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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study investigates the causes of the observed linkage between depression and later onset of cancer. The prevailing view is that cancer in depressed patients results from a weakened immune system. However, molecular biologists have recognized that dysregulation of the ras proto-oncogene results in impaired serotonin and dopamine synthesis manifesting as major depression. A qualitative review of the literature showed that (1) studies using the Minnesota Multiphasic Personality Inventory showed a greater correlation between depression and later cancer onset than those employing other measures and (2) the more related the cancer type was to the Ras oncogene family, the greater the correlation between depression and later cancer onset. These results support the hypothesis that the ras proto-oncogene plays a role in the etiology of depression and could be the common denominator in long-observed depression/cancer linkages. Previous depression/cancer linkage studies are confounded in that they failed to analyze cancer type and accurately diagnose depression.
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PMID:Behavioral genetics of the depression/cancer correlation: a look at the Ras oncogene family and the 'cerebral diabetes paradigm'. 1856 4

Female mice transgenic for the rat proto-oncogene c-erb-B2, under control of the mouse mammary tumor virus (MMTV) promoter (neuN), spontaneously develop metastatic mammary carcinomas. The development of these mammary tumors is associated with increased number of GR-1(+)CD11b(+) myeloid derived suppressor cells (MDSCs) in the peripheral blood (PB), spleen and tumor. We report a complex relationship between tumor growth, MDSCs and immune regulatory molecules in non-mutated neu transgenic mice on a FVB background (FVB-neuN). The first and second tumors in FVB-neuN mice develop at a median of 265 (147-579) and 329 (161-523) days, respectively, resulting in a median survival time (MST) of 432 (201 to >500) days. During tumor growth, significantly increased number of MDSCs is observed in the PB and spleen, as well as, in infiltrating the mammary tumors. Our results demonstrate a direct correlation between tumor size and the number of MDSCs infiltrating the tumor and an inverse relationship between the frequency of CD4(+) T-cells and MDSCs in the spleen. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assessment of enzyme and cytokine transcript levels in the spleen, tumor, tumor-infiltrating non-parenchymal cells (NPCs) and mammary glands revealed a significant increase in transcript levels from grossly normal mammary glands and tumor-infiltrating NPCs during tumor progression. Tumor NPCs, as compared to spleen cells from wild-type (w/t) mice, expressed significantly higher levels of arginase-1 (ARG-1), nitric oxide synthase (NOS-2), vascular endothelial growth factor (VEGF-A) and significantly lower levels of interferon (IFN)-gamma, interleukin (IL)-2 and fms-like tyrosine kinase-3 ligand (Flt3L) transcript levels. Transcript levels in the spleens of tumor-bearing (TB) mice also differed from normal mice, although to a lesser extent than transcript levels from tumor-infiltrating NPCs. Furthermore, both spleen cells and NPCs from TB mice, but not control mice, suppressed alloantigen responses by syngeneic control spleen cells. Correlative studies revealed that the number of MDSCs in the spleen was directly associated with granulocyte colony stimulating factor (G-CSF) transcript levels in the spleen; while the number of MDSCs in the tumors was directly correlated with splenic granulocyte macrophage stimulating factor (GM-CSF) transcript levels, tumor volume and tumor cell number. Together our results support a role for MDSCs in tumor initiation and progressive, T-cell depression and loss of function provide evidence which support multiple mechanisms of MDSC expansion in a site-dependent manner.
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PMID:Myeloid-derived suppressor cells in mammary tumor progression in FVB Neu transgenic mice. 1944 84

The present study aimed to identify the core genes and pathways involved in depression in patients with ovarian cancer (OC) who suffer from high or low-grade depression. The dataset GSE9116 from Gene Expression Omnibus database was analyzed to identify differentially expressed genes (DEGs) in these patients. To elucidate how certain genes could promote depression in patients with OC, pathway crosstalk, protein-protein interaction (PPI) and comprehensive gene-pathway analyses were determined using WebGestalt, ToppGene and Search Tool for the Retrieval of Interacting Genes and gene ontology analysis. Key genes and pathways were extracted from the gene-pathway network, and gene expression and survival analysis were evaluated. A total of 93 DEGs were identified from GSE9116 dataset, including 84 upregulated genes and nine downregulated genes. The PPI, pathway crosstalk and comprehensive gene-pathway analyses highlighted C-C motif chemokine ligand 2 (CCL2), Fos proto-oncogene, AP-1 transcription factor subunit (FOS), serpin family E member 1 (SERPINE1) and serpin family G member 1 (SERPING1) as core genes involved in the promotion of depression in patients with OC. These core genes were involved in the following four pathways 'Ensemble of genes encoding ECM-associated proteins including ECM-affiliated proteins', 'ECM regulators and secreted factors', 'Ensemble of genes encoding extracellular matrix and extracellular matrix-associated proteins' and 'MAPK signaling pathway and IL-17 signaling pathway'. The results from gene expression and survival analysis demonstrated that these four key genes were upregulated in patients with OC and high-grade depression and could worsen patients' survival. These results suggested that CCL2, FOS, SERPINE1 and SERPING1 may serve a crucial role in the promotion of depression in patients with OC. This finding may provide novel markers for predicting and treating depression in patients with OC; however, the underlying mechanisms remain unknown and require further investigation.
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PMID:The core genes involved in the promotion of depression in patients with ovarian cancer. 3178 74


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