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Urological cancers including those of the prostate, bladder, and kidney, are prevalent and often lethal malignancies besides other less common ones like testicular and penile cancers. Current treatments have major limitations like side effects, recurrence, resistance, high costs, and poor quality of life. Nanotechnology offers promising solutions through enhanced diagnostic accuracy, targeted drug delivery, controlled release, and multimodal imaging. This review reflects clinical challenges and nanomedical advances across major urological cancers. In prostate cancer, nanoparticles improve delineation and radiosensitization in radiation therapy, enable fluorescent guidance in surgery, and enhance chemotherapy penetration in metastatic disease. Nanoparticles also overcome bladder permeability barriers to increase the residence time of intravesical therapy and chemotherapy agents. In renal cancer, nanocarriers potentiate tyrosine kinase inhibitors and immunotherapy while gene vectors and zinc oxide nanoparticles demonstrate antiproliferative effects. Across modalities, urological applications of nanomedicine include polymeric, liposomal, and metal nanoparticles for targeted therapy, prodrug delivery, photodynamic therapy, and thermal ablation. Biosafety assessments reveal favorable profiles but clinical translation remains limited, necessitating further trials. In conclusion, nanotechnology holds significant potential for earlier detection, precise intervention, and tailored treatment of urological malignancies, warranting expanded research to transform patient outcomes. [ABSTRACT FROM AUTHOR]

Nuclear factor erythroid 2 (NF-E2)-related factor 3 (NFE2L3), amember of the CNCbZIP subfamily and widely found in a variety of tissues, is an endoplasmic reticulum (ER) membrane-anchored transcription factor that can be released from the ER and moved into the nucleus to bind the promoter region to regulate a series of target genes involved in antioxidant, inflammatory responses, and cell cycle regulation in response to extracellular or intracellular stress. Recent research, particularly in the past 5 years, has shed light on NFE2L3's participation in diverse biological processes, including cell differentiation, inflammatory responses, lipid homeostasis, immune responses, and tumor growth. Notably, NFE2L3 has been identified as a key player in the development and prognosis of multiple cancers including colorectal cancer, thyroid cancer, breast cancer, hepatocellular carcinoma, gastric cancer, renal cancer, bladder cancer, esophageal squamous cell carcinoma, T cell lymphoblastic lymphoma, pancreatic cancer, and squamous cell carcinoma. Furthermore, research has linked NFE2L3 to other cancers such as lung adenocarcinoma, malignant pleural mesothelioma, ovarian cancer, glioblastoma multiforme, and laryngeal carcinoma, indicating its potential as a target for innovative cancer treatment approaches. Therefore, to gain a better understanding of the role of NFE2L3 in disease, this review offers insights into the discovery, structure, function, and recent advancements in the study of NFE2L3 to lay the groundwork for the development of NFE2L3-targeted cancer therapies. [ABSTRACT FROM AUTHOR]

The three most common kinds of urologic malignancies are prostate, bladder, and kidney cancer, which typically cause substantial morbidity and mortality. Early detection and effective treatment are essential due to their high fatality rates. As a result, there is an urgent need for innovative research to improve the clinical management of patients with urologic cancers. A type of small noncoding RNAs of 22 nucleotides, microRNAs (miRNAs) are well-known for their important roles in a variety of developmental processes. Among these, microRNA-21 (miR-21) stands out as a commonly studied miRNA with implications in tumorigenesis and cancer development, particularly in urological tumors. Recent research has shed light on the dysregulation of miR-21 in urological tumors, offering insights into its potential as a prognostic, diagnostic, and therapeutic tool. This review delves into the pathogenesis of miR-21 in prostate, bladder, and renal cancers, its utility as a cancer biomarker, and the therapeutic possibilities of targeting miR-21. [ABSTRACT FROM AUTHOR]

Membrane-type metalloproteinases (including MMP-14 and MMP-15) are enzymes involved in the degradation of extracellular matrix components. In cancer, they are involved in processes such as cellular invasion, angiogenesis and metastasis. Therefore, the aim of this study was to evaluate the expression, content and activity of MMP-14 and MMP-15 in human renal cell carcinoma. Samples of healthy kidney tissue (n = 20) and tissue from clear-cell kidney cancer (n = 20) were examined. The presence and contents of the MMPs were assessed using Western blot and ELISA techniques, respectively. Their activity—both actual and specific—was evaluated using fluorimetric analysis. Both control and cancer human kidney tissues contain MMP-14 and MMP-15 enzymes in the form of high-molecular-weight complexes. Moreover, these enzymes occur in both active and latent forms. Their content in cancer tissues is very similar, but with a noteworthy decrease in content with an increase in the kidney cancer grade for both membrane-type metalloproteinases. Even more notable is the highest content of the investigated enzymes represented by MMP-14 in the control tissues. Considering the actual and specific activity outcomes, MMP-14 dominates over MMP-15 in all of the investigated tissues. Nevertheless, we also noted a significant enhancement of the activity of both metalloproteinases with an increase in the grade of renal cancer. The expression and activity of both enzymes were detected in all examined renal cancer tissues. However, our findings suggest that transmembrane metalloproteinase 14 (MMP-14) plays a much more significant and essential role than MMP-15 in the studied renal carcinoma tissues. Therefore, it seems that MMP-14 could be a promising target in the diagnosis, prognosis and therapy of renal cell carcinoma. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to assess the awareness of genitourinary cancers risk factors among adults in Poland and to identify factors associated with public awareness of risk factors for genitourinary cancers. Methods: This cross-sectional survey was carried out between 1 and 4 March 2024 in a nationwide sample of 2,165 adults in Poland. Quota sampling was used. Data were collected using computer-assisted web interview (CAWI) method. Results: Regardless of the type of cancer (kidney, bladder, or prostate cancer), a family history of cancer was the most recognized risk factor indicated by over half of respondents. Over one-third were aware that chemical exposure increases the risk for bladder cancer (39.4%) or prostate cancer (34.2%). Smoking was recognized as a risk factor for kidney cancer by 40.6% of respondents. Female gender, having higher education, being occupationally active and the presence of chronic diseases were the most important factors (p < 0.05) associated with a higher level of awareness of genitourinary cancers risk factors. Conclusion: This study revealed gaps in public awareness of genitourinary cancers risk factors among adults in Poland, especially lifestyle-related and workplace-related risk factors. [ABSTRACT FROM AUTHOR]

Background: The role of hemoglobin (HGB) in common malignant tumors remains unclear. Methods: A retrospective analysis was conducted to identify the correlation between HGB levels and risk of 15 malignant tumors using 50,085 samples from the National Health and Nutrition Examination Survey. Mendelian Randomization analyses (MRAs) were performed based on genome-wide association study data to assess the causal relationship between HGB levels and these malignant tumors using more than 700,000 samples. The robustness of the MRA results was confirmed through various analytical methods. Fifty-six in-house samples were used to investigate the correlation between HGB levels and the prognosis in prostate cancer (PRCA) using the Kaplan-Meier curve. Results: High HGB levels were associated with a higher risk for patients with cervix cancer, melanoma, and non-melanoma skin cancer (OR > 1.000, p < 0.05). It served as a protective factor for colon cancer, esophagus cancer, stomach cancer, bone cancer, lung cancer, renal cancer, and PRCA (OR < 1.000, p < 0.05). Furthermore, MRAs suggested that elevated HGB levels were correlated with a reduced risk of PRCA (OR = 0.869, p < 0.05), with no significant association observed between this marker and the remaining 14 malignant tumors. No pleiotropy or heterogeneity was found in the ultimate results for MRAs (p-values > 0.05), suggesting the robustness of the results. The results derived from the in-house data revealed a relationship between higher HGB values and a more favorable prognosis in PRCA (p < 0.05). Conclusion: High circulating HGB levels may play a protective prognostic role for PRCA and serve as a protective factor against the occurrence of PRCA. [ABSTRACT FROM AUTHOR]

