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Chemotherapy is the main treatment for patients with lung squamous cell carcinoma (LUSC). However, how chemotherapy affects their immune system is rarely reported. This study was aimed to compare the differences in the immune microenvironment of LUSC patients with or without chemotherapy.

A total of 494 LUSC samples were obtained from The Cancer Genome Atlas (TCGA) database. The immune cell infiltration was evaluated by the ssGSEA algorithm, and the tumor subtype was assayed by ConsensusClusterPlus. The differences in tumor mutation burden (TMB) and clinical information between the two types were then compared. Additionally, the differentially expressed genes (DEGs) between two types were analyzed and hub genes were validated in the GEO database.

LSCC samples in TCGA were divided into three subtypes. Then, combining the tumor subtype and immune scores, the samples were divided into hot and cold tumors. ETC-159 datasheet Regardless of whether LUSC patients received chemotherapy, the survival of the hot tumor group was not significantly prolonged compared with that of the cold tumor group. For LUSC patients who received chemotherapy, the TMB value in hot tumor group was significantly higher. Total 501 DEGs were identified between two groups. The high expressions of hub genes

,

,

,

,

, etc. were also validated in the GSE37745 dataset.

Chemotherapy does not affect the survival and prognosis of LUSC patients, but it significantly increases the TMB value of patients with hot tumor. The DEGs, especially hub genes, such as

,

, and

, may serve as biomarkers to distinguish cold and hot tumors in LUSC.

Chemotherapy does not affect the survival and prognosis of LUSC patients, but it significantly increases the TMB value of patients with hot tumor. The DEGs, especially hub genes, such as CD19, CTLA4, and FCGR3B, may serve as biomarkers to distinguish cold and hot tumors in LUSC.

Early identification of nasopharyngeal carcinoma (NPC) patients with high risk of failure to induction chemotherapy (IC) would facilitate prompt individualized treatment decisions and thus reduce toxicity and improve overall survival rate. This study aims to investigate the value of amide proton transfer (APT) imaging in predicting short-term response of NPC to IC and its potential correlation with well-established prognosis-related clinical characteristics.

A total of 80 pathologically confirmed NPC patients receiving pre-treatment APT imaging at 3T were retrospectively enrolled. Using asymmetry analysis, APT maps were calculated with mean (APT

), 90

percentile (APT

) of APT signals in manually segmented NPC measured. APT values were compared among groups with different histopathological subtypes, clinical stages (namely, T, M, N, and overall stages), EBV-related indices (EBV-DNA), or responses to induction chemotherapy, using Mann-Whitney U test or Kruskal-Wallis H test.

NPC showed significantly htification. However, stationary baseline APT values exhibited no significant correlation with histologic subtypes, clinical stages and EBV-related indices, and showed limited value to predict short-term treatment response to IC.

There are several means of synthetic computed tomography (sCT) generation for magnetic resonance imaging (MRI)-only planning; however, much of the research omits large pelvic treatment regions and female anatomical specific methods. This research aimed to apply four of the most popular methods of sCT creation to facilitate MRI-only radiotherapy treatment planning for male and female anorectal and gynecological neoplasms. sCT methods were validated against conventional computed tomography (CT), with regard to Hounsfield unit (HU) estimation and plan dosimetry.

Paired MRI and CT scans of 40 patients were used for sCT generation and validation. Bulk density assignment, tissue class density assignment, hybrid atlas, and deep learning sCT generation methods were applied to all 40 patients. Dosimetric accuracy was assessed by dose difference at reference point, dose volume histogram (DVH) parameters, and 3D gamma dose comparison. HU estimation was assessed by mean error and mean absolute error in HU value betweused in this study resulted in similarly high dosimetric agreement for MRI-only planning of male and female cancer pelvic regions. The choice of the sCT generation technique can be guided by department resources available and image guidance considerations, with minimal impact on dosimetric accuracy.Multiple myeloma is a blood cancer characterized by clonal proliferation of plasma cells in the bone marrow. In recent years, several new drugs have been added to the therapeutic landscape of multiple myeloma, which have contributed to increased survival rates. However, while the use of therapeutics has evolved, there is still a group of high-risk patients who do not benefit from current treatment strategies. Risk stratification and risk-adapted treatment are crucial to identify the group of patients with urgent need for novel therapies. Gene expression profiling has been introduced as a tool for risk stratification in multiple myeloma based on the genetic make-up of myeloma cells. In this review we discuss the challenge of defining the high-risk multiple myeloma patient. We focus on the standardized analysis of myeloma cancer cells by gene expression profiling and describe how gene expression profiling provides additional insights for optimal risk-adapted treatment of patients suffering from multiple myeloma.

This study aimed to investigate the dosimetric effect and delivery reliability of jaw tracking (JT) with increasing planning target volume (PTV) for lung stereotactic body radiation therapy (SBRT) plans. A threshold of PTV was proposed as a selection criterion between JT and fixed-jaw (FJ) techniques.

