کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10959264 | 1100411 | 2010 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Involvement of stromal p53 in tumor-stroma interactions
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کلمات کلیدی
ECMTSP-1CAFMMPp53SDF-1loss of heterozygosity - از دست دادن هتروزیگوتیسمStroma - استروماinterleukin - اینترلوکینThrombospondin-1 - ترومبوسپوندن-1Cancer - سرطانStromal derived factor 1 - عامل مشتق استروم 1cancer-associated fibroblast - فیبروبلاست وابسته به سرطانLOH - لوهانExtracellular matrix - ماتریکس خارج سلولیmatrix metalloproteinase - ماتریکس متالوپروتئینازwild-type - نوع وحشی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Involvement of stromal p53 in tumor-stroma interactions Involvement of stromal p53 in tumor-stroma interactions](/preview/png/10959264.png)
چکیده انگلیسی
p53 is a major tumor-suppressor gene, inactivated by mutations in about half of all human cancer cases, and probably incapacitated by other means in most other cases. Most research regarding the role of p53 in cancer has focused on its ability to elicit apoptosis or growth arrest of cells that are prone to become malignant owing to DNA damage or oncogene activation, i.e. cell-autonomous activities of p53. However, p53 activation within a cell can also exert a variety of effects upon neighboring cells, through secreted factors and paracrine and endocrine mechanisms. Of note, p53 within cancer stromal cells can inhibit tumor growth and malignant progression. Cancer cells that evolve under this inhibitory influence acquire mechanisms to silence stromal p53, either by direct inhibition of p53 within stromal cells, or through pressure for selection of stromal cells with compromised p53 function. Hence, activation of stromal p53 by chemotherapy or radiotherapy might be part of the mechanisms by which these treatments cause cancer regression. However, in certain circumstances, activation of stromal p53 by cytotoxic anti-cancer agents might actually promote treatment resistance, probably through stromal p53-mediated growth arrest of the cancer cells or through protection of the tumor vasculature. Better understanding of the underlying molecular mechanisms is thus required. Hopefully, this will allow their manipulation towards better inhibition of cancer initiation, progression and metastasis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Seminars in Cell & Developmental Biology - Volume 21, Issue 1, February 2010, Pages 47-54
Journal: Seminars in Cell & Developmental Biology - Volume 21, Issue 1, February 2010, Pages 47-54
نویسندگان
Jair Bar, Neta Moskovits, Moshe Oren,