In this review, we aim to provide a comprehensive assessment of the evolving landscape of the perioperative management in renal cell carcinoma (RCC), emphasizing its dynamic and intricate nature. We explore academic and clinical insights into the perioperative treatment paradigm of RCC. Up-to-date treatment options are discussed and the evolving role of neoadjuvant and adjuvant therapy in RCC is highlighted. [ABSTRACT FROM AUTHOR]

Introduction: This article examines the potential of using liquid biopsy with piRNAs to study cancer survival outcomes. While previous studies have explored the relationship between piRNA expression and cancer patient outcomes, a comprehensive investigation is still lacking. To address this gap, we conducted a systematic review and meta-analysis of existing literature. Methods: We searched major online databases up to February 2024 to identify articles reporting on the role of piRNA in cancer patient survival outcomes. Our meta-analysis used a random-effects model to pool hazard ratios with 95% confidence intervals (CI) and assess the prognostic value of deregulated piRNA-823. For survival analysis, the Kaplan–Meier method and COX analysis were used. Results: Out of 6104 articles screened, 20 met our inclusion criteria. Our analysis revealed that dysregulated piRNA expression is associated with cancer patient survival outcomes. Specifically, our meta-analysis found that overexpression of piR-823 is significantly linked with poorer overall survival in patients with colorectal cancer and renal cell cancer (HR: 3.82, 95% CI = [1.81, 8.04], I2 = 70%). Conclusion: Our findings suggest that various piRNAs may play a role in cancer survival outcomes and that piRNA-823 in particular holds promise as a prognostic biomarker for multiple human cancers. Implications for cancer survivors: Our systematic review and meta-analysis of piRNA-823 has important implications for cancer survivors. Our findings suggest that piRNA-823 can be used as a prognostic biomarker for predicting cancer recurrence and survival rates. This information can help clinicians develop personalized treatment plans for cancer survivors, which can improve their quality of life and reduce the risk of recurrence. [ABSTRACT FROM AUTHOR]

Background: Systemic inflammation and glucose metabolism have been closely related to the survival of cancer patients. Therefore, we aimed to evaluate whether preoperative glucose-to-lymphocyte ratio (GLR) can be used to predict the survival of cancer patients. Methods: We retrospectively examined 2172 cancer patients who underwent surgery from January 1, 2014, to December 31, 2016. There were 240 patients with non-small cell lung cancer (NSCLC), 378 patients with colorectal cancer (CRC), 221 patients with breast cancer (BC), 335 patients with gastric cancer (GC), 270 patients with liver cancer, 233 patients with esophageal cancer (EC), 295 patients with renal cancer, and 200 patients with melanoma. The formula for preoperative GLR calculation was as follows: GLR=glucose/lymphocyte count. The overall survival (OS) was estimated using the Kaplan-Meier method. The predictive factors for OS were determined using multivariate analysis. Results: The Kaplan-Meier analysis showed that the median survival time in the high-GLR group was much shorter than that of those in the low-GLR group for different cancers. Cox multivariate regression analysis reveals that preoperative GLR was an independent factor for predicting overall survival in different tumor types. Conclusion: Elevated preoperative GLR was remarkably associated with a poorer prognosis in patients with NSCLC, CRC, breast cancer, gastric cancer, kidney cancer, liver cancer, esophageal cancer, and melanoma. Preoperative GLR promises to be an essential predictor of survival for cancer patients. [ABSTRACT FROM AUTHOR]

Purpose: The 5-year cancer survival rate among Chinese patients is lower than that among patients in developed countries and varies widely across geographic regions. The aim of this study was to analyse the 5-year relative cancer survival rate in southeastern China, between 2011 and 2021. Patients and Methods: We utilised population-based statistics from 12 cancer registries in Fujian, China. Study population data were up to date as of Dec 31, 2019, and survival outcome status was updated as of Dec 31, 2021. We used the ICD-10 and the ICD-O-3 to categorize all cancer cases. We analysed the 5-year relative survival for cancers combined and different cancer types stratified by sex, urban and rural areas, and age. Survival estimates were stratified according to calendar period (2011– 13, 2014– 15, 2016– 18 and 2019– 21). Results: Ultimately, a total of 160,294 cancer patients were enrolled in the study. In 2011– 13, 2014– 15, 2016– 18 and 2019– 21, the age-standardised 5-year relative survival for cancers combined were 29.1% (95% CI: 28.6– 29.7), 31.5% (95% CI: 31.0– 32.0), 36.8% (95% CI: 36.4– 37.3) and 39.1% (95% CI: 38.7– 39.6), respectively. The age-standardised 5-year relative survival for lung, prostate, larynx, colon-rectum, kidney and bone cancers increased 4.3%, 4.0%, 3.8%, 3.4%, 3.4% and 2.70%, respectively. Cancers with high 5-year relative survival rates (> 60%) in 2019– 21 included thyroid, testis, breast, bladder, cervix, prostate and uterus cancers. The 5-year survival rates in 2019– 2021 was higher for females than for males (47.8% vs 32.0%) and higher in urban areas than in rural areas (41.7% vs 37.1%). Relative survival rates decreased with increasing age. Conclusion: The 5-year cancer survival in Fujian Province increased between 2011 and 2021 but remained at a low level. Building a strong primary public health system may be a key step in reducing the cancer burden in Fujian Province. [ABSTRACT FROM AUTHOR]

Several large cohort studies in cardiovascular disease (CVD) patients have shown an increased incidence of cancer. Previous studies in a myocardial infarction (MI) mouse model reported increased colon, breast, and lung cancer growth. The potential mechanisms could be due to secreted cardiokines and micro-RNAs from pathological hearts and immune cell reprogramming. A study in a MI-induced heart failure (HF) mouse demonstrated an increase in cardiac expression of SerpinA3, resulting in an enhanced proliferation of colon cancer cells. In MI-induced HF mice with lung cancer, the attenuation of tumor sensitivity to ferroptosis via the secretion of miR-22-3p from cardiomyocytes was demonstrated. In MI mice with breast cancer, immune cell reprogramming toward the immunosuppressive state was shown. However, a study in mice with renal cancer reported no impact of MI on tumor growth. In addition to MI, cardiac hypertrophy was shown to promote the growth of breast and lung cancer. The cardiokine potentially involved, periostin, was increased in the cardiac tissue and serum of a cardiac hypertrophy model, and was reported to increase breast cancer cell proliferation. Since the concept that CVD could influence the initiation and progression of several types of cancer is quite new and challenging regarding future therapeutic and preventive strategies, further studies are needed to elucidate the potential underlying mechanisms which will enable more effective risk stratification and development of potential therapeutic interventions to prevent cancer in CVD patients. [ABSTRACT FROM AUTHOR]

