Current Oncology Reports最新文献

Purpose of review: Mesenteric fibrosis (MF) is a hallmark of small intestinal neuroendocrine neoplasms (SI-NEN) and is frequently associated with significant morbidity due to related complications such as intestinal obstruction, ischemia, and cachexia.

Recent findings: Herein we performed a systematic review to discuss the development of MF in SI-NEN. The pathophysiological mechanisms acknowledged as causative for the development of MF include the major components of the tumor microenvironment, such as fibroblasts, endothelial and immune cells and the extracellular matrix, which are involved in a complex interplay activating several signaling pathways that promote profibrotic factors and induce both a desmoplastic reaction and tumor proliferation. Surgery remains the mainstay of treatment, while several medical management options of MF complicating SI-NEN available present rather limited efficacy. MF is a frequent characteristic of SI-NEN that requires particular attention and targeted management to avoid complications.

Introduction: Men from culturally and linguistically diverse (CALD) backgrounds face challenges in accessing equitable and quality healthcare. However, little is known about the patterns of care among men diagnosed with prostate cancer (PCa) from CALD backgrounds. We aimed to map the available literature on patterns of care and treatment outcomes in men from CALD backgrounds who have PCa.

Methods: We used the Johanna Briggs Institute scoping review methodology. We searched five bibliographic databases (Ovid MEDLINE, EMBASE, SCOPUS, CINAHL, and Ovid Emcare) and grey literature. We explored patterns of PCa care extending from screening and early detection to end-of-life care and treatment outcomes.

Results: A total of 7,148 records were identified; 58 studies were included. Most studies were from the United States (US) (n = 41) and used ethnic origin (n = 14), nativity (n = 10), immigration history (n = 11), or country of birth (n = 13) as indicators of CALD. Most studies focused on screening and early detection for PCa (n = 37), specifically prostate-specific antigen (PSA) testing. Twelve papers were on PCa treatment (e.g., surgery, radiation therapy, and active surveillance), five on follow-up and supportive care, and four on treatment outcomes (i.e., change in measured PSA and PCa cancer-specific survival). There were disparities in the PCa care continuum and treatment outcomes between CALD and non-CALD patients. Factors influencing screening and early detection for PCa were systematically summarised and most addressed individual-level determinants.

Conclusions: Key findings from our scoping review emphasised the existence of guideline-discordant care, disparities in PCa screening test use, and differences in PCa treatment received among men from CALD backgrounds. However, little is known about patterns of care in diagnostic modalities, treatment phases, and palliative and end-of-life care.

Purpose of review: The introduction of PSMA-PET/CT scans is expected to increase the incidence of clinically lymph node-positive metastatic hormone-sensitive prostate cancer (mHSPC). The 8th AJCC-TNM classify disease with metastasis limited to pelvic nodes (cN1M0) and nonregional lymph nodes (M1a) as stage IV. To date, there is limited prospective evidence for management of this subgroup. Additionally, no specific recommendations currently exist for managing M1a as a distinct condition but as a part of CHAARTED low volume disease (LVD). Our review examines relevant results from phase III trials examining the management of clinically positive nodal disease over the last decade.

Recent findings: STAMPEDE is the only phase III trial that gave recent data about cN1M0 and isolated M1a management. Cohort sub-analysis of the control arm showed improved failure-free survival after local radiotherapy (RT) plus Androgen Deprivation Therapy (ADT), while metastasis-free survival benefit from Abiraterone Acetate with Prednisolone (AAP) addition was noted when compared to standard of care (SOC), awaiting the overall survival (OS) benefit result. The STAMPEDE H arm showed a marginal significance of M1a stratified OS after RT. Future trials, including PEARLS, ALADDIN and STAMPEDE2, are expected to offer more insights. Interventional Phase III trials directed to clinically node positive patients are still needed to aid deciding on the best management, and nodal metastasis number and size impact on prognosis.

Purpose of review: Isocitrate dehydrogenase wild-type glioblastoma is an extremely aggressive and fatal primary brain tumour, characterised by extensive heterogeneity and diffuse infiltration of brain parenchyma. Despite multimodal treatment and diverse research efforts to develop novel therapies, there has been limited success in improving patient outcomes. Constructing physiologically relevant preclinical models is essential to optimising drug screening processes and identifying more effective treatments.

