The discovery of a class of long noncoding RNAs (lncRNAs), including lncRNAs of the small nucleolar RNA (snoRNA) host gene family, SNHG, has led to growing interest in the study of both snoRNAs themselves and the genes encoding them. Currently, of the 232 known snoRNA genes, only 32 have been confirmed to have lncRNAs. At the same time, a positive correlation has been shown between the expression of lncRNAs and snoRNAs encoded by a common host gene of the SNHG family. Thus, lncRNA of the SNHG1 gene correlates with snoRNAs SNORD22 and SNORD25-31, and lncRNA of the SNHG16 gene, with snoRNAs SNORD1A, SNORD1B, and SNORD1C. There is evidence that SNHG lncRNAs can participate in oncogenesis both through regulatory functions inherent to lncRNAs and by influencing ribosome biogenesis. At the same time, information has accumulated on the "extraribosomal" functions of snoRNAs. In addition to a brief excursion into the biological functions of snoRNAs and SNHG lncRNAs, we present a comprehensive review of data on the role of these two types of noncoding RNAs in the pathogenesis of ovarian cancer, the most insidious cancer of the female reproductive system. The influence of these regulatory RNAs on the main processes of ovarian oncogenesis, such as apoptosis, epithelial-mesenchymal transition, cell cycle control, and DNA methylation mechanisms in this type of cancer is considered. The prospects for clinical application of regulatory RNAs due to their influence on the level of drug resistance are also discussed.

The main functional parts of the glymphatic system are perivascular spaces and surrounding astrocytes. Cerebrospinal fluid enters the brain parenchyma from subarachnoid cisterns through perivascular Virchow-Robin spaces and passes into the interstitium through aquaporin channels in astrocytes. Then, cerebrospinal fluid removes metabolic products and mixes with interstitial fluid. Outflow of cerebrospinal fluid with metabolic products from the brain parenchyma occurs in three ways. The first route is periarterial through intermuscular spaces in the middle layer of cerebral arteries. The second route is perivenous. The third route is lymphatic through meningeal or sinus-associated lymphatic vessels. They provide drainage of macromolecules and immunocompetent cells from the brain to the cervical lymph nodes. Gliomas are accompanied by inhibition of normal cerebrospinal fluid outflow pathways, mainly due to additional intracranial tissue, and compensatory cerebrospinal fluid outflow along the spinal cord. Reduced cerebrospinal fluid release with impaired outflow contribute to accumulation of toxic metabolic products, proinflammatory cytokines and chemokines. Transport of antigens to lymph nodes is inhibited that disrupts antitumor immunity. Impaired cerebrospinal fluid circulation also reduces the effectiveness of intracranial drug delivery. One of the mechanisms of pathogenesis of glioma metastasis is based on migration of tumor cells along classical and meningeal lymphatic pathways. Damage to the latter contributes to metastasis.

The majority of meningiomas - benign tumors with an extremely low metastasis tendency. Only singular observations of extracranial metastasis of WHO Grade I benign meningiomas are described in the literature. Despite the intensive study of meningiomas' molecular biology, there are currently no reliable markers indicating the possibility of their metastasis.

Surgery of meningiomas of the craniocervical region is one of the most difficult parts of neurosurgery due to the closeness of the brainstem, caudal group of the cranial nerves (CNs) and vertebral artery. According to the literature, suffering of the caudal group of CNs is between 20 and 55% according to different authors. In their dysfunction, the recovery of CNs is long-term and requires joint efforts by both the medical team and the patient and his family.

Malignant transformation of fibrous dysplasia in McCune-Albright syndrome is observed in less than 1% of cases, thus osteosarcoma is developing more frequently. According to the search in the PubMed database over the last 5 years, 13 publications were found, but none of them described cerebral cranium damage.

Recent studies have revealed that the tumor microenvironment (TME) mediates neutrophil activation through multicomponent collaborative regulatory mechanisms, serving as a key driver of NETs formation. Cytokines, platelets, and complements activate neutrophil signaling pathways, ultimately forming NETs with protumorigenic properties in the TME. Notably, exogenous stimuli such as surgery, chronic stress, and pathogens can regulate NETs formation by remodeling the TME. However, the regulatory factors that induce NETs formation have not yet been systematically elucidated. Despite the identification of several factors that initiate the formation of NETs, the potential involvement of additional mechanisms remains inadequately understood. There is an urgent need for thorough mechanistic investigations utilizing cell lines and animal models in cancer. These studies will yield essential insights necessary for the formulation of targeted therapeutic approaches. This review delves into the mechanisms behind neutrophil extracellular traps (NETs) formation, tumor microenvironmental regulation of NETs formation, and exogenous stimuli that mediate tumor biological behaviors by inducing NETs. Gaining insight into these mechanisms will enhance our understanding of NETs and aid in crafting more precise strategies to inhibit tumor progression.

