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Uterine Carcinosarcomas (UCS) are a rare type of cancer composed of an admixture of high-grade carcinomatous and sarcomatous elements. Clinicopathological prognostic factors in UCS are well established, but studies that approach the impact of biomarkers in this unusual disease are scarce. The study objective was to evaluate the prevalence and prognostic impact of a panel of prominent biomarkers in uterine carcinosarcoma (UCS) using an immunohistochemical characterization with four biomarkers. The internal database of a single Brazilian institution was carefully explored to select women diagnosed with UCS who were submitted to surgery and postoperative chemotherapy with carboplatin and paclitaxel between January 2012 and December 2017. Tissue microarrays containing UCS samples were evaluated by immunohistochemistry for L1CAM, CDX2, p53 and microsatellite instability markers. A total of 57 cases were included. The mean age was 65.3 years (standard deviation, SD 7.0). L1CAM was negative (score 0, no staining) in 27 (47.4%) patients. Of L1CAM-positive, 10 (17.5%) showed weak (score 1, <10%), 6 (10.5%) showed moderate (score 2, between 10-50%), and 14 (24.6%) showed strong L1CAM staining (score 3, ≧50%). dMMR occurred in 3 (5.3%) cases. The p53 was aberrantly expressed in 15 (26.3%) tumors. CDX2 was positive in 3 (5.3%) patients. The three-year progression-free survival (PFS) rate in the general population of the study was 21.2% (95% CI: 11.7-38.1) and the three-year overall survival (OS) rate was 29.4% (95% CI: 18.1-47.6). By multivariate analysis, the presence of metastases and CDX2-positive were significantly associated with poorer PFS (p < 0.001 and p = 0.002, respectively) and OS (p < 0.001 and p = 0.009, respectively). The strong influence of CDX2 on prognosis requires further investigation. Biological or molecular variability may have impaired the assessment of the impact of the other markers on survival.

This study aimed to describe the demographic and clinical characteristics of cancer patients with COVID-19, exploring factors associated with adverse outcomes. This retrospective cohort study methodically extracted and curated data from electronic medical records (EMRs) of numerous healthcare institutions on cancer patients diagnosed with a confirmed SARS-CoV-2 infection between May 2020 and August 2021, to identify risk factors linked to extended hospitalization and mortality. The retrieved information encompassed the patients' demographic and clinical characteristics, including the incidence of prolonged hospitalization, acute complications, and COVID-19-related mortality. A total of 1446 cancer patients with COVID-19 were identified (mean [Standard deviation] age, 59.2 [14.3] years). Most patients were female (913 [63.1%]), non-white (646 [44.7%]), with non-metastatic (818 [56.6%]) solid tumors (1318 [91.1%]), and undergoing chemotherapy (647 [44.7%]). The rate of extended hospitalization due to COVID-19 was 46% (n = 665), which was significantly impacted by age (p = 0.012), sex (p = 0.003), race and ethnicity (p = 0.049), the presence of two or more comorbidities (p = 0.006), hematologic malignancies (p = 0.013), metastatic disease (p = 0.002), and a performance status ≥ 2 (p = 0.001). The COVID-19-related mortality rate was 18.9% (n = 273), and metastatic disease (<0.001), performance status ≥2 (<0.001), extended hospitalization (p = 0.028), renal failure (p = 0.029), respiratory failure (p < 0.001), sepsis (p = 0.004), and shock (p = 0.040) significantly and negatively influenced survival. The rate of extended hospitalization and COVID-19-specific death in cancer patients was notably high and could be influenced by comorbidities, cancer treatment status, and clinical fragility. These observations may aid in developing risk counseling strategies regarding COVID-19 in individuals diagnosed with cancer.

