Cancer Incidence Research Articles

Patient Enrollment to Industry-Sponsored Versus Federally-Sponsored Cancer Clinical Trials.

The conduct of cancer clinical research in the United States is supported by both private and public sponsors. Industry aims to obtain new drug approvals. Federally-sponsored trials examine a broad set of research questions that are not typically addressed by industry; these trials, which are also more commonly conducted in diverse populations, were recently shown to have contributed to gains of 14 million life-years for patients with cancer. Despite the different mandates, the proportion of patients who might participate in industry-sponsored versus federally-sponsored cancer studies is unknown. We evaluated trial enrollment patterns from 2008 to 2022 using ClinicalTrials.gov data. The ratio of enrollments attributable to industry versus federal sponsors was estimated. A large set of estimates on the basis of different combinations of study characteristics were generated. Point estimates were determined as the mean of combinations and confidence limits by the IQR. Five-year intervals were examined to smooth annual variation. In total, N = 26,080 studies were examined. The estimated enrollment ratio from 2018 to 2022 for all industry-sponsored versus federally-sponsored trials was 8.1 (IQR, 6.2-9.9). For adult trials, the ratio increased from 4.8 (IQR, 4.4-5.3) during 2008-2012 to 9.6 (IQR, 7.4-11.8) during 2018-2022; for trials in children, the ratio increased from 0.7 (IQR, 0.6-0.7) to 2.3 (IQR, 1.8-2.7). Despite increasing cancer incidence, enrollment counts for federally-sponsored trials were flat over the study period. In the United States, there is a growing reliance on industry to conduct cancer clinical research. Underinvestment in federally-sponsored research comes at a cost for both patients and researchers, with lost opportunities for scientific, clinical, and population advances.

Increasing Incidence and Stable Mortality of Pancreatic Cancer in Young Americans

Increasing Incidence and Stable Mortality of Pancreatic Cancer in Young Americans

Spatio-temporal quasi-experimental methods for rare disease outcomes: the impact of reformulated gasoline on childhood haematologic cancer

Abstract Although some pollutants emitted in vehicle exhaust, such as benzene, are known to cause leukaemia in adults with high exposure levels, less is known about the relationship between traffic-related air pollution (TRAP) and childhood haematologic cancer. In the 1990s, the US EPA enacted the reformulated gasoline program in select areas of the U.S., which drastically reduced ambient TRAP in affected areas. This created an ideal quasi-experiment to study the effects of TRAP on childhood haematologic cancers. However, existing methods for quasi-experimental analyses can perform poorly when outcomes are rare and unstable, as with childhood cancer incidence. We develop Bayesian spatio-temporal matrix completion methods to conduct causal inference in quasi-experimental settings with rare outcomes. Selective information sharing across space and time enables stable estimation, and the Bayesian approach facilitates uncertainty quantification. We evaluate the methods through simulations and apply them to estimate the causal effects of TRAP on childhood leukaemia and lymphoma.

Abstract B031: Lean adipocyte-derived lipid decreases metastatic potential of breast cancer cells

Abstract Obesity rates are increasing globally, making it of critical importance to study obesity-linked diseases. Breast cancer is the most common cancer in women, and obesity is associated with both increased incidence and metastatic progression of breast cancer. Metastasis formation depends on a cancer cell leaving the primary site, migrating through the bloodstream, and establishing new growth in a distant site. Both metastasizing cell-intrinsic and metastatic site-dependent factors can help to regulate the effectiveness of this process; however, it is unknown whether obesity-linked metastasis depends on changes to the metastasizing cell and/or changes to the distant metastatic site. This study aims to characterize how the lean versus obese tumor microenvironment impacts breast cancer metastasis and identify adipocyte-derived molecules that modulate the metastatic potential of breast cancer cells. We and others have shown that obesity leads to increased metastasis formation in mouse models of orthotopic breast cancer. However, my preliminary data show that an obese metastatic site is not sufficient to increase metastasis formation in an intravenous injection model of metastasis, emphasizing the importance of the primary tumor microenvironment in programming breast cancer cells for metastasis. Cancer cell stemness helps to mediate metastasis formation and can be assessed in vitro with the mammosphere assay. Importantly, my data demonstrate that a secreted lipid from lean, but not obese, adipocytes potently inhibits the ability of breast cancer cells to form mammospheres. Furthermore, this inhibition induces a G1/S cell cycle arrest. Together, these data suggest that lean adipocytes in the breast cancer tumor microenvironment act in a paracrine manner to decrease the metastatic potential of breast cancer cells. My work demonstrates the role of adipocytes in the regulation of metastasis in breast cancer and provides important insight into the role of the tumor microenvironment in mediating metastasis in lean versus obese conditions. Citation Format: Abigail E. Jackson, Keren I Hilgendorf. Lean adipocyte-derived lipid decreases metastatic potential of breast cancer cells [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Tumor-body Interactions: The Roles of Micro- and Macroenvironment in Cancer; 2024 Nov 17-20; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2024;84(22_Suppl):Abstract nr B031.

