Tristetraprolin (TTP) can inhibit the abnormal proliferation of malignant tumors but there are no studies involving TTP and esophageal squamous cell carcinoma (ESCC). We aimed to determine the effect of TTP on ESCC cell proliferation and to elucidate the underlying mechanism.

The human ESCC cell line, KYSE-510, and the human ESCC cell line, KYSE-150, stably infected with tetracycline-inducible expression (Tet-on-TTP and Tet-on-EV, respectively) were screened with puromycin. After Tet-on-TTP KYSE-150 cells were treated with different concentrations of doxycycline [Dox] (0, 0.5, and 1 ug/mL), the levels of TTP mRNA and protein expression were detected by real-time fluorescent quantitative PCR and western blotting, respectively. The effects of TTP on proliferation and migration were estimated by CCK-8 and Transwell assays, respectively. Cell apoptosis and cell cycle were measured by flow cytometry. Cellular apoptosis-related gene protein expression was determined by western blotting.

TTP overexpression significantly inhibited KYSE-510 and KYSE-150 proliferation. TTP overexpression also significantly inhibited KYSE-150 migration. In addition, TTP expression upregulation promoted the KYSE-150 apoptosis and induced cell cycle arrest in the G2 phase, downregulated Bcl-2 expression, and upregulated Bax expression.

TTP inhibited ESCC cell proliferation, promoted ESCC cell apoptosis, and arrested cell cycle progression in the G2 phase.

Benign stenosis frequently occurs after esophagectomy, causing dysphagia, eating problems, and diminished quality of life. This study aimed to identify risk factors for benign anastomotic stenosis after esophagectomy for cancer.

This retrospective cohort study analyzed patients who underwent esophagectomy at Amsterdam UMC from 2012 until 2022. Intrathoracic and cervical anastomoses were examined separately. Benign anastomotic stenosis was defined as stenosis at the anastomosis causing dysphagia (Ogilvie score ≥2) and requiring at least one endoscopic dilation. Predictive factors were identified using logistic regression.

The study enrolled 902 patients: 605 with intrathoracic and 297 with cervical anastomosis. Of these cases, 91.1 % were a minimally invasive esophagectomy. Stenosis occurred in 18.4 % of the intrathoracic cases and 49.8 % of the cervical cases (p < 0.001). The patients required medians of 4 and 7 dilations, respectively (p = 0.001). The median time to stenosis was 99 days for the intrathor days for the cervical anastomoses (p = 0.001). Intrathoracic stenosis was independently associated with anastomotic leakage (odds ratio [OR], 2.034; 95 % confidence interval [CI], 1.116-3.708). For the patients without leakage, a 2 mm versus a 25 mm circular stapler reduced stenosis risk (OR, 0.486; 95 % CI, 0.294-0.803), whereas use of immunosuppressants (OR, 3.492; 95 % CI, 1.186-10.279]) and chronic pulmonary disease (OR, 2.717; 95 % CI, 1.293-5.707) increased it. For cervical anastomoses, hand-sewn end-to-side anastomosis was protective (OR, 0.454; 95 % CI, 0.234-0.879).

The key risk factors for intrathoracic benign anastomotic stenosis are anastomotic leakage, smaller circular stapler size, use of immunosuppressants, and chronic pulmonary disease. For cervical anastomoses, the hand-sewn end-to side technique is protective compared with the end-to-end technique, whereas use of immunosuppressants and chronic pulmonary disease increases the risk.

Bis-indole-derived compounds including 1,1-bis(3'-indolyl)-1-(3,5-disubstitutedphenyl)methane (DIM-3,5) analogs bind both orphan nuclear receptors 4A1 (NR4A1) and NR4A2, and DIM-3,5 compounds act as dual receptor inverse agonists and inhibit both NR4A1- and NR4A2-regulated responses. Chromatin immunoprecipitation assays show that β1-integrin and the methyltransferase gene G9a are regulated by both NR4A1 and NR4A2 acting as cofactors for Sp1- and Sp4-dependent gene expression. DIM-3,5 treatment results in the loss of one or more of these nuclear factors from the β1-integrin and G9a promoters. Single-cell and RNAseq analyses show that both receptors regulate common (<10%) and unique genes in SW480 colon cancer cells; however, functional enrichment analysis of the differentially expressed genes converges to several common pathways and gene ontology terms.

Humans can perceive five canonical tastes: salty, sour, umami, sweet, and bitter. These tastes are transmitted through the activation of ion channels and receptors. Bitter taste receptors (Taste Family 2 Receptors; T2Rs) are a sub-family of 25 G-protein coupled receptor (GPCR) isoforms that were first identified in type II taste bud cells. T2Rs are activated by a broad array of bitter agonists, which cause an increase in intracellular calcium (Ca2+) and a decrease in cyclic adenosine 3',5'-monophosphate (cAMP). Interestingly, T2Rs are expressed beyond the oral cavity, where they play diverse non-taste roles in cell physiology and disease. Here, we summarize the literature that explores the role of T2Rs in apoptosis. Activation of T2Rs with bitter agonists induces apoptosis in several cancers, the airway epithelia, smooth muscle, and more. In many of these tissues, T2R activation causes mitochondrial Ca2+ overload, a main driver of apoptosis. This response may be a result of T2R cellular localization, nuclear Ca2+ mobilization and/or a remnant of the established immunological roles of T2Rs in other cell types. T2R-induced apoptosis could be pharmacologically leveraged to treat diseases of altered cellular proliferation. Future work must explore additional extra-oral T2R-expressing tissues for apoptotic responses, develop methods for in-vivo studies, and discover high affinity bitter agonists for clinical application.

Despite the importance of genetic testing for risk assessment and treatment in breast cancer, the prognostic impact of germline pathogenic variants (PVs), especially in Asian populations, is unclear. We assessed the impact of germline PVs in patients with early-stage breast cancer. This study included 7278 Japanese multihospital registry patients. PVs of ATM, BRCA1, BRCA2, CDH1, CHEK2, NBN, NF1, PALB2, PTEN, STK11, and TP53 were evaluated. PV and non-PV carriers were matched by age, histology, and stage. Associations between PVs and survival were assessed. The primary outcome was invasive disease-free survival (IDFS). Secondary outcomes included relapse-free survival (RFS), overall survival, and breast cancer-specific survival. We identified 320 (4.4%) patients with BRCA1/2 PVs and 79 (1.1%) with PVs other than BRCA1/2 (non-BRCA1/2). A total of 360 patients (BRCA1/2, n = 289; non-BRCA1/2, n = 71) were matched to 720 noncarriers. Patients with BRCA1/2 PVs had significantly shorter 10-year IDFS (adjusted hazard ratio (aHR) = 2.15; 95% confidence interval (CI), 1.61-2.86; p < 0.001); and RFS (aHR = 1.74; 95% CI, 1.25-2.44; p = 0.001) than noncarriers. Among patients with hormone receptor-positive HER2-negative breast cancer, BRCA1/2 PV carriers exhibited significantly shorter 10-year IDFS than noncarriers, even those with stage I/II disease (total, aHR = 2.23; 95% CI, 1.55-3.23; p < 0.001, Stage I/II, aHR = 2.22; 95% CI, 1.43-3.44; p < 0.001). There was no significant difference in 10-year IDFS between the non-BRCA1/2 PV carrier and noncarrier groups (aHR = 1.40; 95% CI, 0.67-2.93; p = 0.37). Asian patients with breast cancer carrying germline BRCA1/2 PV, even those with a low recurrence risk, have significantly shorter 10-year IDFS than noncarriers.