Recent findings: Traditional in-vitro models have provided critical insights into glioblastoma pathophysiology; however, they are limited in their ability to recapitulate the complex tumour microenvironment and its interactions with surrounding cells. In-vivo models offer a more physiologically relevant context, but often do not fully represent human pathology, are expensive, and time-consuming. These limitations have contributed to the low translational success of therapies from trials to clinic. Organoid and glioblastoma-on-a-chip technology represent significant advances in glioblastoma modelling and enable the replication of key features of the human tumour microenvironment, including its structural, mechanical, and biochemical properties. Organoids provide a 3D system that captures cellular heterogeneity and tumour architecture, while microfluidic chips offer dynamic systems capable of mimicking vascularisation and nutrient exchange. Together, these technologies hold tremendous potential for high throughput drug screening and personalised, precision medicine. This review explores the evolution of preclinical models in glioblastoma modelling and drug screening, emphasising the transition from traditional systems to more advanced organoid and microfluidic platforms. Furthermore, it aims to evaluate the advantages and limitations of both traditional and next-generation models, investigating their combined potential to address current challenges by integrating complementary aspects of specific models and techniques.

Purposeof review: Poly (ADP-ribose) polymerases (PARPs) are enzymes essential for detecting and repairing DNA damage through poly-ADP-ribosylation. In cancer, cells with deficiencies in homologous recombination repair mechanisms often become more dependent on PARP-mediated repair mechanisms to effectively repair dsDNA breaks. As such, PARP inhibitors (PARPis) were introduced into clinical practice, serving as a key targeted therapy option through synthetic lethality in the treatment of cancers with homologous recombination repair deficiency (HRD). Though PARPis are currently approved in the adjuvant setting for several cancer types such as ovarian, breast, prostate and pancreatic cancer, their potential role in the neoadjuvant setting remains under investigation. This review outlines the rationale for using PARPi in the neoadjuvant setting and evaluates findings from early and ongoing clinical trials.

Recent findings: Our analysis indicates that numerous studies have explored PARPi as a neoadjuvant treatment for HRD-related cancers. The majority of neoadjuvant PARPi trials have been performed in breast and ovarian cancer, while phase II/III evidence supporting efficacy in prostate and pancreatic cancers remains limited. Studies are investigating PARPi in the neoadjuvant setting of HRD-related cancers. Future research should prioritize combination strategies with immune checkpoint inhibitors and expand outcome measures to include patient satisfaction and quality-of-life metrics.

Purpose of this review: Acute leukemia (AL) is a hematological neoplasm with rapid progression that affects nutritional status of patients. Assessing nutrition in patients with haematological malignancies poses challenges due to the rapid progression of the disease, the variety of methods for evaluating malnutrition. In this review we will provide evidence of the need of early malnutrition diagnosis thru timely assessment and the implications of malnutrition in patients evolution in patients with AL.

Recent findings: The prevalence of malnutrition ranging from 15 to 26.5% among patients with AL. It is well known that inflammation and cytokine production have been recognized as potential mechanisms of CCS in hematologic malignancies. Regardless of the mechanism underlying Cancer Cachexia Syndrome (CCS) in AML, patients undergoing conditioning chemotherapy and during transplant or antineoplastic treatment. In addition to this, patients with AL undergoing chemotherapy frequently face two main challenges: oral mucositis (OM) and neutropenic colitis (NC). Both conditions challenge nutrition intake and nutrients absorption which make them more susceptible to have nutritional deficits. Malnutrition in patients with acute leukemia face a higher risk of therapy failure, increased rates of relapse, and higher mortality rates. Nutritional status impact patient's prognosis in many ways, malnutrition increases risk of antineoplastic treatment toxicities, hospital stay, and cost, as well reduces quality of life and this condition worsens patient's prognosis.

Purpose of review: While the oncogenic potential of HPV has been well-established in other disease sites (e.g. cervix, vulva, anus), it is increasingly evident that a significant proportion of oropharyngeal cancer cases are related to the virus. Although considerable progress has been made in the understanding of this disease with respect to its underlying biology and clinical behavior, numerous questions persist. From a therapeutic standpoint, HPV-positive oropharyngeal cancer has been shown to be more radiosensitive than HPV-negative disease. However, how HPV mediates this radiosensitivity is relatively uncertain.

