Molecular Biotechnology, Journal Year: 2023, Volume and Issue: unknown
Published: Dec. 25, 2023
Language: Английский
Molecular Biotechnology, Journal Year: 2023, Volume and Issue: unknown
Published: Dec. 25, 2023
Language: Английский
Cancer Letters, Journal Year: 2025, Volume and Issue: unknown, P. 217539 - 217539
Published: Feb. 1, 2025
Language: Английский
Citations
2Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15
Published: Feb. 16, 2024
The nervous and immune systems are the primary sensory interfaces of body, allowing it to recognize, process, respond various stimuli from both external internal environment. These work in concert through mechanisms neuro-immune crosstalk detect threats, provide defense against pathogens, maintain or restore homeostasis, but can also contribute development diseases. Among peripheral neurons (PSNs), nociceptive PSNs particular interest. They possess a remarkable capability noxious periphery transmit this information brain, resulting perception pain activation adaptive responses. Pain is an early symptom cancer, often leading its diagnosis, major source distress for patients as disease progresses. In review, we aim overview within tumors that likely induce cancer pain, exploring range factors etiological elements cellular molecular mediators. addition transmitting central system, capable, when activated, produce release neuropeptides (e.g., CGRP SP) their terminals. have been shown modulate immunity cases inflammation, infection, cancer. PSNs, found solid tumors, play significant role tumor microenvironment, potentially influencing growth anti-tumor discuss current state knowledge about degree innervation tumors. We seek understand whether how may influence associated different mouse models Finally, extent which able functions innervate it.
Language: Английский
Citations
14Oncology Reviews, Journal Year: 2025, Volume and Issue: 18
Published: Jan. 20, 2025
Worldwide, head and neck cancers (HNCs) account for approximately 900,000 cases 500,000 deaths annually, with their incidence continuing to rise. Carcinogenesis is a complex, multidimensional molecular process leading cancer development, in recent years, the role of nerves pathogenesis various malignancies has been increasingly recognized. Thanks abundant innervation region, peripheral nervous system gained considerable interest its possible development progression HNCs. Intratumoral parasympathetic, sympathetic, sensory nerve fibers are emerging as key players potential targets novel anti-cancer pain-relieving medications different tumors, including This review explores nerve-cancer interactions, perineural invasion (PNI), cancer-related axonogenesis, neurogenesis, reprogramming, an emphasis on mechanisms, mediators clinical implications. PNI, adverse histopathologic feature, widely investigated However, prognostic value remains debated due inconsistent results when classified dichotomously (present/absent). Emerging evidence suggests that quantitative qualitative descriptions PNI may better reflect usefulness. The also examines therapies targeting crosstalk highlights influence HPV status tumor innervation. By synthesizing current knowledge, challenges, future perspectives, this offers insights into basis involvement HNCs therapeutic approaches.
Language: Английский
Citations
1Cancers, Journal Year: 2024, Volume and Issue: 16(3), P. 648 - 648
Published: Feb. 2, 2024
Chronic intractable pain affects a large proportion of cancer patients, especially those with metastatic bone disease. Blocking sensory afferents for relief represents an attractive alternative to opioids and other drugs acting in the CNS that nerve blockers are not addictive do affect mental state patient. A distinct subpopulation expresses capsaicin receptor TRPV1. Intrathecal resiniferatoxin, ultrapotent analog, ablates TRPV1-expressing endings exposed cerebrospinal fluid, resulting permanent analgesia women cervical metastasis pelvic bone. High-dose patches effective killers patients chemotherapy-induced peripheral neuropathic pain. However, gaps remain our knowledge since mechanisms by which activates TRPV1 essentially unknown. Most important, it is clear whether or denervation mediated agonists progression. In murine model breast cancer, desensitization was reported accelerate By contrast, resiniferatoxin found block melanoma growth. These observations imply blockade may be indicated some cancers contraindicated others. this review, we explore current field compare analgesic potential antagonism afferent patients.
Language: Английский
Citations
7MedComm, Journal Year: 2024, Volume and Issue: 5(11)
Published: Oct. 31, 2024
Abstract Cancer neuroscience is an emerging field that investigates the intricate relationship between nervous system and cancer, gaining increasing recognition for its importance. The central governs development of directly affects brain tumors, peripheral (PNS) shapes tumor microenvironment (TME) tumors. Both systems are crucial in cancer initiation progression, with recent studies revealing a more role PNS within TME. Tumors not only invade nerves but also persuade them through remodeling to further promote malignancy, creating bidirectional interaction cancers. Notably, immune cells contribute this communication, forming triangular influences protumor inflammation effectiveness immunotherapy. This review delves into mechanisms connecting focusing on how various cell types influence nerve‒tumor interactions, emphasizing clinical relevance nerve‒immune dynamics. By deepening our understanding interplay nerves, cells, has potential reshape biology insights, inspire innovative therapies, improve outcomes patients.
