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A pilot study on acute inflammation and cancer: a new balance between IFN-gamma and TGF-beta in melanoma.

Ma YM, Sun T, Liu YX, Zhao N, Gu Q, Zhang DF, Qie S, Ni CS, Liu Y, Sun BC - J. Exp. Clin. Cancer Res. (2009)

Bottom Line: Recent data have redefined the concept of inflammation as a critical component of tumor progression.In the early phase, inhibitory effects are present.The process that produces these effects is the functional reaction of IFN-gamma secretions from a wound inflammation.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pathology, Tianjin Cancer Hospital, Tianjin Medical University, Tianjin, PR China.

ABSTRACT
Recent data have redefined the concept of inflammation as a critical component of tumor progression. However, there has been little development on cases where inflammation on or near a wound and a tumor exist simultaneously. Therefore, this pilot study aims to observe the impact of a wound on a tumor, to build a new mouse tumor model with a manufactured surgical wound representing acute inflammation, and to evaluate the relationship between acute inflammation or wound healing and the process of tumor growth. We focus on the two phases that are present when acute inflammation influences tumor. In the early phase, inhibitory effects are present. The process that produces these effects is the functional reaction of IFN-gamma secretions from a wound inflammation. In the latter phase, the inhibited tumor is made resistant to IFN-gamma through the release of TGF-beta to balance the inflammatory factor effect on the tumor cells. A pair of cytokines IFN-gamma/TGF-beta established a new balance to protect the tumor from the interference effect of the inflammation. The tumor was made resistant to IFN-gamma through the release of TGF-beta to balance the inflammatory effect on the tumor cells. This balance mechanism that occurred in the tumor cells increased proliferation and invasion. In vitro and in vivo experiments have confirmed a new view of clinical surgery that will provide more detailed information on the evaluation of tumors after surgery. This study also provides a better understanding of the relationship between tumor and inflammation, as well as tumor cell attacks on inflammatory factors.

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To further observe and determine the inflammatory factors in the interaction between tumor and inflammation, results showed that: A.) the level of IFN-γ in the serum in the wound group continued a high level of expression (day 7 p < 0.01, day 11 p < 0.01); B.) in tumor tissue also detected high concentrations compared with the control group (day 7 p < 0.01, day 11 p < 0.01). Interestingly, at the 11th day, the tumor with the TGF-β increased, the result is that: C.) high levels of TGF-β can also be detected in the serum (day 7 p > 0.05, day 11 p < 0.01); D.) the same change in tumor (day 7 p > 0.05, day 11 p < 0.01). The TGF-β level before day 7 is not clear in terms of the present low of expression and secretion of tumor cells. That showed that at this time, the tumor does not have to go through the regulation of TGF-β to go against the ability of IFN-γ. When the IFN-γ-induces inhibition of tumor necrosis and persistence over a period, the role of TGF-β has been demonstrated, giving the tumor cells the ability to fight against the IFN-γ, so that the tumor cells could grow.
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Figure 2: To further observe and determine the inflammatory factors in the interaction between tumor and inflammation, results showed that: A.) the level of IFN-γ in the serum in the wound group continued a high level of expression (day 7 p < 0.01, day 11 p < 0.01); B.) in tumor tissue also detected high concentrations compared with the control group (day 7 p < 0.01, day 11 p < 0.01). Interestingly, at the 11th day, the tumor with the TGF-β increased, the result is that: C.) high levels of TGF-β can also be detected in the serum (day 7 p > 0.05, day 11 p < 0.01); D.) the same change in tumor (day 7 p > 0.05, day 11 p < 0.01). The TGF-β level before day 7 is not clear in terms of the present low of expression and secretion of tumor cells. That showed that at this time, the tumor does not have to go through the regulation of TGF-β to go against the ability of IFN-γ. When the IFN-γ-induces inhibition of tumor necrosis and persistence over a period, the role of TGF-β has been demonstrated, giving the tumor cells the ability to fight against the IFN-γ, so that the tumor cells could grow.

Mentions: Interestingly, after day 7, TGF-β increased in the tumors. The TGF-β level before day 7 day was detected in the category of low expression and secretion of tumor cells (Figure 2). Figure 2 shows that the tumor has to enhance the regulation of TGF-β to fight against IFN-γ. The role of TGF-β has been demonstrated with the IFN-γ-induced inhibition of tumor necrosis and persistence over a period, giving tumor cells the ability to fight IFN-γ and thus resulting in tumor cell growth.