Background: Urinary tract cancers including bladder, kidney, ureter, and pelvis are a common malignancy worldwide with high mortality ratio. Aimed to investigate the prevalence of these cancers, we conducted this study. Methods: In this study, all the information related to ICD10 codes, gender, age and province of residence of individuals were obtained from the data of Iran's cancer registry by the Ministry of Health, Medicine and Medical Education and demographic evidence for each sub-country from the reports of Statistics Center of Iran (SCI). Also, the data of two Iranian national survey studies CASPIAN-III, IV, and V (information related to the care and prevention of non-communicable diseases (NCD) in childhood and adolescence) and STEPs (including information on NCD in adults over 18 years old) were used. The data was analyzed using Poisson regression with mixed effects to estimate the incidence of cancers. Results: Bladder and kidney neoplasm are the most common cancers of the urinary system in Iran. The prevalence of bladder cancer has increased from 5.82 to 11.50 per 100,000 individuals. The increasing trend is growing faster in men compared with women. The incidence of kidney neoplasm has increased over the years (2.03 in 2005 vs. 7.02 in 2020 per 100,000). Having a higher incidence ratio compared with bladder cancer, kidney cancer is responsible for 35.06% of all urinary cancers in 2020 compared with 23.71% in 2005. Both neoplasms of the ureter and renal pelvis were recorded rarely and with lower incidence in both sexes during this period. Conclusion: Considering the increasing trend in the incidence of urinary neoplasms in Iran during these years, the advantage of focusing on the risk of urinary cancers is highlighted. Therefore, investigating the prevalence and incidence of urinary cancers to plan and manage these cancers will result in prevention and reduction of the disease burden on the Iranian society. Future studies in this field can help in the prevention and well-timed diagnosis of these cancers. [ABSTRACT FROM AUTHOR]

Introduction: Polygenic score (PGS) is a valuable method for assessing the estimated genetic liability to a given outcome or genetic variability contributing to a quantitative trait. While polygenic risk scores are widely used for complex traits, their application in uncovering shared genetic predisposition between phenotypes, i.e., when genetic variants influence more than one phenotype, remains limited. Methods: We developed an R package, comorbidPGS, which facilitates a systematic evaluation of shared genetic effects among (cor)related phenotypes using PGSs. The comorbidPGS package takes as input a set of single nucleotide polymorphisms along with their established effects on the original phenotype (Po), referred to as Po-PGS. It generates a comprehensive summary of effect(s) of Po-PGS on target phenotype(s) (Pt) with customisable graphical features. Results: We applied comorbidPGS to investigate the shared genetic predisposition between phenotypes defining elevated blood pressure (systolic blood pressure, SBP; diastolic blood pressure, DBP; pulse pressure) and several cancers (breast cancer; pancreatic cancer, PanC; kidney cancer, KidC; prostate cancer, PrC; colorectal cancer, CrC) using the European ancestry UK Biobank individuals and GWAS meta-analyses summary statistics from independent set of European ancestry individuals. We report a significant association between elevated DBP and the genetic risk of PrC (β [SE] = 0.066 [0.017], p value = 9.64 × 10−5), as well as between CrC PGS and both, lower SBP (β [SE] = −0.10 [0.029], p value = 3.83 × 10−4) and lower DBP (β [SE] = −0.055 [0.017], p value = 1.05 × 10−3). Our analysis highlights two nominally significant relationships for individuals with genetic predisposition to elevated SBP leading to higher risk of KidC (OR [95% CI] = 1.04 [1.0039–1.087], p value = 2.82 × 10−2) and PrC (OR [95% CI] = 1.02 [1.003–1.041], p value = 2.22 × 10−2). Conclusion: Using comorbidPGS, we underscore mechanistic relationships between blood pressure regulation and susceptibility to three comorbid malignancies. This package offers valuable means to evaluate shared genetic susceptibility between (cor)related phenotypes through polygenic scores. [ABSTRACT FROM AUTHOR]

Persistent unilateral nasal obstruction with recurrent epistaxis in an adult should raise suspicion of malignancy. Renal cell carcinoma accounts for 90% of all renal malignancies but rarely manifests as a nasal mass. We describe a case of clear cell renal cell carcinoma metastasizing to the nasal cavity. [ABSTRACT FROM AUTHOR]

Clear cell renal cell carcinoma (KIRC) is the most common subtype of renal cell carcinoma (RCC). This form of cancer is characterized by resistance to traditional therapies and an increased likelihood of metastasis. A major factor contributing to the pathogenesis of KIRC is the alteration of metabolic pathways. As kidney cancer is increasingly considered a metabolic disease, there is a growing need to understand the enzymes involved in the regulation of metabolism in tumorigenic cells. In this context, our research focused on glycine N-acyltransferase (GLYAT), an enzyme known to play a role in various metabolic diseases and cancer. Here, through a bioinformatic analysis of public databases, we performed a characterization of GLYAT expression levels in KIRC cases. Our goal is to evaluate whether GLYAT could serve as a compelling candidate for an in-depth study, given its pivotal role in metabolic regulation and previously established links to other malignancies. The analysis showed a marked decrease in GLYAT expression in all stages and grades of KIRC, regardless of mutation rates, suggesting an alternative mechanism of regulation along the tumor development. Additionally, we observed a hypomethylation in the GLYAT promoter region and a negative correlation between the expression of the GLYAT and the levels of cancer-associated fibroblasts. Finally, the data show a correlation between higher levels of GLYAT expression and better patient prognosis. In conclusion, this article underscores the potential of GLYAT as a diagnostic and prognostic marker in KIRC. [ABSTRACT FROM AUTHOR]

Numerous immunotherapeutic agents, such as immune checkpoint inhibitors (ICIs), have been approved for the treatment of genitourinary (GU) malignancies. While ICIs have improved treatment outcomes and expanded treatment options, they can cause immune-related adverse events (irAEs). The scope of irAEs is broad, and this paper aims to review the rheumatologic side effects associated with immunotherapy drugs approved for bladder cancer and renal cell carcinoma. IrAEs are graded by the common terminology criteria for adverse events (CTCAE), which ranges from 1 to 5. The management of irAEs includes corticosteroids or other immunosuppressive therapies, and it may require discontinuation of immunotherapy. Several real world experience studies suggest that most patients with pre-existing autoimmune diseases treated with ICI did not have to discontinue treatment due to immune-mediated side effects. While data suggest autoimmune side effects are manageable, patients with pre-existing autoimmune diseases are often excluded from immunotherapy clinical trials. Better understanding of these irAEs will improve its safety and expand its use in those with underlying autoimmune disease.

It is quite unusual to have numerous primary malignant tumors at the same time in the same patient. These cancers are classified as metachronous or synchronous. The occurrence of synchronous urologic tumors poses diagnostic and treatment challenges and has always been a subject of controversy in the clinical decision-making process. Unfortunately, no clear standardized management protocols for these patients exist. Therefore, diagnosis and treatment may be difficult, especially with few resources. We present a 75-year-old man with simultaneous prostate and kidney cancers successfully treated at our center. This is one of the rare cases in the English literature with two primary urologic cancers. [ABSTRACT FROM AUTHOR]

Inflammation is a crucial pathological feature in cancers and kidney diseases, playing a significant role in disease progression. Cyclin-dependent kinases CDK4 and CDK6 not only contribute to cell cycle progression but also participate in cell metabolism, immunogenicity and anti-tumor immune responses. Recently, CDK4/6 inhibitors have gained approval for investigational treatment of breast cancer and various other tumors. Kidney diseases and cancers commonly exhibit characteristic pathological features, such as the involvement of inflammatory cells and persistent chronic inflammation. Remarkably, CDK4/6 inhibitors have demonstrated impressive efficacy in treating non-cancerous conditions, including certain kidney diseases. Current studies have identified the renoprotective effect of CDK4/6 inhibitors, presenting a novel idea and potential direction for treating kidney diseases in the future. In this review, we briefly reviewed the cell cycle in mammals and the role of CDK4/6 in regulating it. We then provided an introduction to CDK4/6 inhibitors and their use in cancer treatment. Additionally, we emphasized the importance of these inhibitors in the treatment of kidney diseases. Collectively, growing evidence demonstrates that targeting CDK4 and CDK6 through CDK4/6 inhibitors might have therapeutic benefits in various cancers and kidney diseases and should be further explored in the future. [ABSTRACT FROM AUTHOR]

