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Insight Regarding Cancer Development May Lead To New Treatment Strategies

Cancer is a disease defined by abnormal cell division, development, or protein synthesis.  A wide variety of elements can influence its growth, and while some are controllable, like nutrition, lifestyle choice, activity levels, others like genetic factors are out of our hands.  A recent study from the Tokyo Medical and Dental University details how certain [...]

Cancer is a disease defined by abnormal cell division, development, or protein synthesis.  A wide variety of elements can influence its growth, and while some are controllable, like nutrition, lifestyle choice, activity levels, others like genetic factors are out of our hands.  A recent study from the Tokyo Medical and Dental University details how certain molecules can impact the disease.

The abnormal expression of different classes of molecules is known to be linked to various types of cells becoming cancerous.  The recently discovered group of small, noncoding molecules called microRNAs (miRNAs) fall in this exact category.

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It seems that the absence of miR-146b, as well as miR-146a, can lead to dysregulation of the cell cycle and eventually cause cancers of the blood, including leukemia or lymphoma.  Moreover, key differences were observed depending on which miRNA was absent, along with variations in which type of cancer developed and at what rate.

Investigaror Hiroshi Asahara, M.D., Ph.D., Professor Department of Systems BioMedicine took part in the laboratory testing and noted that: “After the mice had been established, we determined the rate at which they developed tumors, analyzed and characterized their tumor tissue at the cellular and molecular levels, and also focused on key features of their immune cells, specifically their B cells”.

The data collected showed the differences between lacking miR-146a and miR-146b.  “We could also detect any similarities in their cancers to those that develop in humans”, added Dr. Asahara.

The inhibition of either molecule set in motion a series of processes that made the activation of a protein complex called NF-κB impossible.  If either molecule was missing, NF-κB became overactivated, leading to excessive progression of the cell cycle and rapid cell duplication, generating inflammation and tumorigenesis.  This resulted in mouse models presenting high rates of B-cell lymphoma and acute myeloid leukemia.

Lead author Takahiro Mitsumura mentioned that “Mice lacking miR-146b developed malignancy less than those without miR-146a.  There were also differences in histological features within the cells in B-cell lymphomas, including regarding positivity for various tumor markers”.

Dysregulation of miR-146a and miR-146b often appears in many human cancer types, which is why these findings are so important.  Gaining a better understanding of the mechanism involved could lead to improved targeted therapies and increase the quality of life for patients.

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