Abstract C029: PM2.5-induced drug resistance in lung cancer

Abstract Long-term exposure to PM2.5 air pollution is a significant contributor to lung cancer incidence. Our previous studies have shown that such exposure promotes lung cancer progression by activating the EGFR (epidermal growth factor receptor) and AhR (aryl hydrocarbon Receptor) pathways. We observed that in lung cancer cells with EGFR mutations, prolonged PM2.5 exposure induces EGFR activation, resulting in accelerated tumor cell growth both in vitro and in vivo. This suggests that PM2.5 may play a role in the resistance to EGFR-TKI (tyrosine kinase inhibitor) therapies, raising concerns about treatment efficacy. To explore this, we exposed the EGFR-mutant lung cancer cell line to PM2.5 for 90 days. Our results revealed that long-term exposure not only reduced the therapeutic effect of EGFR-TKIs but also increased the expression of cMyc, a gene linked to poor prognosis and drug resistance. We further confirmed that PM2.5-induced EGFR-TKI resistance is driven by the AhR-cMyc pathway. AhR, activated by environmental toxins in PM2.5, increases cMyc expression, leading to drug resistance. When we administered cMyc inhibitors, the PM2.5-exposed cells regained sensitivity to EGFR-TKI therapy. These findings indicate that targeting the AhR-cMyc pathway could be a promising approach to overcome PM2.5-induced resistance in lung cancer treatment. Further research is needed to explore the broader implications of environmental pollution on cancer therapy and to develop strategies to counteract the effects of pollutants like PM2.5. Citation Format: Chi-Yuan Chen, Chieh-Wen Chan, Tong-Hong Wang. PM2.5-induced drug resistance in lung cancer [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Tumor-body Interactions: The Roles of Micro- and Macroenvironment in Cancer; 2024 Nov 17-20; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2024;84(22_Suppl):Abstract nr C029.

Abstract B007: Identification of Asporin as a HER3 ligand exposes a therapeutic vulnerability in metastatic prostate cancer

