Bone metastasis is a common complication of many types of advanced cancer, including breast cancer. Bone metastasis may cause severe pain, fractures, and hypercalcemia, rendering clinical management challenging and substantially reducing the quality of life and overall survival (OS) time of breast cancer patients. Studies have revealed that bone metastasis is related to interactions between tumor cells and the bone microenvironment, and involves complex molecular biological mechanisms, including colonization, osteolytic destruction, and an immunosuppressive bone microenvironment. Agents inhibiting bone metastasis (such as bisphosphate and denosumab) alleviate bone destruction and improve the quality of life of breast cancer patients with bone metastasis. However, the prognosis of these patients remains poor, and the specific biological mechanism of bone metastasis is incompletely understood. Additional basic and clinical studies are urgently needed, to further explore the mechanism of bone metastasis and develop new therapeutic drugs. This review presents a summary of the molecular mechanisms and therapeutic strategies of bone metastasis of breast cancer, aiming to improve the quality of life and prognosis of breast cancer patients and provide a reference for future research directions.

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Background: The number of patients with breast cancer is increasing worldwide, resulting in a growing number of patients with chemotherapy-related cognitive impairment (CRCI), which seriously affects their quality of life. CRCI is associated with inflammatory factors and systemic inflammatory markers such as pan-immune-inflammation value (PIV) and monocyte-to-lymphocyte ratio (MLR), which can reflect the level of inflammation in the body. While the Managing Cancer and Living Meaningfully (CALM) intervention has been demonstrated to alleviate CRCI in patients with breast cancer, the specific mechanism remains unclear. Objective: This study evaluated the impact of the CALM intervention on systemic inflammation. Methods: Ninety patients with breast cancer with CRCI were enrolled and randomized into care as usual (CAU) and CALM intervention groups. All patients were assessed using the Functional Assessment of Cancer Therapy-Cognitive Function (FACT-Cog), Mini-Mental State Exam (MMSE), and Functional Assessment of Cancer Therapy-Breast (FACT-B) before and after the CAU/CALM intervention. The blood levels of inflammatory markers were also analyzed before and after the intervention. Results: Compared to the CAU group, the CALM group showed significantly improved cognitive function and significantly decreased PIV ( P < .05). PIV was significantly negatively correlated with FACT-Cog ( P < .05). The levels of other inflammatory markers, including MLR, neutrophil-to-lymphocyte ratio (NLR), granulocyte-to-lymphocyte ratio (GLR), and systemic immune-inflammation index (SII), were also reduced in the CALM group. Conclusion: PIV is an important marker of inflammation. The CALM intervention may improve the cognitive function of patients by regulating the systemic inflammation marker PIV through the neuroimmune axis.

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Background Camellia oleifera (C.oleifera) is one of the most important wood oil species in the world. C.oleifera was propagated by nurse seedling grafting. Since the morphology of rootstocks has a significant impact on grafting efficiency and seedling quality, it is necessary to understand the molecular mechanism of morphogenesis for cultivating high-quality and controllable rootstocks. However, the genomic resource for this species is relatively limited, which hinders us from fully understanding the molecular mechanisms of seed germination in C.oleifera. Results In this paper, using transcriptome sequencing, we measured the gene expression in the C.oleifera cotyledon in different stages of development and the global gene expression profiles. Approximately 45.4 gigabases (GB) of paired-end clean reads were assembled into 113,582 unigenes with an average length of 396 bp. Six public protein databases annotate 61.5% (68,217) of unigenes. We identified 11,391 differentially expressed genes (DEGs) throughout different stages of germination. Enrichment analysis revealed that DEGs were mainly involved in hormone signal transduction and starch sucrose metabolism pathways. The gravitropism regulator UNE10, the meristem regulators STM, KNAT1, PLT2, and root-specific transcription factor WOX11 all have higher gene expression levels in the CAM2 stage (seed soaking), which indicates that the cotyledon-regulated program for germination had initiated when the seeds were imbibition. Our data showed differentially reprogrammed to multiple hormone-related genes in cotyledons during C.oleifera seed germination. Conclusion Cotyledons play vital roles, both as the main nutrient provider and as one primary instructor for seed germination and seedling growth. Together, our study will significantly enrich the genomic resources of Camellia and help us understand the molecular mechanisms of the development in the seed germination and seedling growth of C.oleifera. It is helpful to culture standard and superior quality rootstock for C.oleifera breeding.

