WordNet

of or relating to interstices
a mass of fungal tissue that has spore-bearing structures embedded in it or on it
the dense colorless framework of a chloroplast
the supporting tissue of an organ (as opposed to parenchyma)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/07/23 20:54:11」(JST)

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In cell biology, stromal cells are connective tissue cells of any organ, for example in the uterine mucosa (endometrium), prostate, bone marrow, and the ovary. They are cells that support the function of the parenchymal cells of that organ. Fibroblasts, immune cells, pericytes, and inflammatory cells are the most common types of stromal cells.

The interaction between stromal cells and tumor cells is known to play a major role in cancer growth and progression.^[1]

Stromal cells (in the dermis layer) adjacent to the epidermis (the very top layer of the skin) release growth factors that promote cell division. This keeps the epidermis regenerating from the bottom while the top layer of cells on the epidermis are constantly being "sloughed" off of the body. Certain types of skin cancers (basal cell carcinomas) cannot spread throughout the body because the cancer cells require nearby stromal cells to continue their division. The loss of these stromal growth factors when the cancer moves throughout the body prevents the cancer from invading other organs.

Stroma is the non malignant host cells.It is an extracellular matrix in which tumor grows.

Stroma (disambiguation)
Stroma of ovary

References[edit]

^ Wiseman BS, Werb Z (May 2002). "Stromal effects on mammary gland development and breast cancer". Science 296 (5570): 1046–9. doi:10.1126/science.1067431. PMC 2788989. PMID 12004111.

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1. 消化管間質腫瘍、平滑筋腫、および消化管の平滑筋肉腫の局所治療 local treatment for gastrointestinal stromal tumors leiomyomas and leiomyosarcomas of the gastrointestinal tract
2. GISTを含む消化管間葉系腫瘍の疫学、分類、臨床像、予後の特徴、および診断方法 epidemiology classification clinical presentation prognostic features and diagnostic work up of gastrointestinal mesenchymal neoplasms including gist
3. 消化管間質腫瘍に対する補助化学療法および術前補助化学療法としてのイマチニブ adjuvant and neoadjuvant imatinib for gastrointestinal stromal tumors
4. 子宮内膜間質腫瘍の分類および治療 classification and treatment of endometrial stromal tumors
5. 子宮肉腫：分類、臨床症状、および診断 uterine sarcoma classification clinical manifestations and diagnosis

English Journal

Pathway modulations and epigenetic alterations in ovarian tumorbiogenesis.

Saldanha SN, Tollefsbol TO.Author information Department of Biology, University of Alabama at Birmingham, Birmingham, Alabama; Department of Biological Sciences, Alabama State University, Montgomery, Alabama.AbstractCellular pathways are numerous and are highly integrated in function in the control of cellular systems. They collectively regulate cell division, proliferation, survival and apoptosis of cells and mutagenesis of key genes that control these pathways can initiate neoplastic transformations. Understanding these pathways is crucial to future therapeutic and preventive strategies of the disease. Ovarian cancers are of three major types; epithelial, germ-cell, and stromal. However, ovarian cancers of epithelial origin, arising from the mesothelium, are the predominant form. Of the subtypes of ovarian cancer, the high-grade serous tumors are fatal, with low survival rate due to late detection and poor response to treatments. Close examination of preserved ovarian tissues and in vitro studies have provided insights into the mechanistic changes occurring in cells mediated by a few key genes. This review will focus on pathways and key genes of the pathways that are mutated or have aberrant functions in the pathology of ovarian cancer. Non-genetic mechanisms that are gaining prominence in the pathology of ovarian cancer, miRNAs and epigenetics, will also be discussed in the review. J. Cell. Physiol. 229: 393-406, 2014. © 2013 Wiley Periodicals, Inc.
Journal of cellular physiology.J Cell Physiol.2014 Apr;229(4):393-406. doi: 10.1002/jcp.24466.
Cellular pathways are numerous and are highly integrated in function in the control of cellular systems. They collectively regulate cell division, proliferation, survival and apoptosis of cells and mutagenesis of key genes that control these pathways can initiate neoplastic transformations. Understa
PMID 24105793

Extracellular Hsp90 mediates an NF-κB dependent inflammatory stromal program: Implications for the prostate tumor microenvironment.

Bohonowych J, Hance M, Nolan K, Defee M, Parsons Ch, Isaacs J.Author information Cell and Molecular Pharmacology, Medical University of South Carolina, Charleston, South Carolina.AbstractBACKGROUND: The tumor microenvironment (TME) plays an essential role in supporting and promoting tumor growth and progression. An inflammatory stroma is a widespread hallmark of the prostate TME, and prostate tumors are known to co-evolve with their reactive stroma. Cancer-associated fibroblasts (CAFs) within the reactive stroma play a salient role in secreting cytokines that contribute to this inflammatory TME. Although a number of inflammatory mediators have been identified, a clear understanding of key factors initiating the formation of reactive stroma is lacking.
The Prostate.Prostate.2014 Apr;74(4):395-407. doi: 10.1002/pros.22761. Epub 2013 Dec 16.
BACKGROUND: The tumor microenvironment (TME) plays an essential role in supporting and promoting tumor growth and progression. An inflammatory stroma is a widespread hallmark of the prostate TME, and prostate tumors are known to co-evolve with their reactive stroma. Cancer-associated fibroblasts (CA
PMID 24338924

Loss of stromal JUNB does not affect tumor growth and angiogenesis.

Braun J, Strittmatter K, Nübel T, Komljenovic D, Sator-Schmitt M, Bäuerle T, Angel P, Schorpp-Kistner M.Author information Division of Signal Transduction and Growth Control DKFZ DKFZ-ZMBH Alliance, German Cancer Research Center (DKFZ), Heidelberg, Germany.AbstractThe transcription factor AP-1 subunit JUNB has been shown to play a pivotal role in angiogenesis. It positively controls angiogenesis by regulating Vegfa as well as the transcriptional regulator Cbfb and its target Mmp13. In line with these findings, it has been demonstrated that tumor cell-derived JUNB promotes tumor growth and angiogenesis. In contrast to JUNB's function in tumor cells, the role of host-derived stromal JUNB has not been elucidated so far. Here, we show that ablation of Junb in stromal cells including endothelial cells (ECs), vascular smooth muscle cells (SMCs) and fibroblasts does not affect tumor growth in two different syngeneic mouse models, the B16-F1 melanoma and the Lewis lung carcinoma model. In-depth analyses of the tumors revealed that tumor angiogenesis remains unaffected as assessed by measurements of the microvascular density and relative blood volume in the tumor. Furthermore, we could show that the maturation status of the tumor vasculature, analyzed by the SMC marker expression, α-smooth muscle actin and Desmin, as well as the attachment of pericytes to the endothelium, is not changed upon ablation of Junb. Taken together, these results indicate that the pro-angiogenic functions of stromal JUNB are well compensated with regard to tumor angiogenesis and tumor growth.
International journal of cancer. Journal international du cancer.Int J Cancer.2014 Mar 15;134(6):1511-6. doi: 10.1002/ijc.28477. Epub 2013 Oct 9.
The transcription factor AP-1 subunit JUNB has been shown to play a pivotal role in angiogenesis. It positively controls angiogenesis by regulating Vegfa as well as the transcriptional regulator Cbfb and its target Mmp13. In line with these findings, it has been demonstrated that tumor cell-derived
PMID 24027048