Abstract Background: Rates of prostate cancer incidence and advanced-stage diagnoses are increasing. Despite curative-intent therapies, nearly all patients with advanced disease progress to metastatic castration-resistant prostate cancer (mCRPC), a lethal form of the disease. There is an urgent unmet need to understand the mechanisms driving prostate cancer progression and identify alternative therapies for patients with mCRPC. It is well-established that cancer-associated fibroblasts (CAF) in the tumor microenvironment secrete factors that enable cancer cells to establish metastases. Asporin (ASPN) is an extracellular protein secreted by a subset of CAF and is associated with worse oncologic outcomes, yet the mechanisms remain poorly understood. In this study, we sought to identify the molecular interactions between the CAF-secreted ASPN and metastatic prostate cancer cells. Methods: ASPN-induced HER2/HER3 activation and downstream signaling was identified by RNA-sequencing and then confirmed by immunoblotting in multiple human metastatic prostate cancer cell lines. Binding interactions were assessed computationally by AlphaFOld2 with Rosetta refinement and substantiated by co-immunoprecipitation assays. CRISPR-cas9 targeting of HER2 and HER3 and therapeutic inhibition of HER2 with Tucatinib were used to determine the role of HER2/HER3 in ASPN-induced signaling and migration. The efficacy of Tucatinib and antibody-drug conjugates (ADC) targeting HER2 (Trastuzumab-deruxtecan) and HER3 (Patritumab-deruxtecan) were assessed in multiple metastatic prostate cancer cell lines in vitro. Trastuzumab-deruxtecan was assessed in PC3 xenografts in vivo. Prostate cancer metastases from 33 patients were assessed by IHC for HER2 and HER3 and by RNAscope for ASPN. Results: We report that ASPN is a novel ligand of HER3 and induces HER3 heterodimerization with its preferred dimerization partner, HER2. ASPN activates established ErbB-associated pathways including Phosphoinositide 3-kinase (PI3K), Mitogen-activated protein kinase (MAPK), and calcium signaling, in multiple metastatic prostate cancer cell lines to promote cell migration. Genetic and molecular inhibition of HER2/HER3 mitigates ASPN-induced signaling and cell migration, suggesting these receptors are required for paracrine activation by ASPN. Importantly, small molecule and ADC therapies targeting HER2/HER3 significantly diminished prostate cancer cell growth in vitro, with enzalutamide-resistant cells showing increased sensitivity. Trastuzumab-deruxtecan nearly resolved tumors in an in vivo xenograft model. Lastly, ASPN+ CAF in the TME of HER2/HER3-expressing metastatic prostate cancer is frequently observed in patient samples, supporting the clinical relevance of these findings. Conclusions: Collectively, these findings indicate ASPN functions as a HER3 ligand to induce cellular migration, and inhibition with anti-HER2/HER3 therapies highlights potential clinical utility for patients with HER2-expressing metastatic prostate cancer. Citation Format: Amanda B. Hesterberg, Hong Yuen Wong, Jorgen Jackson, Monika Antunovic, Brenda L. Rios, Evan Watkins, Riley E. Bergman, Brad A. Davidson, Sarah E. Ginther, Diana Graves, Elliott F. Nahmias, Jared A. Googel, Lillian B. Martin, Violeta Sanchez, Paula Gonzalez Ericsson, Quanhu Sheng, Benjamin P. Brown, Jens Meiler, Ben H. Park, Kerry R. Schaffer, Jennifer B. Gordetsky, Paula J. Hurley. Identification of Asporin as a HER3 ligand exposes a therapeutic vulnerability in metastatic prostate cancer [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Tumor-body Interactions: The Roles of Micro- and Macroenvironment in Cancer; 2024 Nov 17-20; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2024;84(22_Suppl):Abstract nr B007.

Serum urea concentration and risk of 16 site-specific cancers, overall cancer, and cancer mortality in individuals with metabolic syndrome: a cohort study.

The relationship between serum urea concentration and cancer in patients with metabolic syndrome (MetS) remains unclear. This study aimed to investigate the association between serum urea concentration and 16 site-specific cancers, overall cancer incidence, and cancer mortality in individuals with MetS. We analysed the data of 108,284 individuals with MetS obtained from the UK Biobank. The Cox proportional hazards model was used to determine the association between serum urea concentration at recruitment and cancer. The Benjamini-Hochberg correction was used to account for multiple comparisons. Over the median follow-up period of 11.86years, 18,548 new incident cases of cancer were documented. There were inverse associations of urea concentration with overall cancer incidence, and the incidence of oesophageal and lung cancers, with respective hazard ratios (95% confidence intervals) [HR (95% CI)] for the highest (Q4) vs lowest (Q1) urea quartiles of 0.95 (0.91-0.99), 0.68 (0.50-0.92), and 0.76 (0.64-0.90). However, high serum urea concentrations increased the male prostate cancer risk (HR 1.15; 95% CI 1.02-1.30). Although the Cox model indicated a protective effect of higher urea levels against stomach (HR 0.67; 95% CI 0.45-0.98; p = 0.040; FDR 0.120) and colorectal cancer (HR 0.86; 95% CI 0.74-0.99; p = 0.048; FDR 0.123), no strong evidence of association was found after applying the Benjamin-Hochberg correction. Moreover, across the median follow-up period of 13.77years for cancer mortality outcome, 5034 cancer deaths were detected. An "L-shaped" nonlinear dose-response relationship between urea concentration and cancer mortality was discovered (p-nonlinear < 0.001), and the HR (95% CI) for urea concentration Q4 vs Q1 was 0.83 (0.77-0.91). Serum urea concentration can be considered as a valuable biomarker for evaluating cancer risk in individuals with MetS, potentially contributing to personalised cancer screening and management strategies.