Objective To examine the prevalence and prognostic role of tumor microenvironment (TME) markers in uterine carcinosarcoma (UCS) through immunohistochemical characterization. Methods The internal database of our institution was queried out for women with UCS who underwent surgery and thereafter postoperative chemotherapy with carboplatin and paclitaxel between January 2012 and December 2017. Tissue microarrays containing surgical samples of UCS from 57 women were assessed by immunohistochemistry for CD3, CD4, CD8, FOXP3, PD-1, PD-L1, and PD-L2. Results The mean age was 65.3 years (range, 49 to 79 years). For the epithelial component (E), CD3_E and CD4_E were highly expressed in 38 (66.7%) and in 40 (70.1%) patients, respectively, and were significantly associated with more advanced stages ( p  = 0.038 and p  = 0.025, respectively). CD8_E was highly expressed in 42 (73.7%) patients, FOXP3_E 16 (28.1%), PD-1_E 35 (61.4%), PD-L1_E 27 (47.4%) and PD-L2_E 39 (68.4%). For the sarcomatous component (S), the prevalence of high expression was: CD3_S 6 (10.5%), CD4_S 20 (35.1%), CD8_S 44 (77.2%), FOXP3_S 8 (14%), PD-1_S 14 (24.6%), PD-L1_S 14 (24.6%) and PD-L2_S 8 (14%). By multivariate analysis, the CD8/FOXP3_S ratio ( p  = 0.026), CD4_E ( p  = 0.010), PD-L1_E ( p  = 0.013) and PD-L1_S ( p  = 0.008) markers significantly influenced progression-free survival. CD4/FOXP3_S ratio ( p  = 0.043), PD-1_E ( p  = 0.011), PD-L1_E ( p  = 0.036) and PD-L1_S ( p  = 0.028) had a significant association with overall survival. Conclusion Some differences in UCS clinical outcomes may be due to the subtype of TILs and PD-1/PD-L1 axis immune checkpoint signaling.

This study aimed to compare the clinical behavior, clinicopathological and sociodemographic characteristics of patients with early-stage triple-negative breast cancer (TNBC) who belong to the HER2-low and HER2-zero subgroups. This study involved a thorough search in the internal database of a single Brazilian institution to identify women with TNBC who underwent neoadjuvant chemotherapy (NACT) followed by curative surgery within the period from January 2010 to December 2014. HER2 analysis through immunohistochemistry (IHC) and, if required, amplification by in situ hybridization, was conducted using core biopsy samples. The study assesses outcomes of residual cancer burden (RCB), event-free survival (EFS), and overall survival (OS). A total of 170 cases were analyzed, with a mean age of 51.4 years (standard deviation, SD 11.2). The HER2 status was categorized as IHC 0, 1+, or 2+ in 80 (47.1%), 73 (42.9%), and 17 (10%) patients, respectively. No significant differences were observed in the prevalence of clinical pathological characteristics among the subgroups. The absence of significant results for clinicopathological and demographic features hindered the multivariate analysis of HER2 subgroups. Similarly, no significant differences were found in the RCB, EFS, and OS outcomes between HER2 subgroups. The findings of this study suggest that, in early-stage TNBC, the clinical behavior and survival outcomes of the HER2-low subgroup may not differ significantly from those of the HER2-zero subgroup.