The aim is to assess the feasibility and accuracy of a novel quantitative ultrasound (US) method based on global speed-of-sound (g-SoS) measurement using conventional US machines, for breast density assessment in comparison to mammographic ACR (m-ACR) categories.

In a prospective study, g-SoS was assessed in the upper-outer breast quadrant of 100 women, with 92 of them also having m-ACR assessed by two radiologists across the entire breast. For g-SoS, ultrasonic waves were transmitted from varying transducer locations and the image misalignments between these were then related analytically to breast SoS. To test reproducibility, two consecutive g-SoS acquisitions each were taken at two similar breast locations by the same operator.

Measurements were found highly repeatable, with a mean absolute difference ± standard deviation of 3.16 ± 3.79 m/s. Multiple measurements were combined yielding a single g-SoS estimate per each patient, which strongly correlated to m-ACR categories (Spearman's = 0.773). The g-SoS values for categories A-D were 1459.6 ± 0.74, 1475.6 ± 15.92, 1515.6 ± 27.10, and 1545.7 ± 20.62, with all groups (except A-B) being significantly different from each other. Dense breasts (m-ACR C&D) were classified with 100% specificity at 78% sensitivity, with an area under the curve (AUC) of 0.931. Extremely dense breasts (m-ACR D) were classified with 100% sensitivity at 77.5% specificity (AUC = 0.906).

Quantitative g-SoS measurement of the breast was shown feasible and repeatable using conventional US machines, with values correlating strongly with m-ACR assessments.

Question Breast density is a strong predictor of risk for breast cancer, which frequently develops in dense tissue regions. Therefore, density assessment calls for refined non-ionizing methods. Findings Quantitative global speed-of-sound (g-SoS) measurement of the breast is shown to be feasible using conventional US machines, repeatable, and able to classify breast density with high accuracy. Clinical relevance Being effective in classifying dense breasts, where mammography has reduced sensitivity, g-SoS can help stratify patients for alternative modalities. Ideal day for mammography or MRI can be determined by monitoring g-SoS. Furthermore, g-SoS can be integrated into personalized risk assessment.

Herein, nine square planar trans-arylbis(triphenylphosphine)palladium halides (PdX(PPh3)2Ar) were synthesized and fully characterized. The molecular structure of two complexes (1 and 2) have been determined by both X-ray diffraction and described thanks to Hirshfeld surface analysis. Investigation of the antioxidant activities showed that most of the complexes exhibit a strong dose-dependent radical scavenging activity towards DPPH radical as well as in the ABTS radical scavenging test. Complexes 1 [PdI(PPh3)2(4-MeOC6H4)] and 3 [PdCl(PPh3)2(4-MeOC6H4)] showed the highest activity in the DPPH assay with EC50 values of 1.14 ± 0.90 and 1.9 ± 0.87 µM, respectively. In contrast, for the ABTS assay, quercetin (5.56 ± 0.97 µM) was slightly more efficient than the three complexes 1 (5.78 ± 0.98 µM), 2 (7.01 ± 0.98 µM), and 3 (11.12 ± 0.94 µM). The use of kinetic studies as a powerful parameter shows that complexes 1, 2, and 3 displayed the best antioxidant efficiency. The antioxidant effect of the nine palladium complexes has been also evaluated on the enzyme-catalyzed oxidation of the L012 probe (using HRP/H2O2) by using a chemiluminescence technique. As with the last model, complexes 1, 2, and 3 showed the best activity, with EC50 values of 3.56 ± 1.87, 148 0.71, and 5.8 ± 2.60 µM, respectively. Interestingly, those complexes (1, 2, and 3) even exhibited a higher dose-dependent activity than the quercetin (7.06 ± 2.56 µM) used as a standard. Taken together, the combined results reveal that the antiradical and enzyme (HRP) inhibitory activity of complexes decrease following the ligand order of p-OMePh > p-OAcPh >> Ph.

Resection is considered the standard of care for patients with localized esophageal cancer who are "physiologically fit". Patients who do not meet this standard are considered contraindicated to receive surgery. We hypothesized that among patients with non-metastatic esophageal cancer, the consideration of contraindication status would vary based on clinical and demographic factors and would vary between institutions.

We identified patients with non-metastatic gastric and esophageal cancer in the National Cancer Database (NCDB) from 2004 to 2018. Patients were categorized into three groups based on surgical treatment: surgical resection (including endoscopic mucosal resection), resection contraindicated, and refusal of resection based on the coding of the "reason for no surgery" data element. Demographic, clinical, and institutional characteristics were compared between the groups using bivariate and multivariate techniques to identify factors associated with contraindicated status. A subgroup analysis of cT1N0M0 patients was also used to assess every institution in the NCDB's observed-expected ratio for contraindication status.

In total, 144,591 patients with non-metastatic disease met inclusion criteria: 124,972 (86%) underwent resection, 13,793 (10%) were contraindicated for resection, and 5826 (4%) refused resection. Contraindication was associated with age, non-Hispanic Black race, socioeconomic status, Charlson-Deyo score, insurance type, institution characteristics, clinical T-stage, and clinical N-stage. There were 9459 patients who were cT1N0M0 and had no co-morbidities. In this cohort, there were more than 1000-fold differences between individual programs regarding observed-expected ratio of contraindication status when adjusting for clinical and demographic characteristics.

Variation in the assessment of contraindication status varies dramatically between institutions. Underserved minorities, including age, race, and insurance type, are risk factors for being considered contraindicated. These findings highlight the disparities that exist regarding surgical care of non-metastatic esophageal cancer in the United States.

Colorectal cancer is a significant cause of mortality globally, with several factors impacting patient outcomes, including access to healthcare, early detection, and treatment. Despite this, the specific factors affecting incidence of death among colorectal cancer patients in the Amhara region have not been thoroughly investigated. Thus, this study seeks to assess incidence and determinants of mortality among colorectal cancer patients in Amhara Region oncology centers.