Time trends of cancer incidence in young adults (20-49 years) in Italy. A population - based study, 2008-2017.

To evaluate short-term (2008-2017) cancer incidence trends in Italy for individuals aged 20-49 years by sex and cancer type. Observational study from population-based data collected by 20 Italian Cancer Registries, covering 33% of the Italian population. The age-standardized incidence rates (ASRs), overall and stratified by area, sex, cancer site or type, and major age groups (i.e., 20-39, 40-49), were computed. In 2008-2017, cancer incidence rates were almost two times higher in Italian women aged 20-49 than in age-corresponding men (202.2 vs 112.4 per 100,000) on account of elevated rates of breast and thyroid cancers. Contrasting trends emerged according to cancer sites/types. ASRs for female breast cancer increased steadily from 2008 (82.4) to 2014 (86.2) and remained unchanged thereafter (i.e., 86.5 in 2017). During the study period, there was an increase for testicular cancer, skin melanoma in both sexes, and thyroid cancer until 2013 (followed by a slight decrease from 2014 to 2017). Conversely, ASRs consistently declined for colorectal cancer and were substantially stable or slightly decreasing for cervix uteri (from 8.1 to 7.7), ovary (from 7.5 to 6.9) and non-Hodgkin lymphoma (from 8.3 to 7.6 in men and from 5.9 to 5.5 in women). Study findings do not support a unique temporal pattern for the incidence of early-onset cancer in Italy until 2017, as reported in other countries. Increases in incidence documented in both sexes for some tumor sites was counterbalanced by a decrease in other sites. The importance of supporting prevention strategies from the youngest of ages must be emphasized, and the role of anticipated screening should be carefully addressed.

Projected epidemiological trends and burden of liver cancer by 2040 based on GBD, CI5plus, and WHO data.

Incidence of liver cancer as one of the most common cancers worldwide and become the significant contributor for the mortality among cancer patients. The disease burden, risk factors, and trends in incidence and mortality of liver cancer globally was described subsequently estimated the projections of liver cancer incidence or mortality by 2040. Data regarding age-standardized incidence and mortality rates for liver cancer was obtained from multiple databases, including GLOBOCAN 2020, CI5 volumes I-XI, WHO mortality database, and Global Burden of Disease (GBD)-2019. Concentrating on worldwide variations, this thorough analysis offers insights into patterns of incidence and mortality based on gender and age. Our findings encompass significant indicators, including age-standardized rates (ASRs), average annual percentage change (AAPC), and future projections extending up to the year 2040. Liver cancer holds the sixth position in terms of most frequently diagnosed cancers and stands as the sixth leading cause of cancer-related deaths worldwide in 2020, accounting for 905,677 new cases and 782,000 fatalities. Additionally, liver cancer contributed to 12,528,421 age-standardized disability-adjusted life years (DALYs), with an age-standardized DALYs rate of 161.92 in 2019 worldwide. The age-specific incidence rates exhibited significant variations across different regions, showing a fivefold difference in males and females. A significant increase in incidence was observed in North Europe and Asia, while North African countries reported a higher mortality burden (ASR, 10 per 100,000) compared to developed countries. Since last few years, the incidence and mortality rates have increased and attained Annual Average Percentage Change (AAPC) incidence rate of 7.7 (95% CI 3.9-11.6) for men and the highest AAPC mortality rate of 12.2 (95% CI 9.5-15.0) for women. In 2019, Western Europe emerged as the high-risk region for DALYs related to smoking and alcohol consumption, while high-income North America carried a high risk for DALYs associated with a high body-mass index. The projected trend indicates a surge in new liver cancer incident cases, expected to rise from around 905,347 to an estimated 1,392,474 by 2040. This study described the evidence pertinent to higher incidence trends in liver cancer, particularly among both young and older adults, encompassing males and females, as well as those who are HIV-infected and HBsAg positive. A significant rise in the young population poses a significant public health concern that warrants attention from healthcare professionals to prioritize the promotion of health awareness and the development of effective cancer prevention strategies, particularly in many developing countries.