Background Uterine carcinosarcomas (UCS) are rare and aggressive gynecological tumors and the description of biomarkers that can help guide targeted treatments in this disease is a critical gap in current medical research. This study aims to measure the prevalence of trophoblast cell-surface antigen 2 (Trop-2) and folate receptor alpha (FRα) in UCS and evaluate their prognostic significance. Methods This retrospective analysis examined data from female patients diagnosed with UCS who underwent surgery followed by carboplatin and paclitaxel chemotherapy between January 2012 and December 2020. Tissue microarrays from 89 samples were assessed for Trop-2 and FRα expression by IHC. High positivity was defined as a score of ≥ 50% of tumor cells with strong staining intensity for Trop-2 and ≥ 75% with medium or strong staining intensity for FRα. Sociodemographic and clinical features were analyzed alongside progression-free survival (PFS) and overall survival (OS) outcomes. Results The mean age at diagnosis was 66.2 years (Standard Deviation, SD: 7) and the mean body mass index was 28.7 kg/m² (SD: 6.2). Non-white women accounted for 71.6% of cases. Heterologous subtype corresponded to 63.0% of cases, and lymphovascular invasion was observed in 59.2%. Complete resection (R0) was achieved in 66.3% of cases. High expression of Trop-2 and FRα was found in 49.4% and 17.4% of epithelial components, respectively, with no high positivity in sarcomatous components. Negative margins were more common in stage I/II disease ( p  = 0.001), and FRα overexpression correlated with Trop-2 overexpression ( p  = 0.007). On multivariate analysis, advanced stage ( p  = 0.015) and incomplete resection ( p  < 0.001) predicted shorter PFS, while both factors also independently worsened OS ( p  = 0.013 and p  = 0.001, respectively). Lymphadenectomy was associated with improved OS ( p  = 0.025). Conclusion Complete resection and advanced stage were suggested as prognostic factors in UCS. FRα and Trop-2 are increasingly recognized as therapeutic targets and their elevated expression levels in the epithelial component of UCS are promising, although not associated with prognosis in this cohort.

Purpose To investigate breast cancer (BC) incidence and mortality rates among specific racial groups in Brazil. Methods BC incidence was evaluated from 2010 to 2015, using Brazilian Population-Based Cancer Registries, incorporating crude ratios and annual average percentage change (AAPC). Clinical and sociodemographic data from 2000 to 2019 were obtained from Hospital-Based Cancer Registries. Mortality data from 2000 to 2020 were sourced from the National Mortality Information System, comparing White women and Black women. Results Across 13 Brazilian registries, 70,896 new BC cases were reported from 2010 to 2015. The median BC incidence rate was notably higher for White women (101.3 per 100,000) compared to Black women (59.7 per 100,000). In the general population, non-significant decrease in annual BC incidence was observed (AAPC = − 1.2; p  = 0.474). Black women were more likely to live in underdeveloped areas, have lower education levels, live without a partner, and have higher alcohol consumption as compared to White women. A higher proportion of Black women received advanced-stage diagnoses (60.1% versus 50.6%, p  < 0.001). BC-related mortality analysis showed 271,002 recorded deaths, with significant increase in BC-specific mortality rates in both racial groups. Black women displayed an AAPC of 2.3% ( p  < 0.001), while White women demonstrated a moderately elevated AAPC of 0.6% ( p  < 0.001). Conclusion This study underscores the need for targeted policies to address disparities in access to early detection and proper treatment, particularly for Black women in underprivileged regions, aiming to improve the survival rates of Brazilian women grappling with BC.

Purpose This study aimed to describe the clinical and demographic profile of cervical cancer patients exploring risk factors for prolonged use of opioids. Methods The database of the Brazilian National Cancer Institute was queried out and 214 women with cervical cancer diagnosed between January 2014 and December 2015 who underwent isolated external beam radiation therapy (EBRT) or chemoradiotherapy (CRT) with complete response were included. Patients who no longer used opioids 6 months after completion of radiation therapy were classified as stoppers; patients who continued using opioids were non-stoppers. Variables were comparatively evaluated as risk factors for prolonged use of opioids. Results The median age was 49.4 years. Most women were non-white (64.5%) and had ECOG Performance Status (PS) ≥ 1 (76.6%), International Federation of Gynecology and Obstetrics (FIGO) stage II–III (84.1%), and squamous cell carcinoma (82.7%). Smoking and alcohol consumption rates were, respectively, 44.9% and 39.7%. The median time from diagnosis to the onset of EBRT was 111 days (interquartile range 66.2). Most patients underwent CRT (88.8%). The rate of non-stoppers was 65.0%. By multivariate analysis, prescription of strong opioids ( p  = 0.005) and disease recurrence ( p  < 0.001) were suggested as independent factors for prolonged use of opioids. Conclusion The rate of prolonged use of opioids after radiotherapy is alarming. Prescription of strong opioids and disease recurrence might be independent risk factors for its persistent use. Implications for Cancer Survivors These results reveal an unmet and urgent need to implement public multiprofessional support programs with well-established protocols for dependence withdrawal, as well as stricter national measures of control in opioid prescription.

