Tumor-derived exosomes (TDEs) play pivotal roles in several aspects of cancer biology. It is now evident that TDEs also favor tumor growth by negatively affecting anti-tumor immunity. As important sentinels of immune surveillance system, natural killer (NK) cells can recognize malignant cells very early and counteract the tumor development and metastasis without a need for additional activation. Based on this rationale, adoptive transfer of ex vivo expanded NK cells/NK cell lines, such as NK-92 cells, has attracted great attention and is widely studied as a promising immunotherapy for cancer treatment. However, by exploiting various strategies, including secretion of exosomes, cancer cells are able to subvert NK cell responses. This paper reviews the roles of TDEs in cancer-induced NK cells impairments with mechanistic insights. The clinical significance and potential approaches to nullify the effects of TDEs on NK cells in cancer immunotherapy are also discussed.

Multiple factors, including growth factors, are shown to be culprits of cancer outset and persistence. Among growth factors, insulin-like growth factors (IGFs) family are of more importance in the prognosis of blood malignancies. After binding to their corresponding receptor, IGFs initiate PI3K/AKT signaling pathway and increase the translation of intracellular proteins, such as cell division-related proteins. They also stimulate the transcription of cell divisionrelated genes using the Ras-GTP pathway. In addition to organs such as the liver, IGFs are secreted by tumor cells and can cause growth and proliferation of self or tumor cells via autocrine and paracrine methods. Current studies indicate that decreasing the effects of IGF by blocking them, their receptors, or PI3K/AKT pathway using various drugs could help to suppress the division of tumor cells. Here, we delineate the role of the IGF family in hematologic malignancies and their potential mechanisms.

Oncogenic and tumor-suppressive roles of long non-coding RNA make them an appropriate target for expression analysis in cancer studies. In this study, we selected two lncRNAs (EMX2OS and FOXN3-AS1) that are resided near the GWAS-identified SNPs for breast cancer (rs2901157 and rs141061110). These transcripts have been identified in different cancer types as either oncogenes or tumor suppressors. In the present investigation, we aimed to quantify the expression level of EMX2OS and FOXN3-AS1 in 44 breast cancer samples and normal adjacent tissues (ANCTs). The FOXN3-AS1 expression level was significantly increased in breast cancer samples compared with ANCTs (P value ¼ 0.02), Also its amounts could distinguish two sets of samples with an accuracy of 70% (P value ¼ 0.009). We have found an association between FOXN3-AS1 expression and tumor size (P value ¼ 0.02). On the other hand, no significant differences were found in the EMX2OS expression level between two sets of samples (P value ¼ 0.44); however, EMX2OS expression level has a significant association with the age of the patients (P value ¼ 0.03). According to our result, FOXN3-AS1 can be demonstrated as a probable diagnostic marker in breast cancer so we suggest further functional studies to find the precise role of these lncRNAs in breast cancer progression.

Background: Acute lymphoblastic leukemia (ALL) is the most common type of leukemia in children.Several environmental and genetic factors are known to be involved in its development and progression. The angiopoietin-Tie system is one of the most critical factors in angiogenesis, and its possible role in solid tumors and leukemia has been previously investigated. In this study, we examined the expression of these genes in ALL patients (early pre-B-ALL and pre-B-ALL) and compared them with normal samples.Methods: Bone marrow samples were collected from 40 patients (aged 0-19 yr) newly diagnosed with early pre-B-ALL or pre-B-ALL using molecular and flow cytometric tests and from 15 control individuals. For molecular tests, RNA extraction and cDNA synthesis were performed, and Ang1, Ang2, Ang4, Tie1, and Tie2 gene expression was examined by real-time polymerase chain reaction.Results: Ang2, Tie1, and Tie2 gene expression were significantly increased in patients with ALL, whereas Ang1 gene expression was decreased. The Ang4 gene did not show significant expression changes between the two groups. Conclusion:Changes in the expression of the Ang-Tie system indicate a possible role of angiogenesis in ALL prognosis. Moreover, such changes can be considered as potential diagnostic biomarkers or therapeutic targets.

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Introduction: One of the most common types of leukemia is acute myeloid leukemia (AML). Intrinsic and extrinsic factors may lead to AML. Insulin-like growth factor (IGF) is a mitogenic intermediate from the liver that regulates growth and proliferation in response to GH. In this study, we examined the expression of IGF family genes in AML patients (M3 and Non-M3) and compared them with normal samples. Methods Forty bone marrow samples from recently diagnosed AML patients along with 15 samples from subjects without hematological malignancies were collected. For molecular tests, RNA extraction and cDNA synthesis were performed. Finally, IGF1, IGF2, IGFBP3, IGF1R, and IGF2R gene expression were examined by Real-Time PCR. Results IGF1, IGF1R, and IGFBP3 gene expression were significantly increased in patients with AML. In contrast, IGF2 and IGF2R genes did not show significant expression changes between the two groups. Conclusion The expression in this gene family soared in AML patients' bone marrow, compared to normal subjects. This can be caused by malignant cells in the bone marrow. These malignant cells express proteins that increase the number of malignant cells. Moreover, they can be considered as diagnostic biomarkers or therapeutic targets with further research.