Role of metabolic syndrome and lifestyle factors in endometrial cancer risk and prevention

Introduction: The incidence of endometrial cancer, the sixth most common cancer among women, has been rising, especially in developed countries, possibly due to the obesity and diabetes pandemic. The aim of this review is to investigate the connection between metabolic syndrome, its individual components and endometrial cancer risk and to explore the role of lifestyle factors in endometrial cancer prevention. Materials and methods: For this review, we included studies regarding endometrial cancer and metabolic syndrome, obesity, diabetes and hyperglycemia, hypertension, dyslipidemia and several lifestyle factors, from 1994 to 2024. State of knowledge: This paper reviews existing literature on the relationship between metabolic syndrome and endometrial cancer, highlighting the significant role of central obesity, hyperglycemia and diabetes, dyslipidemia, and hypertension as risk factors. Evidence consistently demonstrates that individuals with metabolic syndrome, and its components individually, are at a heightened risk of developing endometrial cancer compared to those without metabolic abnormalities. Biological mechanisms linking metabolic syndrome’s components to endometrial cancer involve complex interplays between metabolic, hormonal or inflammatory factors and signalling pathways. Lifestyle interventions focusing on weight management, physical activity, and eating habits play an important role in reducing endometrial cancer risk and improving overall health outcomes. Conclusion: An understanding of the relationship between metabolic syndrome and endometrial cancer is crucial for improving risk stratification, early detection, and prevention strategies. Addressing metabolic abnormalities and promoting healthy lifestyle behaviours are essential actions against the rising incidence and burden of endometrial cancer.

Proportion of Gleason Score ≥8 Prostate Cancer on Biopsy and Tumor Aggressiveness in Matched Cohorts of East Asian and Non-East Asian Men.

Historically, Asia had a lower prostate cancer (PCa) incidence and mortality compared with Western countries, but the gap is narrowing. Paradoxically, Asians have been reported to present with more advanced disease though more favorable outcomes. Despite PCa becoming an emerging health priority in East Asia, our knowledge remains limited. We compared the prevalence of high-grade PCa on biopsy and disease progression after radical prostatectomy (RP) in East Asian men from Asia and non-East Asian men from Western countries. This retrospective cohort study included men who underwent prostate biopsy and RP at academic centers in Shanghai, China, and Toronto, Canada (2014-2019). The expanded RP cohort included East Asian men from Singapore (n=282) and non-East Asians from Paris (n=192). Primary endpoints included the proportion of men with Gleason score (GS) ≥8 on biopsy and metastasis-free survival (MFS) after RP for GS ≥8. Multivariable logistic regression and Cox proportional hazard models were performed. Propensity score matching was used to reduce imbalances between cohorts. PCa was found on biopsy in 2,343 of 4,905 (48%) East Asians and 2,317 of 3,482 (67%) non-East Asians (P<.001). Prostate-specific antigen (PSA) levels at presentation and the proportion of men with GS ≥8 were higher in East Asians than non-East Asians (12.4 vs 6.6 ng/mL and 15.0% vs 8.8%, respectively; both P<.001). On multivariable analysis, there was no difference in the proportion of men with GS ≥8 between matched cohorts with PSA <20 ng/mL (n=3,572; odds ratio, 1.05 [95% CI, 0.77-1.43]; P=.76). No difference in MFS was found after RP between matched cohorts (hazard ratio, 0.97 [95% CI, 0.55-1.70]; P=.92). This contemporary study demonstrates that East Asian men are equally as likely to harbor aggressive PCa on biopsy as non-East Asian men at PSA levels observed in screening programs, with no difference in disease aggressiveness after RP. The assumption that unfavorable PCa at diagnosis is more common but less aggressive in East Asians should be revisited and viewed in the context of the expected increase in the PCa burden worldwide.