This study aimed to assess the frequency and prognostic significance of programmed cell death ligand 1 (PD-L1) expression and tumor-infiltrating lymphocyte (TIL) subtypes in advanced triple-negative breast cancer (TNBC). A database search was conducted to identify women with previously untreated locally recurrent inoperable or metastatic TNBC treated between January 2018 and December 2022. The inclusion criteria required formalin-fixed paraffin-embedded samples aged less than four years. PD-L1 expression was evaluated using the PD-L1 IHC 22C3 pharmDx assay, and the combined positive score (CPS) was calculated. TIL subtypes were assessed using immunohistochemical staining. The study included 150 patients, with a median age of 51.5 years. The majority of patients were younger than 65 years, postmenopausal, non-white, and had metastatic TNBC. CPS≥10 was observed in 20.9% of cases, mainly in postmenopausal women. No significant differences were found in demographic characteristics and clinicopathological variables across PD-L1 subgroups. Tumors with PD-L1 CPS≥10 had higher expression of CD3+, CD4+, and CD8+ TIL subtypes. Most patients received first-line chemotherapy, with smaller proportions undergoing second, third, and fourth-line treatments. No statistically significant differences were observed in median progression-free survival (PFS) or overall survival (OS) across PD-L1 subgroups in this cohort of chemotherapy-treated patients. This study provides insights into the expression profiles of PD-L1 and TIL subtypes in advanced TNBC. The PD-L1 CPS status did not significantly affect survival outcomes, but variations in TIL subtype composition were observed based on PD-L1 CPS status.

This narrative review explores the mechanisms underlying resistance to cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) in hormone receptor (HR)-positive metastatic breast cancer (MBC), a critical challenge in contemporary oncology. Despite the proven efficacy of CDK4/6i in improving clinical outcomes, both intrinsic and acquired resistance remain substantial challenges. We discuss clinical data that underscore pivotal molecular alterations associated with resistance, including mutations in the Retinoblastoma gene (RB1), germline variants, aberrations in the PIK3CA gene that activate the phosphatidylinositol 3-kinase/protein kinase B (AKT)/mammalian target of rapamycin signaling cascade, and modifications in fibroblast growth factor receptor signaling. Additional resistance mechanisms—such as the loss of the FAT1 tumor suppressor gene and the dysregulation of cell cycle regulators like cyclin E and CDK2—are also explored. The role of circulating tumor DNA analysis in tracking genomic changes during therapy is also considered. Furthermore, the review assesses emerging therapeutic strategies, particularly combination therapies that target alternative pathways to counteract resistance mechanisms. By synthesizing current evidence and providing actionable insights, this review aims to enhance our understanding of endocrine resistance mechanisms among clinical oncologists and gives them some future perspectives to expand strategies to overcome this challenge. Plain language summary Mechanisms of CDK4/6 inhibitor resistance in metastatic breast cancer This review focuses on why some hormone receptor-positive metastatic breast cancers do not respond to CDK4/6 inhibitors, which are effective treatments. It examines both primary and developed resistance to these drugs. Key genetic changes linked to resistance include mutations in the retinoblastoma gene (RB1), variations in the PIK3CA gene activating the PI3K/AKT/mTOR pathway, and changes in fibroblast growth factor receptor (FGFR) signaling. The article also discusses other resistance factors, such as the loss of the FAT1 tumor suppressor gene and disruptions in cell cycle regulators like cyclin E and CDK2. Additionally, the review evaluates how circulating tumor DNA (ctDNA) can help monitor genetic changes during treatment. It highlights new therapeutic strategies, including combination therapies that target different pathways to combat resistance. By compiling and interpreting current research, this review aims to deepen the understanding of how hormone-related resistance mechanisms work. It ultimately seeks to provide oncologists with insights and future directions to improve treatment strategies against resistance in this challenging area of breast cancer care.