Single cell and spatial transcriptomics highlight the interaction of club-like cells with immunosuppressive myeloid cells in prostate cancer DOI Creative Commons
Antti Kiviaho, Sini K. Eerola, Heini Kallio

и другие.

Nature Communications, Год журнала: 2024, Номер 15(1)

Опубликована: Ноя. 16, 2024

Abstract Prostate cancer treatment resistance is a significant challenge facing the field. Genomic and transcriptomic profiling have partially elucidated mechanisms through which cells escape treatment, but their relation toward tumor microenvironment (TME) remains elusive. Here we present comprehensive landscape of prostate TME at multiple points in standard timeline employing single-cell RNA-sequencing spatial transcriptomics data from 120 patients. We identify club-like as key epithelial cell subtype that acts an interface between immune system. Tissue areas enriched with depleted androgen signaling upregulated expression luminal progenitor markers. Club-like display senescence-associated secretory phenotype presence linked to increased polymorphonuclear myeloid-derived suppressor (PMN-MDSC) activity. Our results indicate are associated myeloid inflammation previously deprivation therapy resistance, providing rationale for therapeutic targeting.

Язык: Английский

Aging and cancer DOI Creative Commons
Léa Montégut, Carlos López-Otı́n, Guido Kroemer

и другие.

Molecular Cancer, Год журнала: 2024, Номер 23(1)

Опубликована: Май 18, 2024

Abstract Aging and cancer exhibit apparent links that we will examine in this review. The null hypothesis aging coincide because both are driven by time, irrespective of the precise causes, can be confronted with idea share common mechanistic grounds referred to as ‘hallmarks’. Indeed, several hallmarks also contribute carcinogenesis tumor progression, but some molecular cellular characteristics may reduce probability developing lethal cancer, perhaps explaining why very old age (> 90 years) is accompanied a reduced incidence neoplastic diseases. We discuss possibility process itself causes meaning time-dependent degradation supracellular functions accompanies produces byproduct or ‘age-associated disease’. Conversely, its treatment erode health drive process, has dramatically been documented for survivors diagnosed during childhood, adolescence, young adulthood. conclude connected superior including endogenous lifestyle factors, well bidirectional crosstalk, together render not only risk factor an important parameter must considered therapeutic decisions.

Язык: Английский

Процитировано

43

Complexity made easy: Aggregation‐induced emission small molecules for cancer diagnosis and phototherapies DOI Creative Commons

Luojia Chen,

Si‐Ling Chen,

Yuncong Yuan

и другие.

Aggregate, Год журнала: 2024, Номер unknown

Опубликована: Сен. 2, 2024

Abstract Phototheranostics has garnered sustained attention due to its significant potential for revolutionizing conventional cancer treatment strategies. While being one of the most commonly employed strategies constructing phototheranostic systems by engineering integration photosensitizers (PSs) into nanosystems, nano‐PSs face challenges including complexity in preparation process, low delivery efficiency, and toxicity issues. Contrastingly, burgeoning popularity small molecule PSs characterized aggregation‐induced emission (AIE) become evident arena phototheranostics. This preference is underscored their well‐defined structures, adjustable photophysical properties, toxicity. Therefore, acquiring profound insights pioneering strides achievable through a solitary PS with AIE tumor phototheranostics paramount scientific significance. In this review, we will discuss recent progress properties diagnosis phototherapies representative examples, guided ethos “Complexity made easy”. We also look forward future development direction molecules, central objective advancing research focal emphasis on simplicity, expeditiousness, safety.

Язык: Английский

Процитировано

10

Deciphering mechanical cues in the microenvironment: from non-malignant settings to tumor progression DOI Creative Commons
Yi‐Cheng Zhu,

Jiaoshun Chen,

Chen Chen

и другие.

Biomarker Research, Год журнала: 2025, Номер 13(1)

Опубликована: Янв. 23, 2025

The tumor microenvironment functions as a dynamic and intricate ecosystem, comprising diverse array of cellular non-cellular components that precisely orchestrate pivotal behaviors, including invasion, metastasis, drug resistance. While unraveling the interplay between behaviors represents tremendous challenge, recent research illuminates crucial biological phenomenon known mechanotransduction. Within microenvironment, mechanical cues like tensile stress, shear stiffness play role by activating mechanosensitive effectors such PIEZO proteins, integrins, Yes-associated protein. This activation initiates cascades intrinsic signaling pathways, effectively linking physical properties tissues to their physiological pathophysiological processes morphogenesis, regeneration, immunity. mechanistic insight offers novel perspective on how within impact behaviors. intricacies are yet be fully elucidated, it exhibits distinct attributes from non-malignant tissues, elevated solid stresses, interstitial hypertension, augmented matrix stiffness, enhanced viscoelasticity. These traits exert notable influences progression treatment responses, enriching our comprehension multifaceted nature microenvironment. Through this innovative review, we aim provide new lens decipher contexts, broadening knowledge these factors promote or inhibit thus offering valuable insights identify potential targets for anti-tumor strategies.

Язык: Английский

Процитировано

1

Convergent inducers and effectors of T cell paralysis in the tumour microenvironment DOI
Douglas Hanahan, Olivier Michielin, Mikaël J. Pittet

и другие.

Nature reviews. Cancer, Год журнала: 2024, Номер unknown

Опубликована: Окт. 24, 2024

Язык: Английский

Процитировано

6

Emerging strategies to investigate the biology of early cancer DOI
Ran Zhou, Xiwen Tang, Yuan Wang

и другие.