Ramucirumab, as a vascular endothelial growth factor receptor-2 inhibitor, was first approved in 2014 for treated advanced or metastatic gastric/gastroesophageal junction (GEJ) adenocarcinoma. This study deeply analyzed the efficacy and safety of advanced or metastatic cancer treated with ramucirumab, which included 11 global, double-blind, phase 3 randomized controlled trials with a total of 7410 patients. Subgroup analysis based on different cancer types showed that standard regimens plus ramucirumab significantly increased progression-free survival and overall survival compared with placebo groups in patients with advanced non-small-cell lung cancer (NSCLC), hepatocellular carcinoma, gastric cancer, or GEJ adenocarcinoma. Although a higher proportion of patients achieved overall response and disease control than those treated with placebo, the overall response was not statistically significant between the two groups in advanced NSCLC. Grade 3 or worse treatment-emergent adverse events (TEAEs) that occurred in at least 5% of patients were neutropenia (30.5% in the ramucirumab group vs. 23.5% in the placebo group), leucopenia (14.8% vs. 9.2%), weight decreased (14.2% vs. 8.0%), myalgia (11.7% vs. 7.7%), fatigue (10.9% vs. 7.7%), hypertension (9.2% vs. 2.3%), and anaemia (6.2% vs. 7.7%). In the TEAEs of special interest, the ramucirumab group had a significantly higher incidence of bleeding (mainly grade 1-2 epistaxis and gastrointestinal bleeding), hypertension, proteinuria, liver injury/failure (grade 1-2), venous thromboembolism (grade 1-2), and gastrointestinal perforation (grade ≧3) than the control group.

Aim: To evaluate the relationship between psychological distress and the efficacy of whole-brain radiotherapy (WBRT) in advanced brain metastasis patients. Methods: Brain metastasis patients (40 with psychological distress and 47 without psychological distress) completed distress thermometer tests before WBRT, and progression-free survival (PFS) was acquired during the follow-up period. Results: Psychological distress was a risk factor for poorer PFS in patients treated with WBRT (p < 0.01). The PFS of survivors who underwent WBRT was superior for those without psychological distress (hazard ratio: 0.295; 95% CI: 0.173–0.500; p < 0.01). Conclusion: The survival of brain metastasis patients receiving WBRT was influenced by psychological distress, which negatively affected the treatment outcome and is likely to be a potential risk indicator in advanced cancer patients receiving WBRT.

Background: CD4+ memory T cells (CD4+ MTCs), as an important part of the microenvironment affecting tumorigenesis and progression, have rarely been systematically analyzed. Our purpose was to comprehensively analyze the effect of CD4+ MTC infiltration on the prognosis of colon adenocarcinoma (COAD).Methods: Based on RNA-Seq data, weighted gene co-expression network analysis (WGCNA) was used to screen the CD4+ MTC infiltration genes most associated with colon cancer and then identify hub genes and construct a prognostic model using the least absolute shrinkage and selection operator algorithm (LASSO). Finally, survival analysis, immune efficacy analysis, and drug sensitivity analysis were performed to evaluate the role of the prognostic model in COAD.Results: We identified 929 differentially expressed genes (DEGs) associated with CD4+ MTCs and constructed a prognosis model based on five hub genes (F2RL2, TGFB2, DTNA, S1PR5, and MPP2) to predict overall survival (OS) in COAD. Kaplan–Meier analysis showed poor prognosis in the high-risk group, and the analysis of the hub gene showed that overexpression of TGFB2, DTNA, S1PR5, or MPP2 was associated with poor prognosis. Clinical prediction nomograms combining CD4+ MTC-related DEGs and clinical features were constructed to accurately predict OS and had high clinical application value. Immune efficacy and drug sensitivity analysis provide new insights for individualized treatment.Conclusion: We constructed a prognostic risk model to predict OS in COAD and analyzed the effects of risk score on immunotherapy efficacy or drug sensitivity. These studies have important clinical significance for individualized targeted therapy and prognosis.