Background: Pathogenic germline variants (PGVs) can play a vital role in the oncogenesis process in carriers. Previous studies have recognized that PGVs contribute to early onset of tumorigenesis in certain cancer types, for example, colorectal cancer and breast cancer. However, the reported prevalence data of cancer‐associated PGVs were highly inconsistent due to nonuniform patient cohorts, sequencing methods, and prominent difficulties in pathogenicity interpretation of variants. In addition to the above difficulties, due to the rarity of cases, the prevalence of cancer PGV carriers in young cancer patients affected by late‐onset cancer types has not been comprehensively evaluated to date. Methods: A total of 131 young cancer patients (1–29 years old at diagnosis) were enrolled in this study. The patients were affected by six common late‐onset cancer types, namely, lung cancer, liver cancer, colorectal cancer, gastric cancer, renal cancer, and head–neck cancer. Cancer PGVs were identified and analyzed. based on NGS‐based targeted sequencing followed by bioinformatic screening and strict further evaluations of variant pathogenicity. Results: Twenty‐three cancer PGVs in 21 patients were identified, resulting in an overall PGV prevalence of 16.0% across the six included cancer types, which was approximately double the prevalence reported in a previous pancancer study. Nine of the 23 PGVs are novel, thus expanding the cancer PGV spectrum. Seven of the 23 (30.4%) PGVs are potential therapeutic targets of olaparib, with potential implications for clinical manipulation. Additionally, a small prevalence of somatic mutations of some classic cancer hallmark genes in young patients, in contrast to all‐age patients, was revealed. Conclusion: This study demonstrates the high prevalence of PGVs in young cancer patients with the common late‐onset cancers and the potentially significant clinical implications of cancer PGVs, the findings highlight the value of PGV screening in young patients across lung cancer, liver cancer, colorectal cancer, gastric cancer, renal cancer, or head–neck cancer. [ABSTRACT FROM AUTHOR]

Although the impact of circadian timing on immunotherapy has yet to be integrated into clinical practice, chronoimmunotherapy is an emerging and promising field as circadian oscillations are observed in immune cell numbers as well as the expression of immunotherapy targets, e.g., programmed cell death protein-1 and its ligand programmed death ligand 1. Concurrent retrospective studies suggest that morning infusions may lead to higher effectiveness of immune checkpoint inhibitors in melanoma, non-small cell lung cancer, and kidney cancer. This paper discusses the results of a retrospective study (2016–2022) exploring the impact of infusion timing on the outcomes of all 73 patients with stage IV melanoma receiving immunotherapy at a particular medical center. While the median overall survival (OS) was 24.2 months (95% confidence interval [CI] 9.04–39.8), for a median follow-up of 15.3 months, our results show that having more than 75% of infusions in the afternoon results in shorter median OS (14.9 vs. 38.1 months; hazard ratio 0.45 [CI 0.23–0.86]; p < 0.01) with more expressive impacts on particular subgroups: women, older patients, and patients with a lower tumor burden at the outset of immunotherapy. Our findings highlight the potential benefits of follow-up validation in prospective and translational randomized studies. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate AT1-R expression in normal and cancerous human kidneys, how these expressions are modified, and AT1-R functionality. AT-1R mRNA expression, determined by real-time PCR, was detected in all samples. AT-1R mRNA increased in well-differentiated cancer (G1, p < 0.01) and decreased 2.9-fold in undifferentiated cancer (G4, p < 0.001) compared with normal kidney tissues. Immunocytochemistry analysis showed that the AT-1R was expressed in the normal tubular epithelium. The glomerulus was also immunoreactive, and as expected, the smooth muscle cells of the vessel walls also expressed the receptor. A total of 35 out of 42 tumors were AT-1R positive, with the cell tumors showing varying numbers of immunoreactive cells, which were stained in a diffuse cytoplasmic and membranous pattern. Computer-assisted counting of the stained tumor cells showed that the number of AT-1R-positive cells increased in the well-differentiated cancers. The functionality of AT-1R was assessed in primary cultures of kidney epithelial cells obtained from three G3 kidney cancer tissues and corresponding histologically proven non-malignant tissue adjacent to the tumor. Indeed, Ang II stimulated, in a dose-dependent manner, the 24 h proliferation of normal kidney cells and cancer cells in the primary culture and phosphorylated extracellular regulated kinases 1 and 2. In conclusion, Ang II may be involved in the growth or function of neoplastic kidney tissue. [ABSTRACT FROM AUTHOR]

Cancer stem cells are the root cause of cancer, which, in essence, is a developmental disorder. All-trans retinoic acid (ATRA) signaling via ligand-activation of the retinoic acid receptors (RARs) plays a crucial role in tissue patterning and development during mammalian embryogenesis. In adults, active RARγ maintains the pool of hematopoietic stem cells, whereas active RARα drives myeloid cell differentiation. Various findings have revealed that ATRA signaling is deregulated in many cancers. The enzymes for ATRA synthesis are downregulated in colorectal, gastric, lung, and oropharyngeal cancers. ATRA levels within breast, ovarian, pancreatic, prostate, and renal cancer cells were lower than within their normal counterpart cells. The importance is that 0.24 nM ATRA activates RARγ (for stem cell stemness), whereas 100 times more is required to activate RARα (for differentiation). Moreover, RARγ is an oncogene regarding overexpression within colorectal, cholangiocarcinoma, hepatocellular, ovarian, pancreatic, and renal cancer cells. The microRNA (miR) 30a-5p downregulates expression of RARγ, and miR-30a/miR-30a-5p is a tumor suppressor for breast, colorectal, gastric, hepatocellular, lung, oropharyngeal, ovarian, pancreatic, prostate, and renal cancer. These complementary findings support the view that perturbations to ATRA signaling play a role in driving the abnormal behavior of cancer stem cells. Targeting ATRA synthesis and RARγ has provided promising approaches to eliminating cancer stem cells because such agents have been shown to drive cell death. [ABSTRACT FROM AUTHOR]

Imatinib is mainly metabolised by CYP3A4 and CYP2C8 and is extensively bound to α-acid glycoprotein (AAG). A physiologically based pharmacokinetic (PBPK) model for imatinib describing the CYP3A4-mediated autoinhibition during multiple dosing in gastrointestinal stromal tumor patients with normal renal function was previously reported. After performing additional verification, the PBPK model was applied to predict the exposure of imatinib after multiple dosing in cancer patients with varying degrees of renal impairment. In agreement with the clinical data, there was a positive correlation between AAG levels and imatinib exposure. A notable finding was that for recovery of the observed data in cancer patients with moderate RI (CrCL 20 to 39 mL/min), reductions of hepatic CYP3A4 and CYP2C8 abundances, which reflect the effects of RI, had to be included in the simulations. This was not the case for mild RI (CrCL 40 to 50 mL/min). The results support the finding of the clinical study, which demonstrated that both AAG levels and the degree of renal impairment are key components that contribute to the interpatient variability associated with imatinib exposure. As indicated in the 2020 FDA draft RI guidance, PBPK modelling could be used to support an expanded inclusion of patients with RI in clinical studies. [ABSTRACT FROM AUTHOR]