The mean age of the participants was 48.6 years (SD ± 15). Median survival time was 23.8 months. The overall incidence rate or incidence density of a colorectal cancer mortality rate was 2.9 per 100 person-months (95% CI: 2.5-3.4). Survival rates of colorectal cancer patients 1and 5 year was 69.78% and 16.1%, respectively. The result of the multivariable analysis showed that colorectal cancer patients who had presenting symptoms [AHR = 2.67 (95% CI: 1.95, 3.67)], Base line HGB level < 12.5 mg/dl [AHR = 1.63 (95% CI: 1.12, 2.37)], WHO or ECOG poor performance status [AHR = 2.99 (95% CI: 2.17, 4.12), late stage of cancer [AHR = 2.32 (95% CI: 1.42, 3.79)] and location of tumor on colorectal [AHR = 1.76 (95% CI: 1.20, 2.55)] were significantly associated with mortality of colorectal cancer.

The study highlights significant findings on the survival and mortality of colorectal cancer patients. The overall mortality rate was 2.9 per 100 person-months. Multivariable analysis identified presenting symptoms, low baseline hemoglobin levels, poor performance status, late-stage cancer, and tumor location as significant predictors of mortality. Highlighting the need for early detection and targeted care strategies.

This study explored the value of stomach ultrasound reporting and data system (Su-RADS) and two-dimensional shear wave elastography (2D-SWE) in the diagnosis of benign and malignant lesions of the gastric wall, evaluating the feasibility of combining the two methods for the diagnosis of gastric wall lesions.

113 patients with gastric wall lesions were examined after oral gastric ultrasound contrast agent, and the grades of the gastric wall lesions were classified according to Su-RADS. Moreover, 2D-SWE was performed to measure the E value of the lesions. ROC curves were constructed to evaluate the diagnostic efficacy of Su-RADS, 2D-SWE and their combination for gastric wall lesions.

The cutoff values for Emean and Emax were 8.01 kPa and 11.08 kPa, respectively. The sensitivity and specificity of 2D-SWE were 70.59%, 93.67% and 85.69%, 88.61%, respectively. The diagnostic sensitivity and specificity of Su-RADS were 91.18% and 82.28%, respectively. The AUC of combination of two methods was 0.951, which was greater than that of Su-RADS (0.940) or 2D-SWE alone (0.853, 0.903), and the sensitivity and specificity were 82.35% and 94.94%. The sensitivity and specificity of the combination of the two methods for the diagnosis of malignant gastric lesions were 82.35% and 94.94%, respectively. The AUC was 0.951, and the Youden index was 0.8064. The DeLong test was used to determine the AUC between the combination of two methods and 2D-SWE was P < 0.05.

Compared with Su-RADS or 2D-SWE alone, the combination of the two methods is more effective at diagnosing of gastric wall.And improved the specificity in the diagnosis of gastric wall lesions.

Most people prefer to die at home. Timely and appropriate provision of assistive technology can support people to remain at home in the palliative phase. A state-wide palliative care equipment programme (PCEP) was established in Queensland, Australia, to support coordinated assistive technology provision. The objective of this study was to identify population-wide palliative care equipment needs and their relationship to primary diagnostic categories.

A retrospective, cross-sectional analysis of equipment provided over a 19-month period was conducted. This included types of equipment provided and characteristics of the participants such as rurality, age and diagnostic category.

There were 13 764 approved equipment requests, with a median time between equipment application and death being around 35 days. There were significant differences in the types of equipment typically required across diagnostic categories.

The findings from the study can provide a benchmark for the development of population-wide PCEPs. For practitioners who are new to palliative care, typical trajectories of equipment needs by diagnostic group can help guide equipment planning.

Background: Breast cancer remains the leading cause of cancer-related deaths among women despite advances in early detection. Neoadjuvant chemotherapy (NACT) is now standard for early-stage BC, with vitamin D (VD) emerging as a potential prognostic biomarker considering its positive pleiotropic effects. This review and meta-analysis assess the impact of baseline VD levels on outcomes in BC patients undergoing NACT. Methods: Inclusion criteria required patients to be over 18 years of age, have a pathologically confirmed BC diagnosis, and have their VD levels assessed prior to chemotherapy. Studies were included if they reported odds ratios (ORs) for response and/or hazard ratios (HRs) for PFS with 95% confidence intervals (CIs). A comprehensive literature search of PubMed/MEDLINE and Scopus/ELSEVIER (2014-2024) was conducted, and data were analyzed using fixed- and random-effects models, with Forest plots illustrating the results. Study quality and potential biases were assessed using the MINORS, NOS, and RoB2 scales, and statistical heterogeneity was evaluated with I2 statistics and funnel plots. Results: Six studies were included in the analysis. All studies addressed stages II and III, with three also including stage I. The meta-analysis covered data from 722 patients regarding NACT response and 1033 patients for PFS. The results revealed a 22% reduction in the likelihood of non-response to NACT associated with adequate VD levels (low/deficient VD vs. high/sufficient VD; OR: 0.78; 95% CI: 0.30-1.25; p = 0.001) and a 35% reduction in progression risk with sufficient baseline VD levels (low/deficient VD vs. high/sufficient VD; HR: 0.65; 95% CI: 0.33-0.97; p < 0.001). Conclusions: These findings highlight the significance of maintaining adequate vitamin D levels in BC treatment and encourage further studies to unravel the role of VD on cancer biology.

Malnutrition is a commonly observed side effect in cancer patients, with a 30-85% worldwide prevalence in this population. Existing malnutrition screening tools miss ~ 20% of at-risk patients at initial screening and do not capture the abnormal body composition phenotype. Meanwhile, the gold-standard clinical criteria to diagnose malnutrition use changes in body composition as key parameters, particularly body fat and skeletal muscle mass loss. Diagnostic imaging, such as computed tomography (CT), is the gold-standard in analyzing body composition and typically accessible to cancer patients as part of the standard of care. In this study, we developed a deep learning-based body composition analysis approach over a diverse dataset of 200 abdominal/pelvic CT scans from cancer patients. The proposed approach segments adipose tissue and skeletal muscle using Swin UNEt TRansformers (Swin UNETR) at the third lumbar vertebrae (L3) level and automatically localizes L3 before segmentation. The proposed approach involves the first transformer-based deep learning model for body composition analysis and heatmap regression-based vertebra localization in cancer patients. Swin UNETR attained 0.92 Dice score in adipose tissue and 0.87 Dice score in skeletal muscle segmentation, significantly outperforming convolutional benchmarks including the 2D U-Net by 2-12% Dice score (p-values < 0.033). Moreover, Swin UNETR predictions showed high agreement with ground-truth areas of skeletal muscle and adipose tissue by 0.7-0.93 R2, highlighting its potential for accurate body composition analysis. We have presented an accurate body composition analysis based on CT imaging, which can enable the early detection of malnutrition in cancer patients and support timely interventions.

In this review, we discuss oropharyngeal squamous cell carcinoma (OPSCC) treatment options with a focus on the molecular mechanisms of OPSCC in head and neck squamous cell carcinoma (HNSCC) and head and neck cancers (HNCs). Treatment can be radical intent (aim for cure) or palliative intent (aim for disease control and symptom management). OPSCC is a prominent subset of HNSCCs in Australia and the Western World.