Recent findings: Given that it has been firmly established that patients with HPV-positive oropharyngeal cancer have a significantly improved prognosis as a result of their exquisite response to radiation and can be treated with less-than-standard doses, logical questions pertain to how HPV confers this benefit to infected patients. Although the exact reason for the improved radiosensitivity of HPV-positive oropharyngeal carcinoma is unclear, multiple theories have been proposed. Indeed, it is likely that no single explanation exists for the increased radiosensitivity, and instead, HPV likely exerts its influence through a cascade of activated pathways at both the cellular level and tumor microenvironment. As will be discussed in this review, the proposed mechanisms for HPV-induced radiation response have generally centered on the disruption of such cellular pathways as DNA repair, cell cycle checkpoints, metabolic-induced stress, immunology, and cancer stem cells. Given that HPV-positive oropharyngeal cancer is increasingly recognized as a public health problem, the search to better understand its unique biological radiosensitivity has important societal and treatment-related implications.

Purpose of review: to explore a paradigm shift in the definition of opioid-responsive cancer pain in this hypothesis-driven review. Opioid-responsive cancer pain may be misplaced within the definition of chronic pain, chronic pain takes three months to establish, early effective control is worthwhile to achieve. RECENT: findings, from a bench-to-bed perspective, debates the interpretation of results supporting the hypothesis that opioid-responsive cancer pain could remain 'constant acute pain', with explanations, best solutions, for tolerance and/or addiction, in cancer patients compared to those with chronic pain from other conditions. Unraveling the unique apparent properties of opioid-responsive cancer pain empowers knowledge of the process by which acute pain may have the potential to remain acute in nature and not transition into chronic pain. Findings outlined defend the hypothesis of probable sustained acute nature of opioid-responsive cancer pain, importance of early, sustained pain control, opioid reduction and further exploration of this hypothesis in clinical practice.

Purpose of review: The growth modulation index (GMI) is defined as the ratio between the time to progression of a new line of treatment and the previous line. This ratio can be used to determine whether the new line of treatment brings a clinical benefit. It has been proposed as an outcome in trials evaluating non-cytotoxic drugs. Its interest lies in the intra-patient comparison. The terminology employed to refer to the GMI, as well as its definitions, are highly variable in the literature. Some uses of the GMI are arbitrary and not based on any scientific rationale. Our aim is to describe how the GMI is reported in the scientific literature.

Recent findings: We carried out a scoping review using PubMed, Scopus, Web of Science and BASE (Bielefeld Academic Search Engine). The algorithm was composed of the terms "growth modulation index", "time to progression ratio" and "progression-free survival ratio". Documents in English, with full-text available, published up to 2023, were included. Among 227 included documents, 166 of which discussed GMI specifically. On these 166 documents, 76 reported on observational studies, 62 on interventional studies and 17 on methodological or statistical developments pertaining to the GMI. All were about oncology. Our review highlights significant variability in the reporting and use of the GMI. To address this, we propose standardized reporting guidelines. Additionally, we emphasize the need for methodological and statistical developments to improve the use of the GMI and to develop novel GMI-based trial designs.

Each year, over 84,000 young people in the United States are diagnosed with cancer. These patients face unique burdens that defy historical "adolescent and young adult" and "early-onset cancer" silos. These groups share common vulnerabilities, including financial toxicity, disruptions to education and career development, and inadequate survivorship care. Research efforts to address these shared challenges remain inefficient due to parallel and uncoordinated investigations. Health policy decisions are similarly impacted, with the lack of a unified framework potentially leading to gaps in insurance coverage, disparities in resource allocation, and incomplete data collection on young people diagnosed with cancer. To address these challenges, a collaborative and integrated strategy across clinical care, research, and health policy is urgently needed. By unifying efforts and recognizing the shared experiences of young people with cancer, we can develop more effective support systems, optimize outcomes, and reduce the long-term burden of cancer for this fast-growing and vulnerable population.