Language: Английский
Citations
6Biomolecules, Journal Year: 2023, Volume and Issue: 13(6), P. 983 - 983
Published: June 13, 2023
Both sensory neurons and immune cells, albeit at markedly different levels, express the vanilloid (capsaicin) receptor, Transient Receptor Potential, Vanilloid-1 (TRPV1). Activation of TRPV1 channels in afferent nerve fibers induces local effector functions by releasing neuropeptides (most notably, substance P) which, turn, trigger neurogenic inflammation. There is good evidence that chronic activation or inactivation this inflammatory pathway can modify tumor growth metastasis. expression was also demonstrated a variety mammalian including lymphocytes, dendritic macrophages neutrophils. Therefore, effects agonists antagonists may vary depending on prominent cell type(s) activated and/or inhibited. comprehensive understanding activity cells endings distinct locations necessary to predict outcome therapies targeting channels. Here, we review neuro-immune modulation cancer metastasis, with focus consequences cells. Lastly, potential use modulators therapy discussed.
Language: Английский
Citations
14Cancer Letters, Journal Year: 2025, Volume and Issue: 612, P. 217492 - 217492
Published: Jan. 21, 2025
Language: Английский
Citations
0Journal of Translational Medicine, Journal Year: 2025, Volume and Issue: 23(1)
Published: Feb. 28, 2025
Neural infiltration has been found in various cancers and the infiltrating nerves influence tumor growth dissemination. In non-small cell lung cancer, pan-neuronal marker PGP9.5 was detected by immunohistochemical staining its high expression correlated with poor prognosis. However, existence of nerve fibers mechanism driving neural remains unclear. We first used to assess density patients adenocarcinoma different sizes. Following that, we performed differential analysis univariate Cox prognostic analysis, using public datasets experiments identify gene that triggers is associated cancer progression unfavorable Finally, molecular biology a subcutaneous model were deeply analyze regulates progression. patients, positive within tumors larger than 2 cm diameter significantly higher smaller cm. Bioinformatics suggested NGEF, KIF4A, PABPC1 could be genes trigger are Subsequent co-culture neurons showed increased NGEF cells enhanced axonal neurons. Meanwhile, GSE30219 indicated exhibiting levels sizes, lymph node involvement, reduced overall survival rates. At level mechanisms, knockdown Ephrin-A3 ND7/23 or use ALW-II-41-27 resulted significant decrease neurite outgrowth when co-cultured LA795 cells. animal model, overexpression promoted fibers, these effects inhibited ALW-II-41-27. facilitates through Ephrin-A3/EphA2 pathway, suggesting promising target for disrupting interactions between tumors. Biomaterials focus on anticipated potential treatment option cancer.
Language: Английский
Citations
0Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Journal Year: 2024, Volume and Issue: 1879(4), P. 189121 - 189121
Published: May 23, 2024
Language: Английский
Citations
3International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(4), P. 3671 - 3671
Published: Feb. 12, 2023
Cancer is the leading cause of death and represents a significant economic burden worldwide. The numbers are constantly growing as result increasing life expectancy, toxic environmental factors, adoption Western lifestyle. Among lifestyle stress related signaling pathways have recently been implicated in development tumors. Here we present some epidemiological preclinical data concerning stress-related activation ß-adrenoreceptors (ß-ARs), which contributes to formation, sequential transformation, migration different tumor cell types. We focused our survey on research results for breast lung cancer, melanoma, gliomas published past five years. Based converging evidence, conceptual framework how cancer cells hijack physiological mechanism involving ß-ARs toward positive modulation their own survival. In addition, also highlight potential contribution ß-AR tumorigenesis metastasis formation. Finally, outline antitumor effects targeting ß-adrenergic pathways, methods primarily include repurposed ß-blocker drugs. However, call attention emerging (though yet largely explorative) method chemogenetics, has great suppressing growth either by selectively modulating neuronal groups involved responses affecting or directly manipulating specific (e.g., ß-AR) receptors its microenvironment.
Language: Английский
Citations
7