Purpose: To assess the impact of primary‐site surgery plus systemic therapy compared to systemic therapy alone on overall survival in common metastatic cancer types. Methods: Data sources included Embase, PubMed, and Web of Science (January 1, 1995–March 22, 2023). Randomized controlled trials were included that enrolled patients diagnosed with the 10 most common de novo metastatic cancer types in the Surveillance, Epidemiology, and End Results database and randomized patients to resection of the primary site and systemic therapy versus systemic treatment alone. Random‐effects models were used to pool associations by cancer type. Results: Eight studies with 1774 patients evaluating the efficacy of surgery in breast, renal, stomach, and colorectal cancer were included. There was no statistically significant reduction in risk of all‐cause mortality associated with surgical intervention for metastatic breast (HR = 0.94, 95% CI 0.63–1.40) or renal cancer (HR = 0.79, 95% CI 0.53–1.20), although results were heterogeneous (I2 = 73.7% and 80.6%, respectively). One study evaluating gastrectomy in metastatic stomach cancer found no benefit (HR = 1.09, 95% CI 0.78–1.52), while a small trial suggested that surgery and hyperthermic intraperitoneal chemotherapy might be beneficial for colorectal cancer with peritoneal metastasis (HR = 0.55, 95% CI 0.32–0.95). Conclusions: Few randomized trials have evaluated cancer‐directed surgery among patients with metastatic solid malignancies. [ABSTRACT FROM AUTHOR]

Plasma membrane-derived vesicles, also referred to as large extracellular vesicles (lEVs), are implicated in several pathophysiological situations, including cancer. However, to date, no studies have evaluated the effects of lEVs isolated from patients with renal cancer on the development of their tumors. In this study, we investigated the effects of three types of lEVs on the growth and peritumoral environment of xenograft clear cell renal cell carcinoma in a mouse model. Xenograft cancer cells were derived from patients’ nephrectomy specimens. Three types of lEVs were obtained from pre-nephrectomy patient blood (cEV), the supernatant of primary cancer cell culture (sEV) and from blood from individuals with no medical history of cancer (iEV). Xenograft volume was measured after nine weeks of growth. Xenografts were then removed, and the expression of CD31 and Ki67 were evaluated. We also measured the expression of MMP2 and Ca9 in the native mouse kidney. lEVs from kidney cancer patients (cEV and sEV) tend to increase the size of xenografts, a factor that is related to an increase in vascularization and tumor cell proliferation. cEV also altered organs that were distant from the xenograft. These results suggest that lEVs in cancer patients are involved in both tumor growth and cancer progression.

Spontaneous tumor regression is an increasingly prevalent phenomenon of partial or complete disappearance of primary tumor tissue or associated metastases in the absence of therapeutic intervention. Cases of spontaneous regression have been established in malignant tumors, such as testicular germ cell tumor, renal cell cancer, melanoma, basal cell carcinoma, neuroblastoma, colon cancer, breast cancer, as well as metastases. Breast cancer has increasingly been reported to have a higher rate of spontaneous regression than previously thought. Immunologic response is cited as the forefront of spontaneous regression phenomenon, with the focus on immunologic cell death. This report brings awareness to a case of spontaneous regression observed in invasive ductal carcinoma of the breast and how disruption of the tumor microenvironment can take a variable course even in malignant disease. [ABSTRACT FROM AUTHOR]

Background: The incidence and risk factors of acute kidney injury (AKI) in patients with malignancies receiving immune checkpoint inhibitors (ICIs) are being extensively reported with their widespread application. Objective: This study aimed to quantify the incidence and identify risk factors of AKI in cancer patients treated with ICIs. Methods: We searched the electronic databases of PubMed/Medline, Web of Science, Cochrane and Embase before 1 February 2023 on the incidence and risk factors of AKI in patients receiving ICIs and registered the protocol in PROSPERO (CRD42023391939). A random-effect meta-analysis was performed to quantify the pooled incidence estimate of AKI, identify risk factors with pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) and investigate the median latency period of ICI-AKI in patients treated with ICIs. Assessment of study quality, metaregression, and sensitivity and publication bias analyses were conducted. Results: In total, 27 studies consisting of 24048 participants were included in this systematic review and meta-analysis. The overall pooled incidence of AKI secondary to ICIs was 5.7% (95% CI: 3.7%-8.2%). Significant risk factors were older age (OR: 1.01, 95% CI: 1.00–1.03), preexisting chronic kidney disease (CKD) (OR: 2.90, 95% CI: 1.65–5.11), ipilimumab (OR: 2.66, 95% CI: 1.42–4.98), combination of ICIs (OR: 2.45, 95% CI: 1.40–4.31), extrarenal immune-related adverse events (irAEs) (OR: 2.34, 95% CI: 1.53-3.59), and proton pump inhibitor (PPI) (OR: 2.23, 95% CI: 1.88–2.64), nonsteroidal anti-inflammatory drug (NSAID) (OR: 2.61, 95% CI: 1.90–3.57), fluindione (OR: 6.48, 95% CI: 2.72–15.46), diuretic (OR: 1.78, 95% CI: 1.32–2.40) and angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin-receptor blockers (ARBs) (pooled OR: 1.76, 95% CI: 1.15–2.68) use. Median time from ICIs initiation to AKI was 108.07 days. Sensitivity and publication bias analyses indicated robust results for this study. Conclusion: The occurrence of AKI following ICIs was not uncommon, with an incidence of 5.7% and a median time interval of 108.07 days after ICIs initiation. Older age, preexisting chronic kidney disease (CKD), ipilimumab, combined use of ICIs, extrarenal irAEs, and PPI, NSAID, fluindione, diuretics and ACEI/ARB use are risk factors for AKI in patients receiving ICIs. [ABSTRACT FROM AUTHOR]

Cancer ranks among the five leading causes of death in almost all countries and has important repercussions for individual and public health, the healthcare system, and society in general. Obesity increases the incidence of many types of cancer, but growing evidence suggests that physical activity may decrease risk for developing a variety of obesity-related cancer types, and, in some cases, may improve cancer prognosis and mortality rates. This review summarizes recent evidence on the effect of physical activity on obesity-related cancer prevention and survival. For some cancers, including breast, colorectal, and endometrial cancer, there is strong evidence for a preventative effect of exercise, but for many others, including gallbladder and kidney cancer, and multiple myeloma, evidence is inconsistent or largely lacking. Though many potential mechanisms have been proposed to explain the onco-protective effect of exercise, including improved insulin sensitivity, alterations in sex hormone availability, improved immune function and inflammation, myokine secretion, and modulation of intracellular signaling at the level of AMP kinase, the exact mechanism(s) of action within each cancer subtype remains poorly defined. Overall, a deeper understanding of how exercise can help against cancer and of the exercise parameters that can be altered to optimize exercise prescription is necessary and should be the subject of future investigation. [ABSTRACT FROM AUTHOR]

Background: Removal of tonsils and adenoids is among the most common surgical procedures worldwide. Evidence of increased risk of cancer following such surgery is, however, inconclusive. Methods: We conducted a population-based, sibling-controlled cohort study of 4,953,583 individuals in Sweden with a follow-up during 1980–2016. History of tonsillectomy, adenotonsillectomy, and adenoidectomy was identified from the Swedish Patient Register whereas incident cases of cancer during follow-up were identified from the Swedish Cancer Register. We used Cox models to calculate hazard ratios (HR) with 95% confidence intervals (CI) of cancer in both a population and a sibling comparison. The sibling comparison was used to assess the potential impact of familial confounding, due to shared genetic or non-genetic factors within a family. Results: We found a modestly increased risk for any cancer following tonsillectomy, adenoidectomy, or adenotonsillectomy in both the population (HR 1.10; 95%CI 1.07–1.12) and sibling (HR 1.15; 95%CI 1.10–1.20) comparisons. The association did not differ greatly by type of surgery, age at surgery, or potential indication for surgery, and persisted more than two decades after surgery. An excess risk was consistently observed for cancer of the breast, prostate, thyroid, and for lymphoma in both population and sibling comparisons. A positive association was observed for pancreatic cancer, kidney cancer, and leukemia in the population comparison whereas a positive association was observed for esophageal cancer in the sibling comparison. Conclusions: Surgical removal of tonsils and adenoids is associated with a modestly increased risk of cancer during the decades following the surgery. The association is unlikely attributed to confounding due to shared genetic or non-genetic factors with a family. [ABSTRACT FROM AUTHOR]