We looked at the current conventional treatment options with an overview of recent advances and future endeavours.

We identified that radiotherapy is the primary management for OPSCC in most countries, including the USA, UK, NZ, and Australia. In contrast, surgery is only considered for superficial OPSCC or neck surgery. If surgery is incomplete, then definitive management still requires radiotherapy.

Molecular therapy is largely at the preclinical stage, with cetuximab, nivolumab, pembrolizumab, Lenvatinib, and bevacizumab being tested clinically currently.

Esophageal squamous cell carcinoma (ESCC) is a malignant tumor with high incidence and mortality rates worldwide. This study aimed to investigate the correlation between LINC-PINT polymorphisms and ESCC risk in the Hainan Han population.

A total of 391 patients with ESCC and 452 healthy controls were enrolled to evaluate the effect of LINC-PINT SNPs (single nucleotide polymorphisms) on ESCC susceptibility. Associations were evaluated by calculating odds ratios (OR) and 95% confidence intervals (CIs). Multifactor dimensionality reduction analysis was performed to explore the association between SNP-SNP interactions and ESCC susceptibility. We further determined the correlation between clinical indicators and SNP in patients with ESCC.

Our study showed that rs157916 (OR 0.63, p = 0.011) and rs157928 (OR 0.80, p = 0.021) were associated with a decreased risk of ESCC. Stratified analysis indicated that rs157916 could decrease the risk of ESCC in people aged >64 years, in males, and non-drinkers (OR 0.58, p = 0.042; OR 0.58, p = 0.010; OR 0.62, p = 0.025, respectively). Rs16873842 was related to a decreased risk of ESCC in males (OR 0.70, p = 0.015). Rs7801029 was associated with ESCC risk in females (OR 0.39, p = 0.033) and non-drinkers (OR 0.68, p = 0.040). Rs7781295 decreased the ESCC risk in smokers (OR 0.58, p = 0.046) and drinkers (OR 0.58, p = 0.046). In addition, rs157928 played a protective role in ESCC risk in females (OR 0.39, p = 0.033) and non-smokers (OR 0.32, p = 0.006). Additionally, the best predictive model for ESCC was a combination of rs157916, rs16873842, rs7801029, rs7781295, rs28662387, and rs157928.

Our study revealed that LINC-PINT polymorphisms were associated with ESCC risk.

Human Papillomavirus (HPV) is a widespread infection associated with various cancers, including cervical, oropharyngeal, anal, and genital cancers. This infection contributes to 5 % of global cancer cases annually, affecting approximately 625,600 women and 69,400 men. Cervical cancer remains the most prevalent HPV-linked cancer among females, with the highest incidence seen in low and middle-income countries (LMICs). While most HPV infections are transient, factors such as HPV variants, age, gender, and socioeconomic status influence transmission risks. HPV is categorized into high-risk (HR-HPV) and low-risk types, with strains like HPV 16 and 18 displaying distinct demographic patterns. The intricate pathogenesis of HPV involves genetic and epigenetic interactions, with HPV oncogenes (E6 and E7) and integration into host DNA playing a pivotal role in driving malignancies. Early diagnostics, utilizing HPV DNA testing with surrogate markers such as p16, and advanced molecular techniques like PCR, liquid biopsy, and NGS, significantly impact the management of HPV-induced cancers. Effectively managing HPV-related cancers demands a multidisciplinary approach, including immunotherapy, integrating current therapies, ongoing trials, and evolving treatments. Prevention via HPV vaccination and the inclusion of cervical cancer screening in national immunization programs by conventional Pap smear examination and HPV DNA testing remains fundamental.Despite the preventability of HPV-related cancers, uncertainties persist in testing, vaccination, and treatment. This review article covers epidemiology, pathogenesis, diagnostics, management, prevention strategies, challenges, and future directions. Addressing issues like vaccine hesitancy, healthcare disparities, and advancing therapies requires collaboration among researchers, healthcare providers, policymakers, and the public. Advancements in understanding the disease's molecular basis and clinical progression are crucial for early detection, proper management, and improved outcomes.

The burden of cancer is increasing globally and is having a negative impact on people's physical, mental and financial health. On the other hand, developing countries are not progressing to prevent the disease at the same rate as the disease burden increases. The development of strategies for cancer prevention, control and treatment that contribute to the community's improved health requires knowledge of cancer epidemiologic data. There is relatively little epidemiologic evidence of nasopharyngeal, tongue and laryngeal cancer in southern Ethiopia. This study aimed to assess the epidemiological burden of nasopharyngeal, tongue and laryngeal cancer among patients treated at Hawassa University Comprehensive and Specialised Hospital (HUCSH) between 2013 and 2019.

A cross-sectional retrospective review was conducted among 3,002 patients who attended the oncologic care at HUCSH. Data were retrieved between February and May 2020. Data were entered using Epi-data version 3.1 and the data were then exported to IBM SPSS version 22 (IBM Corporation, Armonk, NY, USA) for further processing and analysis. A descriptive analysis was done.

A total of 280 (9.3%) new head and neck cancer (HNC) patients were identified over a period of 7 years. Nasopharyngeal cancer accounts for more than one-fourth (26.4%) of all HNCs, followed by tongue 15% and laryngeal 14.6% cancers. Males constituted nearly two-thirds of the cases. The overall caseloads doubled over the retrieved years.

According to this study, nasopharyngeal, tongue and laryngeal cancer is a more prominent cause of morbidity. According to place, person and time, the frequency of nasopharyngeal, tongue and laryngeal cancer steadily rose in both sexes and across all age categories. Therefore, immediate intervention is needed nationwide to monitor the disease's explosive growth.

Combined radiotherapy and immune checkpoint inhibition is a potential treatment option for head and neck squamous cell carcinoma (HNSCC). Immunocompetent mouse models can help to successfully develop radio- immunotherapy combinations and to increase our understanding of the effects of radiotherapy on the tumor microenvironment for future clinical translation. Therefore, the aim of this study was to develop a homogeneous, reproducible HNSCC model originating from the Mouse Oral Cancer 1 (MOC1) HNSCC cell line, and to explore the radiotherapy-induced changes in its tumor microenvironment, using flow cytometry and PD-L1 microSPECT/CT imaging.

In vivo growing tumors originating from the parental MOC1 line were used to generate single cell derived clones. These clones were screened in vitro for their ability to induce programmed cell death ligand 1 (PD-L1) and major histocompatibility complex class I (MHC-I) following IFNγ exposure. Clones with different IFNγ sensitivity were inoculated in C57BL/6 mice and assessed for tumor outgrowth. The composition of the tumor microenvironment of a stably growing (non)irradiated MOC1-derived clone was assessed by immunohistochemistry, flow cytometry and PD-L1 microSPECT/CT.