Age differences in the treatment of lung cancer-a cohort study among 42,000 patients from Germany.

We aimed to describe treatment of lung cancer patients in Germany based on health claims data, focusing particularly on differences by age. Using the German Pharmacoepidemiological Research Database (GePaRD, ~ 20% of the German population) we identified lung cancer patients diagnosed in 2015-2018 based on a previously developed algorithm and followed them until death, end of continuous insurance or end of 2020. We described initial treatment patterns after diagnosis and survival, stratified among others by age. We included 42,629 incident lung cancer patients (58% male). Surgery within three months after diagnosis was performed in 36%, 31%, 29% and 18% of patients aged < 50, 50-69, 70-79 and ≥ 80, respectively. Among patients without surgery, systemic therapy was administered in 77%, 72%, 54% and 25% of patients aged < 50, 50-69, 70-79 and ≥ 80, respectively. Monoclonal antibodies were administered in 15-30% of patients across age groups, and 4% to 15% received protein kinase inhibitors. Overall, 21% of patients remained untreated. In the age groups < 50, 50-69, 70-79 and ≥ 80, this proportions was 9%, 12%, 22% and 48%, respectively. In conclusion, our study provides a comprehensive overview of the therapy of lung cancer patients in Germany and quantitatively demonstrates the considerable differences between age groups. In terms of clinical cancer registration, the results are useful to estimate the completeness of data for the different types of treatment.

POORLY DIFFERENTIATED CLUSTERS IN COLORECTAL CARCINOMA: ASSOCIATION WITH OTHER HISTOPATHOLOGICAL PROGNOSTIC PARAMETERS INCLUDING TUMOUR BUDDING

Objective: In India, colorectal carcinoma (CRC) ranks third in terms of cancer incidence. Pathologists are essential when it comes to determining the stage, examining surgical margins, and recording the histopathologic prognostic factors. A new prognostic grading system is proposed named poorly differentiated clusters (PDCs), which are defined by neoplastic clusters of 5 cells lacking glandular structure in the invasive front of the stroma. It is significant for cancer-specific and recurrence-free survival in CRC patients, reflecting the biological aggressiveness of the tumor. Aim of the study was to analyse of PDCs in colorectal carcinomas and association with other histopathological prognostic factors. Methods: The Hematoxylin and Eosin (HandE)-stained slides of 76 histopathologically diagnosed CRC resection specimens were reviewed. Poorly differentiated clusters (PDC) were assessed into under 200x power. The correlation of PDC with other histopathological prognostic parameters like tumor size, site, grade, laterality, lymphovascular invasion, perineural invasion, T stage, N stage, and tumor budding was analyzed using descriptive statistics and the Chi-square test with SPSS version 26.0. Results: There was no significant association between PDC and age, tumor location, tumor size, histological grade, LVI, PNI, or lymphnode status. Where a significant association was noted between the sex and PDC grade (P value = 0.035), T stage and PDC grade (P value = 0.045), and N stage and PDC grade is significant (P value = 0.001). Conclusion: PDCs may be considered, along with other clinical-pathological parameters, a promising prognostic factor for the management of patients with CRC and should be included in pathological reports, but it still needs standardization and further validation. At the same time, tumor budding can become an irreplaceable histological indicator for identifying a high malignant potential carcinoma and poor prognosis in CRCS, thus indicating the need for aggressive postoperative management to improve the prognosis of the patient. PDC is important for the survival of CRC patients, indicating the aggressiveness of the tumor both in terms of cancer-specific survival and freedom from recurrence. PDC may help to identify patients who need a more intensive postoperative follow-up and the possibility of adjuvant therapy.