Finding new targets is necessary for understanding tumorigenesis and developing cancer therapeutics. DExH-box helicase 9 (DHX9) plays a central role in many cellular processes but its expression pattern and prognostic value in most types of cancer remain unclear. In this study, we extracted pan-cancer data from TCGA and GEO databases to explore the prognostic and immunological role of DHX9. The expression levels of DHX9 were then verified in tumor specimens by western blot and immunohistochemistry (IHC). The oncogenic roles of DHX9 in cancers were further verified by in vitro experiments. We first verified that DHX9 is highly expressed in most tumors but significantly decreased in kidney and thyroid cancers, and it is prominently correlated with the prognosis of patients with different tumors. The phosphorylation level of DHX9 was also increased in cancers. Enrichment analysis revealed that DHX9 was involved in Spliceosome, RNA transport and mRNA surveillance pathway. Furthermore, DHX9 expression exhibited strong correlations with immune cell infiltration, immune checkpoint genes, and tumor mutational burden (TMB)/microsatellite instability (MSI). In liver, lung, breast and renal cancer cells, the knockdown or depletion of DHX9 significantly affected the proliferation, metastasis and EMT process of cancer cells. In summary, this pan-cancer investigation provides a comprehensive understanding of the prognostic and immunological role of DHX9 in human cancers, and experiments indicated that DHX9 was a potential target for cancer treatment. [ABSTRACT FROM AUTHOR]

Cigarette chemicals are harmful to Deoxyribonucleic Acid (DNA). Cells have a strict time repairing DNA damage due to cigarette toxins. Additionally, they break the DNA regions that guard against cancer. Cancer is caused by the accumulation of DNA damage in one cell over time. There are around sixteen cancers which cause risk to human beings due to smoking as follows-cancer of the lung, cancers of the mouth (Squamous cell carcinomas), throat, nose, and sinuses, cancers of the esophagus, cancers of the bladder and ureter (Urothelial carcinoma/transitional cell carcinoma), cancers of kidney (Renal cell carcinoma), cancer of the pancreas (Pancreatic adenocarcinoma), cancer of the stomach (Adenocarcinomas), cancer of the liver (Cholangiocarcinoma), cancer of the cervix and ovary (Ovarian cancers). However, smokers often pass away from other smoking-related conditions, including heart disease, stroke, or emphysema. About 10% to 15% of the smokers acquire lung cancer. People who never smoked or who have quit smoking years ago have also been reported to die from lung cancer. In this research, people suffering from cancer and healthy people were separated using Decision Tree, AdaBoost, and aimed to evaluate a specific gene and smoking history algorithms. [ABSTRACT FROM AUTHOR]

miRNA-93 is a member of the miR-106b-25 family and is encoded by a gene on chromosome 7q22.1. They play a role in the etiology of various diseases, including cancer, Parkinson's disease, hepatic injury, osteoarthritis, acute myocardial infarction, atherosclerosis, rheumatoid arthritis, and chronic kidney disease. Different studies have found that this miRNA has opposing roles in the context of cancer. Recently, miRNA-93 has been downregulated in breast cancer, gastric cancer, colorectal cancer, pancreatic cancer, bladder cancer, cervical cancer, and renal cancer. However, miRNA-93 is up-regulated in a wide variety of malignancies, such as lung, colorectal, glioma, prostate, osteosarcoma, and hepatocellular carcinoma. The aim of the current review is to provide an overview of miRNA-93's function in cancer disorder progression and non-cancer disorders, with a focus on dysregulated signaling pathways. We also give an overview of this miRNA's function as a biomarker of prognosis in cancer and emphasize how it contributes to drug resistance based on in vivo, in vitro, and human studies. AEB9GaMjYR7aRambjWnbpG Video Abstract [ABSTRACT FROM AUTHOR]

Purpose: To systematically review studies focused on screening programs for renal cell carcinoma (RCC) and provide an exhaustive overview on their clinical impact, potential benefits, and harms. Methods: A systematic review of the recent English-language literature was conducted according to the European Association of Urology guidelines and the PRISMA statement recommendations (PROSPERO ID: CRD42021283136) using the MEDLINE, Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov databases. Risk-of-bias assessment was performed according to the QUality In Prognosis Studies (QUIPS) tool. Results: Overall, nine studies and one clinical trials were included. Eight studies reported results from RCC screening programs involving a total of 159 136 patients and four studies reported screening cost-analysis. The prevalence of RCC ranged between 0.02 and 0.22% and it was associated with the socio-demographic characteristics of the subjects; selection of the target population decreased, overall, the screening cost per diagnosis. Conclusions: Despite an increasing interest in RCC screening programs from patients and clinicians there is a relative lack of studies reporting the efficacy, cost-effectiveness, and the optimal modality for RCC screening. Targeting high-risk individuals and/or combining detection of RCC with other health checks represent pragmatic options to improve the cost-effectiveness and reduce the potential harms of RCC screening. [ABSTRACT FROM AUTHOR]

Extracellular vesicles (EVs) are ideal for liquid biopsy, but distinguishing cancer cell‐derived EVs and subpopulations of biomarker‐containing EVs in body fluids has been challenging. Here, we identified that the glycoproteins CD147 and CD98 define subpopulations of EVs that are distinct from classical tetraspanin+ EVs in their biogenesis. Notably, we identified that CD147+ EVs have substantially higher microRNA (miRNA) content than tetraspanin+ EVs and are selectively enriched in miRNA through the interaction of CD147 with heterogeneous nuclear ribonucleoprotein A2/B1. Studies using mouse xenograft models showed that CD147+ EVs predominantly derive from cancer cells, whereas the majority of tetraspanin+ EVs are not of cancer cell origin. Circulating CD147+ EVs, but not tetraspanin+ EVs, were significantly increased in prevalence in patients with ovarian and renal cancers as compared to healthy individuals and patients with benign conditions. Furthermore, we found that isolating miRNAs from body fluids by CD147 immunocapture increases the sensitivity of detecting cancer cell‐specific miRNAs, and that circulating miRNAs isolated by CD147 immunocapture more closely reflect the tumor miRNA signature than circulating miRNAs isolated by conventional methods. Collectively, our findings reveal that CD147 defines miRNA‐enriched, cancer cell‐derived EVs, and that CD147 immunocapture could be an effective approach to isolate cancer‐derived miRNAs for liquid biopsy. [ABSTRACT FROM AUTHOR]