Low in vitro inducibility of MHC-I and PD-L1 by IFNγ was associated with increased tumor outgrowth of MOC1 clones in vivo. Flow cytometry analysis of cells derived from a stable in vivo growing MOC1 clone MOC1.3D5low showed expression of MHC-I and PD-L1 on several cell populations within the tumor. Upon irradiation, MHC-I and PD-L1 increased on leukocytes (CD45.2+) and cancer associated fibroblasts (CD45.2-/EpCAM-/CD90.1+). Furthermore, PD-L1 microSPECT/CT showed increased tumor uptake of radiolabeled PD-L1 antibodies with a heterogeneous spatial distribution of the radio signal, which co-localized with PD-L1+ and CD45.2+ areas.

PD-L1 and MHC-I inducibility by IFNγ in vitro is associated with tumor outgrowth of MOC1 clones in vivo. In tumors originating from a stably growing MOC1-derived clone, expression of these immune-related markers was induced by irradiation shown by flow cytometry on several cell populations within the tumor microenvironment such as immune cells and cancer associated fibroblasts. PD-L1 microSPECT/CT showed increased tumor uptake following radiotherapy, and autoradiography showed correlation of uptake with areas that are heavily infiltrated by immune cells. Knowledge of radiotherapy-induced effects on the tumor microenvironment in this model can help optimize timing and dosage for radio- immunotherapy combination strategies in future research.

To facilitate rapid, efficient, and accurate detection of miR-96-5p associated with gastric cancer (GC), we developed a bioanalytical platform by integrating surface-enhanced Raman spectroscopy with lateral flow assay (SERS-LFA). With these SERS-LFA strips, miR-96-5p within the specimen competed with Au rhombic dodecahedron (AuRD) conjugated single-stranded DNA (ssDNA) to bond to the immobilized hairpin DNA (hpDNA) probe on the T line. Consequently, higher abundance of miR-96-5p led to reduced conjugation of AuRD on the T line, thereby resulting in diminished SERS intensity. The biosensor exhibited a detection time of approximately 30 min and demonstrated a low limit of detection (LOD) for miR-96-5p in PBS buffer solution, down to 3.7 fM. To validate its clinical utility for the early diagnosis of patients with different degrees of gastric lesions, we performed quantitative evaluations in cohorts that included healthy individuals, patients with mild intraepithelial neoplasia, patients with severe intraepithelial neoplasia, as well as patients diagnosed with GC. The results obtained from the SERS-LFA strips were in agreement with those obtained from the quantitative real-time polymerase chain reaction (qRT-PCR). Given the accomplishments, this biosensor has significant potential for the clinical diagnosis of GC, offering a promising avenue for timely detection and improved patient prognoses.

Colorectal adenomas are recognized as precursors to colorectal cancer through the adenoma-carcinoma sequence. Identifying modifiable dietary factors that may inhibit cancer progression is critical, but epidemiologic studies in Asian populations are scarce.

This study explored the impact of fish and meat intake on colorectal adenoma risk among Koreans. The study enrolled asymptomatic adults who visited Seoul National University Hospital Healthcare System Gangnam Center for health check-ups from May to December 2011. All participants underwent screening colonoscopy and completed a validated food frequency questionnaire. The study included 536 adenoma patients, 135 high-risk adenoma patients and 1,122 adenoma-free controls. Using multivariate logistic regression, we calculated odds ratios (ORs) and 95% confidence intervals (CIs) for fish and meat intake related to colorectal adenoma status, significant at p < 0.05.

The intake of total fish, meat, red meat, chicken or processed meat showed no clear association with the prevalence of colorectal adenoma after adjusting for age, education, smoking status, alcohol intake, physical activity, body mass index, metabolic syndrome, colorectal cancer family history, total energy intake, and total fruit and vegetable intake. However, higher fish intake was associated with lower odds of high-risk colorectal adenoma, with a significant trend observed across quartiles (P for trend = 0.04). This trend was more pronounced among men than women (P for trend = 0.01).

In conclusion, we observed a significant inverse association between high fish intake and the prevalence of high-risk adenoma, but there were no clear associations between red and processed meat or chicken in the Korean population.

A definitive understanding of the interplay between protein binding/migration and membrane curvature evolution is emerging but needs further study. The mechanisms defining such phenomena are critical to intracellular transport and trafficking of proteins. Among trafficking modalities, exosomes have drawn attention in cancer research as these nano-sized naturally occurring vehicles are implicated in intercellular communication in the tumor microenvironment, suppressing anti-tumor immunity and preparing the metastatic niche for progression. A significant question in the field is how the release and composition of tumor exosomes are regulated. In this perspective article, we explore how physical factors such as geometry and tissue mechanics regulate cell cortical tension to influence exosome production by co-opting the biophysics as well as the signaling dynamics of intracellular trafficking pathways and how these exosomes contribute to the suppression of anti-tumor immunity and promote metastasis. We describe a multiscale modeling approach whose impact goes beyond the fundamental investigation of specific cellular processes toward actual clinical translation. Exosomal mechanisms are critical to developing and approving liquid biopsy technologies, poised to transform future non-invasive, longitudinal profiling of evolving tumors and resistance to cancer therapies to bring us one step closer to the promise of personalized medicine.

Drug resistance is a major challenge in the treatment of advanced cholangiocarcinoma (CCA). Understanding the mechanisms of drug resistance can aid in identifying novel prognostic biomarkers and therapeutic targets to improve treatment efficacy. This study established 5-fluorouracil- (5-FU) and gemcitabine-resistant CCA cell lines, KKU-213FR and KKU-213GR, and utilized comparative proteomics to identify differentially expressed proteins in drug-resistant cells compared to parental cells. Additionally, bioinformatics analyses were conducted to explore the biological and clinical significance of key proteins. The drug-resistant phenotypes of KKU-213FR and KKU-213GR cell lines were confirmed. In addition, these cells demonstrated increased migration and invasion abilities. Proteomics analysis identified 81 differentially expressed proteins in drug-resistant cells, primarily related to binding functions, biological regulation, and metabolic processes. Protein-protein interaction analysis revealed a highly interconnected network involving MET, LAMB1, ITGA3, NOTCH2, CDH2, and NDRG1. siRNA-mediated knockdown of these genes in drug-resistant cell lines attenuated cell migration and cell invasion abilities and increased sensitivity to 5-FU and gemcitabine. The mRNA expression of these genes is upregulated in CCA patient samples and is associated with poor prognosis in gastrointestinal cancers. Furthermore, the functions of these proteins are closely related to the epithelial-mesenchymal transition (EMT) pathway. These findings elucidate the potential molecular mechanisms underlying drug resistance and tumor progression in CCA, providing insights into potential therapeutic targets.