A pilot study on acute inflammation and cancer: a new balance between IFN-gamma and TGF-beta in melanoma.

Ma YM, Sun T, Liu YX, Zhao N, Gu Q, Zhang DF, Qie S, Ni CS, Liu Y, Sun BC - J. Exp. Clin. Cancer Res. (2009)

To further observe and determine the inflammatory factors in the interaction between tumor and inflammation, results showed that: A.) the level of IFN-γ in the serum in the wound group continued a high level of expression (day 7 p < 0.01, day 11 p < 0.01); B.) in tumor tissue also detected high concentrations compared with the control group (day 7 p < 0.01, day 11 p < 0.01). Interestingly, at the 11th day, the tumor with the TGF-β increased, the result is that: C.) high levels of TGF-β can also be detected in the serum (day 7 p > 0.05, day 11 p < 0.01); D.) the same change in tumor (day 7 p > 0.05, day 11 p < 0.01). The TGF-β level before day 7 is not clear in terms of the present low of expression and secretion of tumor cells. That showed that at this time, the tumor does not have to go through the regulation of TGF-β to go against the ability of IFN-γ. When the IFN-γ-induces inhibition of tumor necrosis and persistence over a period, the role of TGF-β has been demonstrated, giving the tumor cells the ability to fight against the IFN-γ, so that the tumor cells could grow.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2683570&req=5

Figure 2: To further observe and determine the inflammatory factors in the interaction between tumor and inflammation, results showed that: A.) the level of IFN-γ in the serum in the wound group continued a high level of expression (day 7 p < 0.01, day 11 p < 0.01); B.) in tumor tissue also detected high concentrations compared with the control group (day 7 p < 0.01, day 11 p < 0.01). Interestingly, at the 11th day, the tumor with the TGF-β increased, the result is that: C.) high levels of TGF-β can also be detected in the serum (day 7 p > 0.05, day 11 p < 0.01); D.) the same change in tumor (day 7 p > 0.05, day 11 p < 0.01). The TGF-β level before day 7 is not clear in terms of the present low of expression and secretion of tumor cells. That showed that at this time, the tumor does not have to go through the regulation of TGF-β to go against the ability of IFN-γ. When the IFN-γ-induces inhibition of tumor necrosis and persistence over a period, the role of TGF-β has been demonstrated, giving the tumor cells the ability to fight against the IFN-γ, so that the tumor cells could grow.
Mentions: Interestingly, after day 7, TGF-β increased in the tumors. The TGF-β level before day 7 day was detected in the category of low expression and secretion of tumor cells (Figure 2). Figure 2 shows that the tumor has to enhance the regulation of TGF-β to fight against IFN-γ. The role of TGF-β has been demonstrated with the IFN-γ-induced inhibition of tumor necrosis and persistence over a period, giving tumor cells the ability to fight IFN-γ and thus resulting in tumor cell growth.

Bottom Line: Recent data have redefined the concept of inflammation as a critical component of tumor progression.In the early phase, inhibitory effects are present.The process that produces these effects is the functional reaction of IFN-gamma secretions from a wound inflammation.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pathology, Tianjin Cancer Hospital, Tianjin Medical University, Tianjin, PR China.

ABSTRACT
Recent data have redefined the concept of inflammation as a critical component of tumor progression. However, there has been little development on cases where inflammation on or near a wound and a tumor exist simultaneously. Therefore, this pilot study aims to observe the impact of a wound on a tumor, to build a new mouse tumor model with a manufactured surgical wound representing acute inflammation, and to evaluate the relationship between acute inflammation or wound healing and the process of tumor growth. We focus on the two phases that are present when acute inflammation influences tumor. In the early phase, inhibitory effects are present. The process that produces these effects is the functional reaction of IFN-gamma secretions from a wound inflammation. In the latter phase, the inhibited tumor is made resistant to IFN-gamma through the release of TGF-beta to balance the inflammatory factor effect on the tumor cells. A pair of cytokines IFN-gamma/TGF-beta established a new balance to protect the tumor from the interference effect of the inflammation. The tumor was made resistant to IFN-gamma through the release of TGF-beta to balance the inflammatory effect on the tumor cells. This balance mechanism that occurred in the tumor cells increased proliferation and invasion. In vitro and in vivo experiments have confirmed a new view of clinical surgery that will provide more detailed information on the evaluation of tumors after surgery. This study also provides a better understanding of the relationship between tumor and inflammation, as well as tumor cell attacks on inflammatory factors.

Show MeSH
Related in: MedlinePlus