A total of 28 patients with early-stage non-small-cell lung cancer were retrospectively included. The PTVs ranged from 4.88 cc to 68.74 cc, prescribed with 48 Gy in four fractions. Three-partial-arc volumetric modulated arc therapy (VMAT) plans with FJ and with JT were created for each patient with the same optimization objectives. These two sets of plans were compared using metrics, including conformity index (CI), V

, R

, D

, dose-volume parameters of organs at risk, and monitor units (MUs). The ratio of small subfields (<3 cm in either dimension), %SS, was acquired as a surrogate for the small-field uncertainty. Statistical analyses were performed to evaluate the correlation between the differences demand of delivery reliability for lung SBRT.

Although the effect of pseudogene ANXA2P2 on some tumors has been reported in a few literatures, the therapeutic potential and prognostic value of ANXA2P2 in ovarian serous cystadenocarcinoma (OV) have not been elucidated.

The correlation for ANXA2P2 expression patterns to prognostic characteristics, tumor immune microenvironment, immune cell infiltration level, tumor mutation burden (TMB), tumor microsatellite instability (MSI), drug sensitivity, and pathway function enrichment were investigated in pan-carcinoma

TCGA and GTEx databases. Subsequently, the role of ANXA2P2 expression levels in the pathway enrichments and prognosis prediction in OV were further explored using weighted correlation network analysis (WGCNA) analysis, gene mutation analysis, and risk-independent prognostic analysis.

ANXA2P2 was frequently overexpressed in a variety of tumors compared with normal tissues. The correlation analysis for prognostic characteristics, tumor immune microenvironment, immune cell infiltration level, Tal prognosis prediction, and give new hope for OV patients.

In summary, our findings might provide a helpful foundation for prospective explorative researches, afford new strategies for the clinical treatment, deal prognosis prediction, and give new hope for OV patients.Acute myeloid leukemia (AML) with nucleophosmin 1 (NPM1) mutations exhibits distinct biological and clinical features, accounting for approximately one-third of AML. Recently, the N 6-methyladenosine (m6A) RNA modification has emerged as a new epigenetic modification to contribute to tumorigenesis and development. However, there is limited knowledge on the role of m6A modifications in NPM1-mutated AML. In this study, the decreased m6A level was first detected and high expression of fat mass and obesity-associated protein (FTO) was responsible for the m6A suppression in NPM1-mutated AML. FTO upregulation was partially induced by NPM1 mutation type A (NPM1-mA) through impeding the proteasome pathway. Importantly, FTO promoted leukemic cell survival by facilitating cell cycle and inhibiting cell apoptosis. Mechanistic investigations demonstrated that FTO depended on its m6A RNA demethylase activity to activate PDGFRB/ERK signaling axis. Our findings indicate that FTO-mediated m6A demethylation plays an oncogenic role in NPM1-mutated AML and provide a new layer of epigenetic insight for future treatments of this distinctly leukemic entity.Interferon regulatory factor 8 (IRF-8) is a transcription suppressor that functions through associations with other transcription factors, contributing to the growth and differentiation of bone marrow cells and the activation of macrophages. IRF-8 expression profoundly affects pathogenic processes ranging from infections to blood diseases. Interleukin-9 (IL-9) is a multipotent cytokine that acts on a variety of immune cells by binding to the IL-9 receptor (IL-9R) and is involved in a variety of diseases such as cancer, autoimmune diseases, and other pathogen-mediated immune regulatory diseases. Studies have shown that IL-9 levels are significantly increased in the serum of patients with diffuse large B-cell lymphoma (DLBCL), and IL-9 levels are correlated with the DLBCL prognostic index. The activator protein-1 (AP-1) complex is a dimeric transcription factor that plays a critical role in cellular proliferation, apoptosis, angiogenesis, oncogene-induced transformation, and invasion by controlling basic and induced transcription of several genes containing the AP-1 locus. The AP-1 complex is involved in many cancers, including hematological tumors. In this report, we systematically review the precise roles of IL-9, IRF-8, and AP-1 in tumor development, particularly with regard to DLBCL. Finally, the recent progress in IRF-8 and IL-9 research is presented; the possible relationship among IRF-8, IL-9, and AP-1 family members is analyzed; and future research prospects are discussed.

Previous findings indicated that polymorphism in gene catechol-O-methyltransferase (COMT) had been linked to chemotherapy-related cognitive impairment (CRCI). Nevertheless, the motivation of COMT polymorphisms in regulating cognitive impairment in breast cancer survivors with disparate status of human epidermal growth factor receptor 2 (HER2) was still vague.

The current research aimed to evaluate the regulation of the risk by COMT genotype on CRCI in breast cancer survivors with disparate status of HER2.

Breast cancer survivors (103 with HER2- and 118 with HER2+) underwent neuropsychological tests before and after chemotherapy, containing event- and time-based prospective memory (EBPM and TBPM). Three single-nucleotide polymorphisms (SNPs) were estimated by providing peripheral blood, containing COMT (rs165599, rs737865, and rs4680).

The EBPM and TBPM performances was lower as compared with these before chemotherapy (z = -7.712, z = -2.403, respectively,

< 0.01). Furthermore, the EBPM and TBPM performances of HER2- group survivors were lower than those of HER2+ group survivors after chemotherapy (z = -7.