Small extracellular vesicles (sEVs) are emerging as critical mediators of intercellular communication in the tumor microenvironment (TME). Here, we investigate the mechanisms by which sEVs derived from neutrophils treated with the cholesterol metabolite, 27-hydroxycholesterol (27HC), influence breast cancer progression. sEVs released from 27HC treated neutrophils enhance epithelial-mesenchymal transition (EMT) and stem-like properties in breast cancer cells, resulting in loss of adherence, increased migratory capacity and resistance to cytotoxic chemotherapy. Decreased microRNAs (miRs) within the sEVs resulted in activation of the WNT/β-catenin signaling pathway in recipient cells and suggest that this may be a predominant pathway for stem-like phenotype and EMT. Our findings underscore a novel mechanism by which 27HC-modulated neutrophils contribute to breast cancer pathophysiology through EV-mediated intercellular communication, suggesting potential therapeutic targets in cancer treatment.

Many patients undergo dose reduction or early termination of chemotherapy to reduce chemoradiotherapy-related toxicity, which may increase their risk of survival. However, this strategy may result in underdosing patients with locally advanced esophageal squamous cell carcinoma (LA-ESCC). This study aimed to analyze the relationship between the relative dose intensity (RDI) and survival outcomes in patients with LA-ESCC.

This retrospective study assessed patients with LA-ESCC (cT2N + M0, cT3-4NanyM0) receiving neoadjuvant chemoradiotherapy (NCRT) with curative-intent esophagectomy. The patients received 2 courses of paclitaxel plus carboplatin (TC) combination radiotherapy prior to undergoing surgery. During NCRT, RDI was computed, defined as the received dose as a percentage of the standard dose, and the incidence of dose delays was estimated (≥ 7 days in any course cycle). The best RDI cutoff value (0.7) was obtained using ROC curve. The Kaplan-Meier survival curves were compared using the log-rank test, the treatment effect was measured using hazard ratios (HR) and 95% confidence intervals (CI).

We included 132 patients in this study, divided into RDI < 0.7 and RDI ≥ 0.7 groups using cut-off value of 0.7. RDI grade was an independent prognostic factor for OS. Baseline demographic and clinical characteristics were well balanced between the groups. There was no evidence that patients with RDI < 0.7 experienced less toxicity or those with RDI ≥ 0.7 resulted in more toxicity. However, patients with RDI < 0.7 who were given reduced doses had a worse overall survival [HR 0.49, 95% CI 0.27-0.88, P = 0.015]. The risk of a lower RDI increased with a longer dose delay time (P < 0.001).

The RDI below 0.7 for avoiding chemoradiotherapy toxicity administration led to a reduction in the dose intensity of treatment and decreased overall survival.

We analyzed trends in cancer incidence and regional disparities of eight major types of cancer in Korea.

This retrospective cohort study used the data of 17 cities/provinces from the Korea Central Cancer Registry (1999-2020) in South Korea. Age-standardized incidence rates (per 100,000 person-years), between-group variance (per 100,000 person-years)2, and annual percentage changes ( %) were calculated for the eight most common malignancies. Joinpoint regression was utilized to identify the points at which significant changes occur in cancer incidence or regional disparity trends over time to characterize these trends.

The incidence of stomach cancer decreased as regional disparity decreased and that of colorectal cancer initially increased but recently declined, showing fluctuations in regional disparity. The incidence and regional disparity in liver cancer decreased. The incidence of lung cancer remained stable, with reduced regional disparities. The incidence of breast cancer rose with increasing regional disparity, whereas the incidence of cervical cancer decreased, accompanied by decreased regional disparity. A significant increase in prostate cancer was found, with initially reduced regional disparities but later showed a resurgence. The incidence of thyroid cancer fluctuated alongside variations in regional disparities.

This study revealed cancer incidence and regional variations in each cancer type in Korea. More studies are needed to understand the underlying factors and potential interventions for reducing cancer incidence and addressing regional disparity.

Human papilloma virus (HPV) is an etiological factor of head and neck squamous cell carcinoma (HNSCC). To investigate the role of HPV antigen in anti-tumor immunity, we established mouse models by expressing HPV16 E6 and E7 in a SCC tumor cell line. We obtained two HPV antigen-expressing clones (C-225 and C-100) transplantable into C57BL/6 recipients. We found that C-225 elicited complete eradication in C57BL/6 mice (eradicated), whereas C-100 grew progressively (growing). We examined immune tumor microenvironment (TME) using flow cytometry and found that eradicated or growing tumors exhibited differential immune profiles that may influence the outcome of anti-tumor immunity. Surprisingly, the percentage of CD8 and CD4 tumor-infiltrating lymphocytes (TILs) was much higher in growing (C-100) than eradicated (C-225) tumor. However, the TILs upregulated PD-1 and LAG-3 more potently and exhibited impaired effector functions in growing tumor compared to their counterparts in eradicated tumor. C-225 TME is highly enriched with myeloid cells, especially polymorphonuclear (PMN) myeloid-derived suppressor cells (MDSC), whereas the percentage of M-MDSC and tumor-associated macrophages (TAMs) was much higher in C-100 TME, especially M2-TAMs (CD206+). The complete eradication of C-225 depended on CD8 T cells and elicited anti-tumor memory responses upon secondary tumor challenge. We employed DNA sequencing to identify differences in the T cell receptor of peripheral blood lymphocytes pre- and post-secondary tumor challenge. Lastly, C-225 and C-100 tumor lines harbored different somatic mutations. Overall, we uncovered differential immune TME that may underlie the divergent outcomes of anti-tumor immunity by establishing two SCC tumor lines, both of which express HPV16 E6 and E7 antigens. Our experimental models may provide a platform for pinpointing tumor-intrinsic versus host-intrinsic differences in orchestrating an immunosuppressive TME in HNSCCs and for identifying new targets that render tumor cells vulnerable to immune attack.

The proportional trends of HPV-associated oropharyngeal squamous cell carcinoma (OPSCC) according to various factors have not been analyzed in detail in previous studies. We aimed to evaluate the trends of HPV-associated OPSCC in the United States.

This retrospective cohort study included 13,081 patients with OPSCC from large population-based data using Surveillance, Epidemiology, and End Results (SEER) 2010-2017 database, 17 Registries. Patients were diagnosed with OPSCC primarily in the base of tongue (BOT), posterior pharyngeal wall (PPW), soft palate (SP), and tonsil and were tested for HPV infection status. We analyzed how the proportional trends of patients with OPSCC changed according to various demographic factors. Additionally, we forecasted and confirmed the trend of HPV (+) and (-) patients with OPSCC using the autoregressive integrated moving average (ARIMA) model.

The proportion of patients who performed the HPV testing increased every year, and it has exceeded 50% since 2014 (21.95% and 51.37% at 2010 and 2014, respectively). The HPV-positive rates tended to increase over past 7 years (66.37% and 79.32% at 2010 and 2016, respectively). Positivity rates of HPV were significantly higher in OPSCC located in the tonsil or BOT than in those located in PPW or SP. The ARIMA (2,1,0) and (0,1,0) models were applied to forecast HPV (+) and (-) patients with OPSCC, respectively, and the predicted data generally matched the actual data well.