Phosphatidylcholine (PC), a core component of eukaryotic cell membranes essential for maintaining membrane integrity, has emerged as a critical regulator in oncogenic metabolic reprogramming. Accumulating evidence reveals that dysregulated PC metabolism constitutes a central mechanism driving malignant tumor progression. This review systematically delineates the biosynthetic pathways (Kennedy pathway, PEMT pathway, Lands cycle) and catabolic processes (phospholipase-mediated hydrolysis via PLA2, PC-PLC, and PLD) governing PC homeostasis. We highlight how PC metabolic networks orchestrate pro-tumorigenic effects via multifaceted mechanisms, such as enhancing membrane biosynthesis to support rapid tumor proliferation, activating some proliferative signaling cascades coupled with apoptosis suppression, remodeling the immunosuppressive microenvironment, et al. Notably, small-molecule inhibitors targeting key PC metabolic enzymes (e.g., RSM-932A, FIPI) demonstrate promising anti-tumor efficacy in preclinical models, though therapeutic outcomes are constrained by metabolic plasticity and tumor heterogeneity. By integrating recent advances in lipidomics and spatial metabolomics, this synthesis not only deciphers the evolutionary logic underlying PC-driven oncogenesis but also proposes innovative therapeutic strategies combining metabolic inhibitors with immune checkpoint modulators. Our analysis provides a conceptual framework for targeting phospholipid vulnerabilities in cancer, paving the way for precision oncology applications.

Pancreatic carcinosarcoma is a rare and aggressive malignancy that can mimic pancreatic adenocarcinomas in presentation but often has different disease biology and different responses to conventional treatment for pancreatic adenocarcinoma. Case reports have documented a 5-year overall survival of approximately 13% only if the disease is caught at an earlier stage and is amenable to multi-modality treatment, including surgery, chemotherapy, and radiation. In the advanced stage, treatments do not often provide benefit, and patients may decline rapidly. There are currently no studies demonstrating survival benefits with chemotherapy in patients with metastatic carcinosarcoma, owing to both the rarity and the often late diagnosis of this aggressive entity. We present a case of a 71-year-old male patient diagnosed with metastatic pancreatic carcinosarcoma who received four lines of palliative-intent treatment: gemcitabine and nab-paclitaxel, modified FOLFIRINOX, GTX, and doxorubicin. With careful selection of chemotherapeutic regimen as well as his ability to tolerate four lines of treatment, this resulted in an unprecedented 26-month survival. We also reviewed the literature on the histopathology, diagnosis, and treatment of this rare entity.

Since cancer is often linked to the aging process, the importance of cellular senescence in cancer has come under the spotlight. While senescence in cancer cells can serve as a natural barrier against cancer due to its proliferation arrest, its secretory phenotypes and alterations in the surface proteome can paradoxically promote or suppress tumor progression. Senescent cancer-associated fibroblasts, endothelial cells, and immune cells can also contribute to cancer promotion. During therapeutic interventions for cancer, not only their therapeutic effects, but also therapy-induced senescence may have an impact on cancer outcomes. Senotherapeutics, therapy targeting senescent cells, have been reported as novel cancer therapy in recent studies, and the combination of senescence induction and senotherapeutics has been increasingly recognized. Although some clinical trials of senotherapeutic drugs for cancer with or without senescence-inducible therapy are ongoing, there is as yet no satisfactory clinical application. With further research into targeting senescence in oncology, it is expected that senotherapeutics, particularly in combination with senescence-inducing therapy, will become a novel therapeutic strategy.

Pulmonary carcinoids (PCs) are rare neoplasms involving typical and atypical carcinoids (TCs and ACs), defined histologically by absent or focal necrosis and mitotic counts (<2/mm2 vs. 2-10/mm2), respectively. Although uncommon overall, TCs and ACs represent the most frequent non-hematologic malignancies in the pediatric population. However, significantly less is known about PC in AYAs, a population often overlooked or analyzed within pediatric or adult cohorts. In this critical review, we analyzed existing literature on PCs in the AYA population using a question-and-answer format, emphasizing the substantial gap in current knowledge in this field and the urgent unmet clinical need for future scientific proposals. First, we analyzed epidemiology and the data availability about the association between PCs in AYA patients and genetic syndromes that typically reach the maximal diagnostic incidence within this age group. We then reviewed the available literature about the pathologic characteristics, clinical presentation, and treatment strategies for localized and metastatic disease in PC AYA patients. According to our findings, a significant lack of age-specific evidence and the need for international collaboration and prospective, AYA-focused clinical studies were underscored. Advancing research in this area is essential to improve understanding and develop tailored, evidence-based therapeutic approaches for this peculiar population.