Nature reviews. Cancer, Год журнала: 2024, Номер 24(12), С. 850 - 866

Опубликована: Окт. 21, 2024

Язык: Английский

Процитировано

5

Exposomal determinants of non-genetic plasticity in tumor initiation DOI

Davide Carra,

Silvana C. E. Maas, José A. Seoane

и другие.

Trends in cancer, Год журнала: 2025, Номер unknown

Опубликована: Фев. 1, 2025

Язык: Английский

Процитировано

0

Aromatics from fossil fuels and breast cancer DOI Creative Commons
Leena Hilakivi‐Clarke,

Theresa Krista Jolejole,

Joas Lucas da Silva

и другие.

iScience, Год журнала: 2025, Номер unknown, С. 112204 - 112204

Опубликована: Март 1, 2025

Polycyclic aromatic hydrocarbons (PAHs) from fossil fuels initiate breast cancer in animal models, and humans a link between PAH exposure risk has been established. In women, it takes approximately two decades for PAH-exposed cells to progress diagnosable cancer, the needs happen during time window when is vulnerable PAHs. Further, not everyone exposed high levels of PAHs develops cancer. are most likely lead initiation among individuals who were utero through pregnant mothers environmental pollutants or maternal obesity both. These early life exposures shown increase daughter's later susceptibility by causing daughter (1) an number structures which place, (2) suppression, perhaps epigenetically, ability repair DNA damage caused inhibiting expression tumor suppressor genes, (3) persistent gut dysbiosis, then impacts immune microenvironment. Among that may be volatile BTEX compounds. Thus, aromatics involved efforts should directed toward reducing human these compounds prevent

Язык: Английский

Процитировано

0

A Multifunctional Fluorescent Probe: Selective Visualization of Mitochondria and Tumor Cells with Viscosity/Polarity Responsiveness DOI
Fengjun Hu,

Fawei Zhu,

Lei Yang

и другие.

Sensors and Actuators B Chemical, Год журнала: 2025, Номер unknown, С. 137644 - 137644

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0

Oncometabolites at the crossroads of genetic, epigenetic and ecological alterations in cancer DOI Creative Commons
Letizia Lanzetti

Cell Death and Differentiation, Год журнала: 2024, Номер unknown

Опубликована: Окт. 23, 2024

Abstract By the time a tumor reaches clinical detectability, it contains around 10 8 –10 9 cells. However, during formation, significant cell loss occurs due to death. In some estimates, could take up thousand generations, over ~ 20-year life-span of tumor, reach which would correspond “theoretical” generation ~10 30 These rough calculations indicate that cancers are under negative selection. The fact they thrive implies “evolve”, and their evolutionary trajectories shaped by pressure environment. Evolvability cancer is function its heterogeneity, be at genetic, epigenetic, ecological/microenvironmental levels [1]. principles were summarized in proposed classification Evo (evolutionary) Eco (ecological) indexes used label index addresses cell-autonomous heterogeneity (genetic/epigenetic). describes ecological landscape (non-cell-autonomous) terms hazards survival resources available. reciprocal influence components critical, as can trigger self-sustaining loops shape evolvability [2]. Among various hallmarks [3], metabolic alterations appear unique intersect with both components. This partly because altered metabolism leads accumulation oncometabolites. oncometabolites have traditionally been viewed mediators non-cell-autonomous microenvironment. now increasingly recognized inducers genetic epigenetic modifications. Thus, uniquely positioned crossroads cancer. this review, mechanisms action will summarized, together roles phenotypic evolvability. An perspective impact on natural history presented.

Язык: Английский

Процитировано

4

Clinical research framework proposal for ketogenic metabolic therapy in glioblastoma DOI Creative Commons
Tomás Duraj,

Miriam Kalamian,

Giulio Zuccoli

и другие.

BMC Medicine, Год журнала: 2024, Номер 22(1)

Опубликована: Дек. 5, 2024

Abstract Glioblastoma (GBM) is the most aggressive primary brain tumor in adults, with a universally lethal prognosis despite maximal standard therapies. Here, we present consensus treatment protocol based on metabolic requirements of GBM cells for two major fermentable fuels: glucose and glutamine. Glucose source carbon ATP synthesis growth through glycolysis, while glutamine provides nitrogen, carbon, glutaminolysis. As no can grow without anabolic substrates or energy, simultaneous targeting glycolysis glutaminolysis expected to reduce proliferation if not all cells. Ketogenic therapy (KMT) leverages diet-drug combinations that inhibit glutaminolysis, signaling shifting energy metabolism therapeutic ketosis. The glucose-ketone index (GKI) standardized biomarker assessing biological compliance, ideally via real-time monitoring. KMT aims increase substrate competition normalize microenvironment GKI-adjusted ketogenic diets, calorie restriction, fasting, also glycolytic glutaminolytic flux using specific inhibitors. Non-fermentable fuels, such as ketone bodies, fatty acids, lactate, are comparatively less efficient supporting long-term bioenergetic biosynthetic demands cancer cell proliferation. proposed strategy may be implemented synergistic priming baseline well other tumors driven by regardless their residual mitochondrial function. Suggested best practices provided guide future research oncology, offering shared, evidence-driven framework observational interventional studies.

Язык: Английский

Процитировано

4