospects for improving chemotherapy and immunotherapy therapeutic outcomes in breast cancer treatment. We hope to provide a deeper understanding of the neurobiological underpinnings of breast cancer and pave the way for the discovery of innovative therapeutic targets and prognostic markers.
    Keywords:  Breast cancer; Cancer neuroscience; Cancer treatment; Innervation; Neurotransmitter
    DOI:  https://doi.org/10.1016/j.heliyon.2025.e42293
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