This large population-based study suggests that the proportional trends of HPV (+) patients with OPSCC has increased and will continue to increase. However, the trends of HPV (+) and (-) patients differed greatly according to various demographic factors. These results present a direction for establishing appropriate preventive measures to deal with HPV-related OPSCC in more detail.

The purpose of this study was to describe an approach to cervical brachytherapy for a patient with a complete bicorporeal uterus and locally advanced cervical cancer (LACC).

The patient was a 53-year-old woman with a complete bicorporeal uterus, diagnosed with stage IIB cervical squamous cell carcinoma due to contact bleeding. The patient underwent concurrent chemoradiotherapy (CCRT), external beam pelvic radiotherapy with 45 Gy/25 fractions, and weekly cisplatin (40 mg/m2). Brachytherapy was administered following the completion of external beam radiotherapy.

The brachytherapy, which was CT (Computed Tomography)-guided using two CT-compatible tandems and two CT-compatible ovoids, delivered a prescription dose of HRCTV D90 was 6 Gy*5F, which achieved satisfactory dose coverage. The patient's final HRCTV D90 EQD210 was 84.9 Gy, and IRCTV D90 EQD210 was 63.5 Gy. Rectum D2cc EQD23 was 66.03 Gy, bladder D2cc EQD23 was 75.57 Gy, sigmoid D2cc EQD23 was 63.93 Gy, and intestine D2cc EQD23 was 65.86 Gy. Follow-up at 1 year was CR.

For patients with cervical cancer and a complete bicorporeal uterus, using double tandems combined with double ovoids is a feasible treatment method to ensure adequate dose coverage without causing additional damage. This method is also applicable to patients with endometrial cancer.

Renin-angiotensin-aldosterone system inhibitors (RAAS-I) have been shown to prolong overall survival in patients with liver metastasized colorectal cancer in combination with antiangiogenic treatment. The effects of RAAS-I combined with neoadjuvant chemotherapy on colorectal cancer liver metastasis remain unexplored. We aimed to study the response of patients undergoing liver resection to RAAS-I in combination with neoadjuvant therapy to elucidate their potential benefits.

Between February 2005 and May 2012, 62 patients fulfilled the inclusion criteria for distant metastasis (cM1) and comparable computed tomography or magnetic resonance tomography scans in the Picture Archiving Communication System of our center before and after neoadjuvant chemotherapy. Follow-up data and clinicopathological characteristics were collected from a prospective database and retrospectively investigated. The chemotherapeutic response to liver metastasis was evaluated according to the Response Evaluation Criteria in Solid Tumors criteria 1.1.

Comparing the average reduction of measured lesions, a significant response to chemotherapy was detected in the patients receiving RAAS-I (n = 24) compared to those who did not (n = 38) (P = 0.031). Interestingly, the effect was more distinctive when the size reduction was compared between high responses with more than 50% size reduction of all measured lesions (P = 0.011). In the subgroup analysis of patients receiving bevacizumab treatment, high responses to chemotherapy were observed only in the RAAS-I cohort (28.6% versus 0%, P = 0.022).

For neoadjuvantly treated patients, concomitant antihypertensive treatment with RAAS-I showed a higher total size reduction of liver metastasis as a sign of treatment response, especially in combination with antiangiogenic treatment with bevacizumab.

There is a paucity of research on the supply of the hematology and oncology workforce despite projected shortages in the United States Over the past 15 years of the hematology and oncology match (HOM), we hypothesized that there would be more growth in the number of training positions relative to applicants, higher match rates for US allopathic graduates relative to non-US allopathic graduates, and fewer applicants matching at their top fellowship choices.

This was a national, retrospective cohort study of all applicants in the HOM (2009-2023). Match rates and applicant-to-training position ratios were calculated and compared over time with Pearson tests.

Growth in the number of annual training positions (426-708; 66% increase) exceeded growth in the number of interested applicants (706-945; 34% increase; P < .001). Annual applicant-to-training position ratios decreased from 1.7 to 1.3 (r = -0.813; P < .001). Match rates increased over the study period for both US allopathic graduates (79%-88%; r = 0.761; P = .001) and non-US allopathic graduates (45%-63%; r = 0.801; P < .001). During each year, match rates for US allopathic graduates exceeded those for non-US allopathic graduates (P < .001). From 2018 to 2023, US allopathic graduates (83%) had higher match rates than US osteopathic graduates (60%) and international medical graduates (50%; P < .001). The percentage of applicants that matched at one of their top three fellowship choices increased from 53% to 60% (r = 0.480; P = .070). Fewer available annual training positions went unfilled over the study period (3%-0.3%; r = - 0.870; P < .001).

Match rates have increased in the HOM but remain competitive especially for non-US allopathic graduates. Future investigation is needed to understand disparities in match outcomes by additional applicant and fellowship program characteristics. Ongoing surveillance of HOM outcomes remains critical given the projected shortages in the US hematology and oncology workforce.

At present, there are few options for third line and above treatment of advanced gastric cancer and the single drug effect is poor. HER2 positive gastric cancer is an important subtype of gastric cancer and has certain immune characteristics. The combination of HER2 inhibitor and PD-1 inhibitor has a synergistic effect, and anti-tumor drugs targeting HER2 can play an anti-angiogenesis role by downregulating VEGF. We report a patient with HER2-positive gastric cancer who developed post-operative tumor recurrence and metastasis after adjuvant chemotherapy and radiotherapy. Trastuzumab combined with albumin paclitaxel was used as second-line treatment with progression-free survival for 9 months. In third line treatment, we retained trastuzumab and combined it with camrelizumab and apatinib. During the treatment period, although the patient stopped taking the drugs due to the side effects of camrelizumab and apatinib, he achieved a PFS of 10.4 months. Considering the good effect of the third line treatment, we added another PD-1 inhibitor and continued to combine trastuzumab treatment. We found that the patient still benefited from the treatment and continued to survive for another 4 months. At present, the patient is treated with DisitamabVedotin (HER2-ADC) combined with PD-1 inhibitor, and no overall survival outcome has been observed.

In this chapter, we aim to bridge basic molecular and cellular principles surrounding membrane curvature generation with rewiring of cellular signals in cancer through multiscale models. We describe a general framework that integrates signaling with other cellular functions like trafficking, cell-cell and cell-matrix adhesion, and motility. The guiding question in our approach is: how does a physical change in cell membrane configuration caused by external stimuli (including those by the extracellular microenvironment) alter trafficking, signaling and subsequent cell fate? We answer this question by constructing a modeling framework based on stochastic spatial continuum models of cell membrane deformations. We apply this framework to explore the link between trafficking, signaling in the tumor microenvironment, and cell fate. At each stage, we aim to connect the results of our predictions with cellular experiments.