Ferroptosis suppressor protein 1 (FSP1) has emerged as a critical regulator of ferroptosis, an iron-dependent form of programmed cell death with significant therapeutic potential in cancer treatment. Despite rapidly expanding research, current knowledge on FSP1 remains fragmented across various tumor types and experimental contexts. The aim of this review is to systematically integrate the latest evidence regarding the molecular structure, biological functions, and regulatory mechanisms controlling FSP1 expression, emphasizing its involvement in tumor progression and resistance to therapy. Readers can expect comprehensive coverage of FSP1's structural characteristics, enzymatic roles, transcriptional and post-transcriptional regulation, and its pathological significance in hepatocellular carcinoma, colorectal cancer, pancreatic cancer, gastric cancer, breast cancer, lung cancer, and leukemia. We further evaluate emerging therapeutic strategies targeting FSP1 aimed at overcoming resistance and improving clinical outcomes. Relevant studies were systematically identified by searching PubMed, Web of Science, and Embase databases, focusing particularly on the recent and impactful literature to guide future research directions.

The treatment landscape for EGFR-mutated metastatic non-small cell lung cancer (mNSCLC) has evolved significantly with multiple combination regimens demonstrating superiority over single agent Osimertinib over the past two years. Recent trials such as FLAURA2 and MARIPOSA have explored intensified front-line regimens, with FLAURA2 demonstrating improvement in PFS with the addition of chemotherapy to Osimertinib and MARIPOSA, showing both a PFS and OS benefit with a novel combination regimen of Amivantamab and Lazertinib. However, these regimens are associated with significantly higher toxicity to patients and pose a huge financial and logistical burden to the health care system; therefore, treatment selection must therefore be individualized, considering disease biology, patient fitness, and toxicity burden. Post-progression strategies remain challenging due to resistance mechanisms like EGFR C797S mutations and MET amplification and the lack of data post-progression on novel first-line combinations. Ongoing trials are investigating fourth-generation EGFR TKIs, MET inhibitors, antibody-drug conjugates, and bispecific antibodies in subsequent lines. While regimens like Amivantamab-Lazertinib show promise even in second-line settings, toxicity, cost, and access remain barriers. As therapeutic options expand, biomarker-driven sequencing and personalized care will be critical to optimizing long-term outcomes in EGFR-mutated mNSCLC.

Treatment of locally advanced rectal cancer (LARC), clinical stages II-III, typically involves multimodal treatment options. Over the past decade, the role of radiation therapy as a neoadjuvant treatment for LARC has evolved and is currently a part of total neoadjuvant therapy (TNT). Some recently published studies advocate for the omission of radiation therapy entirely, while others report on a non-operative approach that emphasizes the use of higher radiation therapy doses. This review aims to evaluate the latest literature on the current role of radiation therapy in the management of LARC, with a discussion of how to best select the most appropriate treatment protocol based on individual patient and tumor characteristics, comorbidities, and personal needs and preferences.

Dose-dense chemotherapy shortens the interval between chemotherapy cycles and has shown improved outcomes in high-risk breast cancer patients. We retrospectively evaluated the efficacy and safety of dose-dense chemotherapy in 80 breast cancer patients treated at our hospital from 2020 to 2024. The regimen included epirubicin and cyclophosphamide followed by paclitaxel or docetaxel, with pegfilgrastim support. The overall treatment completion rate was 82.5%. Of the 80 patients, 55 underwent neoadjuvant chemotherapy, and the pathological complete response rate was significantly higher in triple-negative breast cancer (59.1%) compared to that in luminal-type cancer (9.1%). Common adverse events included anemia, liver dysfunction, myalgia, and peripheral neuropathy. Febrile neutropenia occurred in 8.8% of patients, with some cases linked to pegfilgrastim body pod use, particularly in individuals with low subcutaneous fat. Notably, two patients developed pneumocystis pneumonia, potentially associated with steroid administration. Despite these toxicities, most were manageable and resolved after treatment. Our findings support the efficacy of dose-dense chemotherapy, particularly in triple-negative breast cancer, while highlighting the importance of individualized supportive care and vigilance regarding hematologic and infectious complications.

The treatment landscape of metastatic hormone-sensitive prostate cancer (mHSPC) has transformed significantly with the advent of triplet therapy involving androgen deprivation therapy (ADT), docetaxel, and androgen receptor signalling inhibitors (ARSIs). While clinical guidelines increasingly support early intensification, real-world practice remains challenged by patient heterogeneity, evolving evidence, and limited consensus on treatment sequencing. This narrative review integrates evidence from landmark trials, clinical guidelines, and expert insights from oncologists managing mHSPC in India. Findings affirm that triplet therapy, particularly with darolutamide, improves survival in high-volume disease and underscores the need for personalized treatment based on disease burden, comorbidities, and genomic profiles. The review also highlights gaps in real-world data, sequencing strategies, and biomarker-driven therapy, reinforcing the need for precision medicine and locally relevant evidence to guide treatment. Ultimately, optimizing mHSPC management requires harmonizing guideline-based approaches with individualized, real-world decision making to improve patient outcomes.

