75; P = 0.001) were prognostic factors for OS. Patients with oligometastasis (P = 0.009) and those with IMDC favorable (P = 0.044) or intermediate (P = 0.002) risk had significantly longer OS with TKI + SBRT. The median TTS were 21.5, 6.4, and 9.0 months in patients receiving SBRT before first-line TKI failure, SBRT after first-line TKI failure, and first-line TKI alone (P < 0.001). Five patients (5.9%) experienced SBRT-related grade 3 toxicities.
 
  Combining SBRT with TKIs is tolerable and associated with longer OS in selected patients, such as those with oligometastasis and favorable or intermediate risk.
 Combining SBRT with TKIs is tolerable and associated with longer OS in selected patients, such as those with oligometastasis and favorable or intermediate risk.
  We developed and validated a contrast-enhanced spectral mammography (CESM)-based radiomics nomogram to predict neoadjuvant chemotherapy (NAC)-insensitive breast cancers prior to treatment.
 
  We enrolled 117 patients with breast cancer who underwent CESM examination and NAC treatment from July 2017 to April 2019. The patients were grouped randomly into a training set (n = 97) and a validation set (n = 20) in a ratio of 82. 792 radiomics features were extracted from CESM images including low-energy and recombined images for each patient. Optimal radiomics features were selected by using analysis of variance (ANOVA) and least absolute shrinkage and selection operator (LASSO) regression with 10-fold cross-validation, to develop a radiomics score in the training set. A radiomics nomogram incorporating the radiomics score and independent clinical risk factors was then developed using multivariate logistic regression analysis. With regard to discrimination and clinical usefulness, radiomics nomogram was evaluated using the area under the receiver operator characteristic (ROC) curve (AUC) and decision curve analysis (DCA).
 
  The radiomics nomogram that incorporates 11 radiomics features and 3 independent clinical risk factors, including Ki-67 index, background parenchymal enhancement (BPE) and human epidermal growth factor receptor-2 (HER-2) status, showed an encouraging discrimination power with AUCs of 0.877 [95% confidence interval (CI) 0.816 to 0.924] and 0.81 (95% CI 0.575 to 0.948) in the training and validation sets, respectively. DCA revealed the increased clinical usefulness of this nomogram.
 
  The proposed radiomics nomogram that integrates CESM-derived radiomics features and clinical parameters showed potential feasibility for predicting NAC-insensitive breast cancers.
 The proposed radiomics nomogram that integrates CESM-derived radiomics features and clinical parameters showed potential feasibility for predicting NAC-insensitive breast cancers.
  Whether the original dosimetric constraints of neuro-optic structures (NOS) are appropriate for patients with nasopharyngeal carcinoma (NPC) undergoing intensity-modulated radiotherapy (IMRT) remains controversial. The present study compared the survival rates and radiation-induced optic neuropathy (RION) occurrence between T4 NPC patients whose NOS were irradiated with a near maximum dose received by 2% of the volume (D2%) >55 Gy and ≤55 Gy. Moreover, the NOS dosimetric parameters and their correlation with RION occurrence were also evaluated.
 
  In this retrospective study, 256 T4 NPC patients treated with IMRT between May 2009 and December 2013 were included. Patient characteristics, survival rates, dosimetric parameters, and RION incidence were compared between the D2% ≤55 Gy and D2% >55 Gy groups.
 
  The median follow-up durations were 87 and 83 months for patients in the D2% >55 Gy and D2% ≤55 Gy groups, respectively. The 5-year localrecurrence-freesurvival rates were 92.0 and 84.0% in the D2% >55 Gy and D2% ≤55 Gy groups (P = 0.043), respectively. There was no significant difference in the 5-year overall survival (OS) between both groups (D2% >55 Gy, 81.6%; D2% ≤55 Gy, 79.4%; P = 0.586). No patients developed severe RION (Grades 3-5), and there was no significant difference (P = 0.958) in the incidence of RION between the two groups. The maximum dose of NOS significantly affected the RION incidence, with a cutoff point of 70.77 Gy.
 
  Appropriately looseningNOS dosimetric constraints in order to ensure a more sufficient dose to the target volume can provide a better 5-year localrecurrence-freesurvivaland acceptable neuro-optic toxicityin T4 NPC patientsundergoing IMRT.
 Appropriately loosening NOS dosimetric constraints in order to ensure a more sufficient dose to the target volume can provide a better 5-year local recurrence-free survival and acceptable neuro-optic toxicity in T4 NPC patients undergoing IMRT.Rhabdoid tumors are rare aggressive malignancies in infants and young children with a poor prognosis. The most common anatomic localizations are the central nervous system, the kidneys, and other soft tissues. Rhabdoid tumors share germline and somatic mutations in SMARCB1 or, more rarely, SMARCA4, members of the SWI/SNF chromatin-remodeling complex. Rhabdoid tumor predisposition syndrome (RTPS) is a condition characterized by a high risk of developing rhabdoid tumors, among other features.  https://www.selleckchem.com/products/msc2530818.html  RTPS1 is characterized by pathogenic variants in the SMARCB1 gene, while RTPS2 has variants in SMARCA4. Interestingly, germline variants of SMARCB1 and SMARCA4 have been identified also in patients with Coffin-Siris syndrome. Children with RTPS typically present with tumors before 1 year of age and in a high percentage of cases develop synchronous or multifocal tumors with aggressive clinical features. The diagnosis of RTPS should be considered in patients with rhabdoid tumors, especially if they have multiple primary tumors and/or in individuals with a family history. Because germline mutations result in an increased risk of carriers developing rhabdoid tumors, genetic counseling, and surveillance for all family members with this condition is recommended.Glioblastoma (GBM), one of the deadliest primary brain malignancies, is characterized by a high recurrence rate due to its limited response to existing therapeutic strategies such as chemotherapy, radiation therapy, and surgery. Several mechanisms and pathways have been identified to be responsible for GBM therapeutic resistance. Glioblastoma stem cells (GSCs) are known culprits of GBM resistance to therapy. GSCs are characterized by their unique self-renewal, differentiating capacity, and proliferative potential. They form a heterogeneous population of cancer stem cells within the tumor and are further divided into different subpopulations. Their distinct molecular, genetic, dynamic, and metabolic features distinguish them from neural stem cells (NSCs) and differentiated GBM cells. Novel therapeutic strategies targeting GSCs could effectively reduce the tumor-initiating potential, hence, a thorough understanding of mechanisms involved in maintaining GSCs' stemness cannot be overemphasized. The mitochondrion, a regulator of cellular physiological processes such as autophagy, cellular respiration, reactive oxygen species (ROS) generation, apoptosis, DNA repair, and cell cycle control, has been implicated in various malignancies (for instance, breast, lung, and prostate cancer).