Aim: Cancers are Turkey's second most common cause of mortality, following cardiovascular diseases. Tobacco and obesity are the two major etiological factors for cancer progression, which are highly prevalent in Turkey. This study aimed to evaluate the new cancer cases in Turkey attributable to these two main risk factors. Materials and Methods: The tobacco-related cancers based on the International Agency for Research on Cancer (IARC) monographs were esophagus, oral cavity, gastric, pancreatic, larynx, lung, renal, and bladder cancers, and the obesity-related cancers based on the IARC's and World Cancer Research Fund (WCRF)/American Institute for Cancer Research (AICR) Continuous Update Project's reports were esophagus, colon, rectum, gallbladder, pancreas, kidney, ovary, endometrium, and breast cancers. The cancer incidences were obtained from the national cancer statistics. A lag time of at least 10 years was considered adequate to observe past exposures' effects on new cancer cases. The prevalence of tobacco smoking was based on the Peto-Lopez approach. The obesity prevalence was obtained from the National Burden of Disease and Cost-Effectiveness Project Household Survey, 2003 Report in Turkey. Using these incidence and prevalence data, we estimated the population-attributable fractions (PAF) of cancers attributable to smoking and obesity in Turkey. Results: For tobacco-related cancers, the highest PAFs were found in lung cancer (89.8%), larynx cancer (86%), oral cavity and pharynx cancer (77.2%) in males, and larynx cancer (46.5%), lung cancer (43%), and esophagus cancer (31.4%) in females. For obesityrelated cancers, the highest PAFs were found in esophagus adenocarcinoma (31.4%), kidney cancer (19.8%), gallbladder cancer (15.1%) in males, and esophagus adenocarcinoma (33.9%), endometrium cancer (32.8%), and postmenopausal breast cancer (22.8%) in females. When all tobacco-related cancers were considered, 41,283 cases in males and 3,853 cases in females were attributable to tobacco smoking, and when all obesity-related cancer types were considered, the number of attributable cancer cases to obesity was 2,653 in men and 7,387 in women. Conclusion: The current avoidable cancer burden in Turkey shows that eliminating tobacco smoking and obesity may prevent more than 50,000 cancer cases in Turkey. [ABSTRACT FROM AUTHOR]

Patients with cancer represent a unique patient population with increased susceptibility to kidney disease. Drug-induced acute kidney injury (AKI) in patients with cancer is a common problem. Cisplatin is a highly effective treatment used in many solidorgan cancers and causes AKI in 30% of patients, increasing the risk of chronic kidney disease development. Most preclinical cisplatin toxicity studies have been completed in mice without cancer. We believe that the physiology of patients with cancer is not adequately represented in preclinical models, and the objective of this study was to determine how lung cancer will alter the nephrotoxicity of cisplatin. A genetically engineered mouse model and a syngeneic xenograft model of lung cancer were used. Mice were divided into the following four groups: 1) noncancer/vehicle, 2) noncancer/cisplatin, 3) cancer/vehicle, and 4) cancer/cisplatin. Mice were administered cisplatin via intraperitoneal injection once a week for 4 wk. Animals were euthanized 72 h following their final cisplatin injection. Mice with lung cancer had increased renal toxicity, injury, and fibrosis following repeated low doses of cisplatin. In addition, lung cancer alone induced kidney injury and fibrosis in the kidney before cisplatin treatment. In conclusion, this is the first study that we are aware of that assesses the impact of cancer on the kidney in conjunction with the nephrotoxicity of cisplatin. We believe that cancer is providing the first hit to the kidney and the subsequent damage from repeated doses of cisplatin becomes unsurmountable, leading to AKI and progression to chronic kidney disease. NEW & NOTEWORTHY Patients with cancer have impaired kidney function and increased susceptibility to nephrotoxic agents. Cisplatin is a commonly used chemotherapeutic with nephrotoxicity as the dose-limiting side effect. Cisplatin nephrotoxicity is almost exclusively studied in mice without cancer. Our current preclinical models do not adequately represent the complexity of patients with cancer. This study demonstrates increased renal toxicity, injury, and fibrosis in mice with lung cancer, which is exacerbated with cisplatin treatment. These results highlight the necessity of using preclinical models that more accurately capture the altered physiology of patients with cancer treated with cisplatin. [ABSTRACT FROM AUTHOR]

Background: The epidemiology of renal impairment in patients with cancer remains unclear. We aimed to clarify associations between various cancer sites and renal impairment. Methods: We reviewed data from 5674 patients aged ≥ 18 years receiving cancer treatment at a single hospital facility. The primary endpoints were the occurrence of acute kidney injury (AKI), a 30% decrease in the estimated glomerular filtration rate (eGFR), or death. Survival time was defined as the time from study enrolment to AKI occurrence. Kaplan–Meier and Cox proportional hazard analyses were performed. Results: Hazard ratios (HRs) for AKI occurrence and a ≥ 30% decline in eGFR were significantly higher for kidney, urinary tract, pancreatic, liver, and gallbladder cancers than for colon cancer. Compared with colon cancer, digestive tract cancer showed a significantly higher HR for AKI occurrence alone. The HRs for a ≥ 30% decline in eGFR were significantly higher for patients aged 71‒77 years or ≥ 78 years than for those aged < 68 years, and for patients with eGFR ≥ 90 mL/min/1.73 m2 or 30–44 mL/min/1.73 m2 than for those with eGFR = 45‒59 mL/min/1.73 m2. Conclusions: Kidney, urinary, hepatobiliary, or pancreatic cancer are associated with a higher risk of AKI development and eGFR decrease than other cancers. Renal function changes should be more closely monitored in patients with these cancers. [ABSTRACT FROM AUTHOR]

Renal cancer is one of the most common malignancies, and its incidence is increasing year by year, second only to prostate and bladder cancers. Therefore, early screening is of great significance to prevent and improve the prognosis of patients with renal cancer. Therefore, this study intends to observe the early diagnostic value of miR-15b-5p combined with Colour ultrasound imaging in renal cell carcinoma. In this study, the clinical samples of 76 patients with renal cell carcinoma diagnosed by pathology in our hospital from April 2020 to June 2022 were retrospectively collected as the research objects. Another 100 healthy people who underwent general physical examination in our hospital during the same period were selected to detect the expression level of miR-15b-5 in serum by RT-PCR together with the 76 experimental samples. Colour ultrasound imaging was used to detect the blood flow distribution around and inside the kidney of the patients with renal cancer, and the parameters were measured and compared with the gold standard for statistical analysis. The expression level of miR-15b-5 in renal cell carcinoma group was significantly higher than that in control group. Most of them showed renal hamartoma (40.79%). Benign renal tumors were mainly characterized by type I and II blood flow, while malignant renal tumors were characterized by type III and IV blood flow. Compared with the pathological gold standard, the diagnostic accuracy of ultrasound imaging was founded to be about 81.25%. Further ROC analysis showed that ultrasound imaging combined with miR-15b-5 detection could effectively improve the early screening value of renal cell carcinoma. We observed that miR-15b-5 has a specific expression level in the serum of patients with renal cell carcinoma, and its combination with ultrasound imaging can significantly improve the early detection of renal cell carcinoma. This approach is envisaged to be highly useful for, early diagnosis, intervention and management of patients with renal cell carcinoma. [ABSTRACT FROM AUTHOR]

Atopic dermatitis is a chronic inflammatory intensively pruritic skin disease. Patients with moderate-to-severe atopic dermatitis or with difficult-to-treat areas are candidates for systemic therapy, especially when topical therapy is inadequate. Currently, we have available not only conventional immunosuppressive systemic therapy, but also targeted biological therapy, which has shown a remarkable reduction in clinical severity with a good safety profile. Dupilumab has been approved to treat moderate-to-severe atopic dermatitis. Even though the therapy has been available for more than 3 years, there are still limited data regarding the treatment of patients with concomitant cancer. Previous immunosuppressive treatment for atopic dermatitis, such as cyclosporine or azathioprine, poses a safety risk for patients with malignant disease. We present a case series of three patients with advanced cancer and severe atopic dermatitis treated with dupilumab for an average of 17 months with a great response toward atopic dermatitis without cancer recurrence. One patient had colorectal cancer' the second and the third both had cancer duplicity—colorectal and kidney cancer and penile squamous cell carcinoma with prostate cancer. Our cases suggest that dupilumab can safely control atopic dermatitis in patients with advanced cancer. [ABSTRACT FROM AUTHOR]