Fine needle aspiration cytology diagnoses of follicular thyroid carcinoma: results from a multicenter study in Asia

Background: This study was designed to compare diagnostic categories of thyroid fine needle aspiration cytology (FNAC) and incidence of thyroid tumors in the multi-institutional Asian series with a special focus on diagnostic category IV (suspicious for a follicular neoplasm) and follicular thyroid carcinomas (FTCs). Methods: Distribution of FNAC categories, incidence of thyroid tumors in resection specimens and cytologic diagnoses of surgically confirmed follicular adenomas (FAs) and FTCs were collected from 10 institutes from five Asian countries and were compared among countries and between FAs and FTCs. Results: The frequency of category IV diagnoses (3.0%) in preoperative FNAC were significantly lower compared to those in Western countries (10.1%). When comparing diagnostic categories among Asian countries, category IV was more frequent in Japan (4.6%) and India (7.9%) than in Taiwan (1.4%), Korea (1.4%), and China (3.6%). Similarly, incidence of FAs and FTCs in surgical resection specimens was significantly higher in Japan (10.9%) and India (10.1%) than in Taiwan (5.5%), Korea (3.0%), and China (2.5%). FTCs were more commonly diagnosed as category IV in Japan (77.5%) than in Korea (33.3%) and China (35.0%). Nuclear pleomorphism, nuclear crowding, microfollicular pattern, and dyshesive cell pattern were more common in FTCs compared with FAs. Conclusions: Our study highlighted the difference in FNAC diagnostic categories of FTCs among Asian countries, which is likely related to different reporting systems and thyroid cancer incidence. Cytologic features such as nuclear pleomorphism, nuclear crowding, microfollicular pattern, and dyshesive cell pattern were found to be useful in diagnosing FTCs more effectively.

A Systemic Review on Phytochemicals and Novel Approaches for the Management of Hepatic Cancer

Introduction: Hepatic cancer, an aggressive tumour that often develops along with cirrhosis and chronic liver disease like infections with the hepatitis B and hepatitis C viruses, while nonalcoholic steatohepatitis, is linked to metabolic syndrome or diabetes mellitus. It is the third most prevalent cause of cancer-related mortality globally and ranks fifth in cancer incidence. According to GLOBOCON, the prevalence is expected to rise by 55.0% and the fatalities by 56.4% in the near future. Objective: The present review offered natural plant-based substances and compounds having curative effects on liver cancer, along with novel drug delivery systems and nanocarrier-based therapies. Methods: The literature has been taken from PubMed, Google Scholar, SciFinder, Springer Nature, Bentham Science, PLOS one, or other internet sites. Result: Treatment for heterogeneous malignancy is multidimensional, and care guidelines differ depending on the specialty and location. Several nutritional herbal remedies and their active phytoconstituents may have an abundance of impacts on the management of liver cancer, including preventing the growth and spread of tumor cells, shielding the body from liver carcinogens, boosting the effects of chemotherapy and immunomodulating the body. Conclusion: The treatment of liver cancer involves multidisciplinary and multimodel therapy. The literature is a compilation of extract, compounds, and novel approaches like nanoparticles, microsphere, liposomes, niosomes, phytosomes and microparticles. These approaches not only manage cancer but also boost the immunity of the individuals.

Efficacy of chondroitin sulfate as an emerging biomaterial for cancer-targeted drug delivery: A short review.

The global increase in cancer incidence over the past decade highlights the urgent need for more effective therapeutic strategies. Conventional cancer treatments face challenges such as drug resistance and off-target toxicity, which affect healthy tissues. Chondroitin sulfate (CHDS), a naturally occurring bioactive macromolecule, has gained attention because of its biocompatibility, biodegradability, and low toxicity, positioning it as an ideal candidate for cancer-targeted drug delivery systems. This review highlights the potential of CHDS as an emerging biomaterial in cancer therapy, focusing on its unique biological properties and applications in drug delivery platforms. Furthermore, we discuss the advantages of CHDS-based biomaterials in enhancing cancer treatment efficacy and minimizing side effects, in order to provide a comprehensive reference for future research on CHDS-based cancer therapeutics.

The incidence of kidney cancer in Iran: a systematic review and meta-analysis

The incidence of kidney cancer in Iran: a systematic review and meta-analysis

Analysis of clinical characteristics and risk factors on serrated polyps with synchronous advanced adenoma in elderly and non-elderly people: a retrospective cohort study

ObjectivesSerrated polyps (SPs) with synchronous advanced adenoma (AA) may increase the incidence of colorectal cancer. However, current studies do not address this combination of SPs and AAs in detail with...