Studies about the influence of weekday of esophagectomy on survival are limited and show conflicting results. This study aimed to explore whether weekday of esophagectomy affects patient's survival outcomes.

Patients who underwent esophagectomy in a grade-A tertiary hospital from January 2015 to December 2016 were enrolled. The primary outcome was 5-year overall survival (OS). The secondary outcomes were 5-year disease-free survival (DFS) and days of hospitalization. The impact of weekday surgery on 5-year OS and DFS were evaluated with Cox regression, and impact on days of hospitalization was assessed using logistic regression. Propensity score matching (PSM) analysis was used to balance the confounding factors.

A total of 1478 patients were included. The 5-year OS and DFS were 63.77% and 59.26% respectively. Multivariate analyses adjusted for covariables indicated that weekday was not significantly associated with OS (P = 0.076), nor days of hospitalization (P = 0.824), but it appeared to be associated with DFS (P = 0.044). Additionally, PSM analysis showed no significant effect of weekday on the 5-year OS, nor DFS and days of hospitalization.

In patients diagnosed with squamous esophageal cancer, the survival outcome of patients was not influenced by weekday.

Background Early detection of breast cancer is crucial for effective treatment and minimizing mortality, requiring effective screening methods like self-examination, clinical examination, and mammography. However, not all women in Saudi Arabia comply with these examinations, and studies examining its practice and barriers of low uptake are scant. The aim of this study is to investigate factors influencing breast cancer screening behavior among women in Saudi Arabia. Methods This cross-sectional study involving 806 women from October to November 2022 used an online questionnaire for the data collection process, including questions about demographic characteristics, awareness assessment, breast cancer screening behavior, symptoms, risk factors, and screening programs. Factors affecting the screening behavior were analyzed using the logistic regression model with adjusted odds ratio (AOR) and 95% confidence interval (CI). Results Among the 806 women who participated in the study, 479 (59.4%) were under 40 years old, and half of them were urban residents (n = 394, 48.9%). Only 134 subjects (16.6%) had a history of breast screening. Social media (n = 519, 64.5%) was the predominant source of screening information. The primary obstacles to breast cancer screening were the absence of tumor symptoms (n = 333, 41.3%), insufficient knowledge about early detection (n = 249, 31%), lack of time (n = 245, 30%), fear of discovering a tumor (n = 187, 23%), and lack of awareness about screening centers (n = 155, 19%). In regression analysis, predictive factors for breast cancer screening behavior were as follows: age over 40 years old (AOR: 2.56; 95% CI: 1.70-3.87), residents of big cities (AOR: 3.57; 95% CI: 1.02-12.56), positive family history of breast cancer (AOR: 2.53; 95% CI: 1.50-4.28), proximity to the screening center (AOR: 2.56; 95% CI: 1.22-5.39), and using contraceptive pills for more than five years (AOR: 1.78; 95% CI: 1.04-3.04), and were statistically significant (all p-values < 0.05). Conclusions In this study, the most perceived barriers to BSE were the absence of tumor symptoms, followed by insufficient knowledge about early detection, lack of time, fear of discovering a tumor, and lack of awareness about screening centers. Additionally, the predictive factors for breast cancer screening behavior were as follows: age over 40 years old, residents of big cities, positive family history of breast cancer, proximity to the screening center, and using contraceptive pills for more than five years. Given the identified factors affecting breast self-examination behavior in this study, public education initiatives are crucial for raising awareness, facilitating self-examination, and ultimately improving health outcomes and reducing breast cancer treatment costs in society.

Head and neck cancer (HNC) refers to the epithelial malignancies of the upper aerodigestive tract. HNCs have a constant yet slow-growing rate with an unsatisfactory overall survival rate globally. The development of new blood vessels from existing blood conduits is regarded as angiogenesis, which is implicated in the growth, progression, and metastasis of cancer. Aberrant angiogenesis is a known contributor to human cancer progression. Representing a promising therapeutic target, the blockade of angiogenesis aids in the reduction of the tumor cells oxygen and nutrient supplies. Despite the promise, the association of existing anti-angiogenic approaches with severe side effects, elevated cancer regrowth rates, and limited survival advantages is incontrovertible. Exosomes appear to have an essential contribution to the support of vascular proliferation, the regulation of tumor growth, tumor invasion, and metastasis, as they are a key mediator of information transfer between cells. In the exocrine region, various types of noncoding RNAs (ncRNAs) identified to be enriched and stable and contribute to the occurrence and progression of cancer. Mounting evidence suggest that exosome-derived ncRNAs are implicated in tumor angiogenesis. In this review, the characteristics of angiogenesis, particularly in HNC, and the impact of ncRNAs on HNC angiogenesis will be outlined. Besides, we aim to provide an insight on the regulatory role of exosomes and exosome-derived ncRNAs in angiogenesis in different types of HNC.

Iodine is involved in the synthesis of thyroid hormones and plays a crucial role in human life. Both iodine deficiency and excess are common issues in certain populations. Iodine also has extrathyroidal effects on organs that can uptake it independently of thyroid hormones. Recently, multiple clinical studies have shown a connection between iodine intake and metabolic disorders, such as metabolic syndrome, obesity, diabetes, hypertension, and dyslipidemia. However, the results of these studies have been inconsistent, and the mechanisms behind these associations are still not well understood. Therefore, in this review, we aim to examine the recent research progress regarding the relationship between iodine and metabolic disorders, along with the relevant mechanisms.

Breast cancer has become a severe public health concern and one of the leading causes of cancer-related death in women worldwide. Several genes and mutations in these genes linked to breast cancer have been identified using sophisticated techniques, despite the fact that the exact cause of breast cancer is still unknown. A commonly used feature for identifying driver mutations is the recurrence of a mutation in patients. Nevertheless, some mutations are more likely to occur than others for various reasons. Sequencing analysis has shown that cancer-driving genes operate across complex networks, often with mutations appearing in a modular pattern. In this work, as a retrospective study, we used TCGA data, which is gathered from breast cancer patients. We introduced a new machine-learning approach to examine gene functionality in networks derived from mutation associations, gene-gene interactions, and graph clustering for breast cancer analysis. These networks have uncovered crucial biological components in critical pathways, particularly those that exhibit low-frequency mutations. The statistical strength of the clinical study is significantly boosted by evaluating the network as a whole instead of just single gene effects. Our method successfully identified essential driver genes with diverse mutation frequencies. We then explored the functions of these potential driver genes and their related pathways. By uncovering low-frequency genes, we shed light on understudied pathways associated with breast cancer. Additionally, we present a novel Monte Carlo-based algorithm to identify driver modules in breast cancer. Our findings highlight the significance and role of these modules in critical signaling pathways in breast cancer, providing a comprehensive understanding of breast cancer development. Materials and implementations are available at: [https://github.com/MahnazHabibi/BreastCancer].