Renal cancer is responsible for over 100,000 yearly deaths and is principally discovered in computed tomography (CT) scans of the abdomen. CT screening would likely increase the rate of early renal cancer detection, and improve general survival rates, but it is expected to have a prohibitively high financial cost. Given recent advances in artificial intelligence (AI), it may be possible to reduce the cost of CT analysis and enable CT screening by automating the radiological tasks that constitute the early renal cancer detection pipeline. This review seeks to facilitate further interdisciplinary research in early renal cancer detection by summarising our current knowledge across AI, radiology, and oncology and suggesting useful directions for future novel work. Initially, this review discusses existing approaches in automated renal cancer diagnosis, and methods across broader AI research, to summarise the existing state of AI cancer analysis. Then, this review matches these methods to the unique constraints of early renal cancer detection and proposes promising directions for future research that may enable AI-based early renal cancer detection via CT screening. The primary targets of this review are clinicians with an interest in AI and data scientists with an interest in the early detection of cancer. [ABSTRACT FROM AUTHOR]

This article discusses a case of pseudomesothelioma, a condition where cancers can mimic malignant pleural mesothelioma (MPM) clinically, histologically, and radiologically. The case involves a 62-year-old ex-smoker with a history of asbestos exposure who presented with shortness of breath and cough. Initially, the patient was thought to have community-acquired pneumonia, but follow-up imaging revealed pleural thickening characteristic of MPM. However, further testing confirmed a diagnosis of squamous cell lung cancer, highlighting the importance of accurate tissue diagnosis in cases that resemble MPM. Pseudomesotheliomas are rare and are often associated with poor prognosis, particularly in male smokers with a history of asbestos exposure. [Extracted from the article]

Targeted therapies with antiangiogenic drugs (e.g., sunitinib) and immune checkpoint inhibitors (e.g., anti-PD-1 antibodies) are the standard of care for patients with metastatic renal cell carcinoma. Although these treatments improve patient survival, they are rarely curative. We previously hypothesized that advanced cancers might be treated without drugs by using artificial diets in which the levels of specific amino acids (AAs) are manipulated. In this work, after showing that AA manipulation induces selective anticancer activity in renal cell carcinoma cells in vitro, we screened 18 artificial diets for anticancer activity in a challenging animal model of renal cell carcinoma. The model was established by injecting murine renal cell carcinoma (Renca) cells into the peritoneum of immunocompetent BALB/cAnNRj mice. Mice survival was markedly improved when their normal diet was replaced with our artificial diets. Mice fed a diet lacking six AAs (diet T2) lived longer than mice treated with sunitinib or anti-PD-1 immunotherapy; several animals lived very long or were cured. Controlling the levels of several AAs (e.g., cysteine, methionine, and leucine) and lipids was important for the anticancer activity of the diets. Additional studies are needed to further evaluate the therapeutic potential and mechanism of action of this simple and inexpensive anticancer strategy. [ABSTRACT FROM AUTHOR]

Cancer immunotherapy has now entered clinical practice and has reshaped the standard of care for many cancer patients. With these new strategies, specific toxicities have emerged, and renal side effects have been described. In this review, we will describe the causes of acute kidney injury in CAR T cell, immune checkpoint inhibitors and other cancer immuno-therapy recipients. CAR T cell therapy and bispecific T cell engaging antibodies can lead to acute kidney injury as a consequence of cytokine release syndrome, tumor lysis syndrome, sepsis or specific CAR T cell infiltration. Immune checkpoint blockade most often results in acute tubular interstitial nephritis, but glomerular diseases have also been described. Although the pathophysiology remains mostly elusive, we will describe the mechanisms of renal damage in these contexts, its prognosis and treatment. As the place of immunotherapy in the anti-cancer armamentarium is exponentially increasing, close collaboration between nephrologists and oncologists is of utmost importance to provide the best standard of care for these patients. [ABSTRACT FROM AUTHOR]

While we previously revealed RSK4 as a therapeutic target in lung and bladder cancers, the wider role of this kinase in other cancers remains controversial. Indeed, other reports instead proposed RSK4 as a tumour suppressor in colorectal and gastric cancers and are contradictory in breast malignancies. One explanation for these discrepancies may be the expression of different RSK4 isoforms across cancers. Four RNAs are produced from the RSK4 gene, with two being protein-coding. Here, we analysed the expression of the latter across 30 normal and 33 cancer tissue types from the combined GTEx/TCGA dataset and correlated it with clinical features. This revealed the expression of RSK4 isoforms 1 and 2 to be independent prognostic factors for patient survival, pathological stage, cancer metastasis, recurrence, and immune infiltration in brain, stomach, cervical, and kidney cancers. However, we found that upregulation of either isoform can equally be associated with good or bad prognosis depending on the cancer type, and changes in the expression ratio of isoforms fail to predict clinical outcome. Hence, differential isoform expression alone cannot explain the contradictory roles of RSK4 in cancers, and further research is needed to highlight the underlying mechanisms for the context-dependent function of this kinase. [ABSTRACT FROM AUTHOR]

According to the World Health Organization (WHO) categorization of Body Max Index, obesity is frequently measured in clinical practice by expressing body weight as a function of height (BMI). There is good evidence that obesity raises the risk of many cancers, such as esophageal adenocarcinoma, postmenopausal breast, pancreatic, colorectal, endometrial, liver cancer and kidney cancer. The study aims to summarize current evidence regarding Obesity as a risk factor for different cancers. The PubMed database and EBSCO Information Services were utilised to choose the articles. In our review, all pertinent articles related to our subject and other publications were used. Other articles that have nothing to do with this subject were not included. The group members looked through a certain format in which the data had been extracted. Obesity is a significant risk factor for the occurrence and progression of many cancer types especially when it comes to GI cancers such as colorectal, gastric, and liver cancer. This has been linked to multiple pathophysiological reasons such as lower immunological response in obese patients. However, it is worth noting that in many cases strong evidence has not been established for obesity as a risk factor, and some studies suggest that sex may play a critical role when it comes to obesity as a risk factor for cancer. [ABSTRACT FROM AUTHOR]

Background: Immunotherapy with immune checkpoint inhibitors (ICI) has revolutionized cancer therapy. However, therapeutic targeting of inhibitory T cell receptors such as PD-1 not only initiates a broad immune response against tumors, but also causes severe adverse effects. An ideal future stratified immunotherapy would interfere with cancer-specific cell surface receptors only. Methods: To identify such candidates, we profiled the surface receptors of the NCI-60 tumor cell panel via flow cytometry. The resulting surface receptor expression data were integrated into proteomic and transcriptomic NCI-60 datasets applying a sophisticated multiomics multiple co-inertia analysis (MCIA). This allowed us to identify surface profiles for skin, brain, colon, kidney, and bone marrow derived cell lines and cancer entity-specific cell surface receptor biomarkers for colon and renal cancer. Results: For colon cancer, identified biomarkers are CD15, CD104, CD324, CD326, CD49f, and for renal cancer, CD24, CD26, CD106 (VCAM1), EGFR, SSEA-3 (B3GALT5), SSEA-4 (TMCC1), TIM1 (HAVCR1), and TRA-1-60R (PODXL). Further data mining revealed that CD106 (VCAM1) in particular is a promising novel immunotherapeutic target for the treatment of renal cancer. Conclusion: Altogether, our innovative multiomics analysis of the NCI-60 panel represents a highly valuable resource for uncovering surface receptors that could be further exploited for diagnostic and therapeutic purposes in the context of cancer immunotherapy. [ABSTRACT FROM AUTHOR]