At diagnosis, metastatic prostate cancer (PC) is sensitive to androgen deprivation therapy (ADT), and patients are usually referred to as having castration-sensitive prostate cancer (mCSPC). The combination of ADT and androgen receptor pathway inhibitors (ARPI) is the current standard of care for mCSPC. This study aimed to review the literature on economic evaluations and health economic models related to mCSPC. A literature search was performed covering Medline, Embase, and Scopus with additional grey literature sources. Studies with data on health economic evaluations focusing on Europe or North America were relevant. 18 peer-reviewed articles and 10 grey literature documents were included. The majority (n = 23) had a deterministic Markov structure and applied either Markov cohort or partitioned survival models. Evaluations investigated various types of ADT-based combinations, comparing the addition of ARPI, chemotherapy agents, or radiation therapy to ADT alone. We concluded that economic evaluations in the field of PC are widely published, and there are a large number of publications even in the specific subgroup of mCSPC. Regardless of the investigated interventions, most studies applied similar methodologies and simulated patients from the mCSPC state until the development of mCRPC or death.

Tissue-resident memory T (TRM) cells have emerged as critical sentinels in the control of cancer metastasis, yet their precise roles across different tumor types and tissues remain underappreciated. Here, we review current insights into the mechanisms governing TRM cell seeding and retention in pre-metastatic niches, their effector functions in eliminating disseminated tumor cells, and their dynamic crosstalk with local stromal and myeloid populations. Here, we highlight evidence for organ-specific variability in TRM cell-mediated immunity, discuss strategies for therapeutically harnessing these cells-ranging from vaccination and checkpoint modulation to chemokine axis manipulation-and explore their promise as prognostic biomarkers. Finally, we outline key knowledge gaps and future directions aimed at translating TRM cell biology into targeted interventions to prevent and treat metastatic disease.

Post-translational modifications (PTMs) of proteins, as the core mechanism for dynamically regulating follicular development, affect the maintenance of mammalian fertility by precisely coordinating granulosa cell-oocyte interaction, metabolic reprogramming, and epigenetic remodeling. Dysregulation of these modifications directly contributes to major reproductive diseases, including polycystic ovary syndrome (PCOS) and premature ovarian insufficiency (POI). Post-translational modifications regulate follicular development through intricate mechanisms. Thus, this review systematically synthesizes recent advances in PTMs, encompassing traditional ones such as phosphorylation, ubiquitination, and acetylation, alongside emerging modifications including lactylation, SUMOylation, and ISGylation, thereby constructing a more comprehensive PTM landscape of follicular development. Furthermore, this study dissects the molecular interaction networks of these PTMs during follicular activation, maturation, and ovulation, and uncovers the common mechanisms through which PTM dysregulation contributes to pathological conditions, including hyperandrogenism in PCOS and follicular depletion in POI. Finally, this review ultimately provides a theoretical basis for improving livestock reproductive efficiency and precise intervention in clinical ovarian diseases.

Uterine fibroids are benign smooth muscle tumors that affect ~70% of women, with Black women being affected at a disproportionate rate. The growth of these tumors is driven by estrogen and progesterone. Driver mutations in genes such as MED12, HMGA2, and FH also play roles in the development and growth of fibroids. Despite their high prevalence, the pathogenesis of fibroids remains largely unknown, leading to a lack of effective therapeutic options. Non-coding RNAs (ncRNAs), including miRNAs (e.g., miR-21, miR-29, miR-200), lncRNAs (e.g., H19, MIAT, XIST), and circRNAs, are important regulatory RNAs that are becoming increasingly implicated in the aberrant expression of protein-coding genes functionally associated with ECM production, cell proliferation, apoptosis, and inflammation in fibroids. Race/ethnicity, MED12 mutations, and ovarian steroids influence the expression of ncRNA expression, further implicating their relevance to fibroid pathogenesis. Therapeutic targeting of these dysregulated ncRNAs in fibroids could enable more precise and individualized non-hormonal-based treatment for this common gynecologic tumor.

Cancer cells predominantly utilize aerobic glycolysis for energy production, preferentially converting glucose (Glu) to pyruvate (PA) and subsequently to lactate (LA). This metabolic reprogramming results in extracellular LA accumulation, acidifying the tumor microenvironment (TME) and facilitating tumor invasion and metastasis. The dynamics of Glu, PA, and LA are pivotal to tumor initiation and progression. This review comprehensively discussed therapeutic strategies targeting these key metabolites and systematically evaluates electrochemical and fluorescence-based techniques for their dynamic monitoring. We highlight the critical role of these monitoring approaches in advancing early cancer diagnosis, enabling personalized treatment, and accelerating anticancer drug development.