Effects of Fermented Kimchi Consumption on Anthropometric and Blood Cardiometabolic Indicators: A Systematic Review and Meta-Analysis of Intervention Studies and Prospective Cohort Studies.

Increasing global kimchi consumption has prompted interest in its health impact. However, comprehensive reviews of the influence of kimchi on cardiometabolic risk factors, especially meta-analyses, remain limited. This review assessed the impact of fermented kimchi consumption on cardiometabolic risk factors by systematically reviewing human intervention and prospective cohort studies, and conducting a meta-analysis of intervention studies. A literature search of PubMed, EMBASE, Scopus, Web of Science, RISS, KISS, and ScienceON databases was conducted through April 30, 2024. The inclusion criteria encompassed studies that examined the effects of fermented kimchi, without any added ingredients or lactic acid bacteria, on health outcomes, including anthropometric measures, blood pressure, cardiometabolic and glycemic indicators, inflammatory cytokines, and the incidence of related chronic diseases. Data extraction and quality evaluation were conducted independently by 3 researchers. Pooled effect sizes were calculated as weighted mean differences (WMDs) with 95% CIs employing random-effects models. Five intervention studies (205 participants) and 4 prospective cohort studies (42 455 participants) were selected. A meta-analysis of the intervention studies revealed a significant reduction in fasting blood glucose (WMD: -1.93 mg/dL; 95% CI: -3.82, -0.03; I2 = 17.4%) following the consumption of fermented kimchi. After excluding studies that contributed to increased heterogeneity, significant inverse associations were observed between fermented kimchi consumption and triglycerides (WMD: -28.9 mg/dL; 95% CI: -53.2, -4.5; I2 = 0.0%), systolic blood pressure (WMD: -3.48 mmHg; 95% CI: -5.95, -1.01, I2 = 0.0%), and diastolic blood pressure (WMD: -2.68 mmHg; 95% CI: -4.75, -0.62; I2 = 0.0%). Prospective cohort studies linked higher kimchi intake with a lower incidence of cancer and metabolic syndrome and an increased likelihood of achieving normal body weight. This review supports beneficial effects of fermented kimchi on cardiometabolic health. However, due to the limited number of studies, these findings should be interpreted cautiously, highlighting the need for further research in diverse populations. PROSPERO registration No. CRD42024532020.

Body mass index and breast cancer risk in premenopausal and postmenopausal East Asian women: a pooled analysis of 13 cohort studies.

It has been suggested that the association between body mass index and breast cancer risk differs between Asian women and Western women. We aimed to assess the associations between body mass index and breast cancer incidence in East Asian women. Pooled analyses were performed using individual participant data of 319,189 women from 13 cohort studies in Japan, Korea, and China. Participants' height and weight were obtained by measurement or self-reports at cohort baseline. Breast cancer was defined as code C50.0-C50.9 according to the International Classification. Using a Cox proportional hazards model, hazard ratios of breast cancer were estimated for each body mass index category, with the reference group set as the group with a body mass index of 21 to < 23 kg/m2. The hazard ratio for a 5kg/m2 increase in body mass index was also calculated. During a mean 16.6 years of follow-up, 4819 women developed breast cancer. Similar to Westerners, a steady increase in breast cancer risk with increasing body mass index was observed in postmenopausal women, but the slope of the risk increase appeared to slow at a body mass index of 26-28 kg/m2. In premenopausal women, the inverse association seen in Westerners was not observed. The risk of developing breast cancer after 50 years of age increased slightly with increasing body mass index, which was more pronounced in the older birth cohort. There was no significant association between body mass index and the risk of developing breast cancer before 50 years of age, but the risk estimates changed from positive to negative as the birth cohort got younger. In East Asia, the role of body mass index in breast cancer in premenopausal women may be changing along with the increase in obesity and breast cancer. The increased risk of postmenopausal breast cancer with a higher body mass index was as robust as that of Western women.