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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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A wound model was built in C57BL/B16 tumor-bearing mouse to determine the influence on melanoma by inflammation. When the tumor grew to 0.5 cm3, we created a wound beyond the tumor in the opposite site of the mouse's body. A.) The results show gradual reduction of the tumor volume when the wound was building; the tumor volume reached the minimum at day 7 (shown in black box, p < 0.01). After day 7, the tumor inhibitory effect of the wound (inflammation) weakened gradually. On about day 11 of the inflammatory group compared with the control group, tumor volume almost as same as the control group at day 13 (shown in black box, p > 0.05). B.) The cross-section of the tumor showed that the tumor necrosis with hemorrhage occurred in different proportions of times and groups. On day 7, the group wound tumors were smaller than the control group, and the area with necrotic tissue is greater than the control group (p < 0.01). After 11 days, the tumor volume in the wound group was increased, but in the cross-section area of necrotic tissue rather than in the control group (p > 0.05). The necrotic percentage after day 11 showed the tumor through a mechanism to adapt the wounds caused by inflammation induced necrosis, promoted the emergence of proliferation.
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Figure 1: A wound model was built in C57BL/B16 tumor-bearing mouse to determine the influence on melanoma by inflammation. When the tumor grew to 0.5 cm3, we created a wound beyond the tumor in the opposite site of the mouse's body. A.) The results show gradual reduction of the tumor volume when the wound was building; the tumor volume reached the minimum at day 7 (shown in black box, p < 0.01). After day 7, the tumor inhibitory effect of the wound (inflammation) weakened gradually. On about day 11 of the inflammatory group compared with the control group, tumor volume almost as same as the control group at day 13 (shown in black box, p > 0.05). B.) The cross-section of the tumor showed that the tumor necrosis with hemorrhage occurred in different proportions of times and groups. On day 7, the group wound tumors were smaller than the control group, and the area with necrotic tissue is greater than the control group (p < 0.01). After 11 days, the tumor volume in the wound group was increased, but in the cross-section area of necrotic tissue rather than in the control group (p > 0.05). The necrotic percentage after day 11 showed the tumor through a mechanism to adapt the wounds caused by inflammation induced necrosis, promoted the emergence of proliferation.

Mentions: To determine if inflammation has an inhibitory effect on the melanoma cells, a wound mouse model was built. When the tumor grew to a specific size, we created a wound in the opposite side of the mouse's body. The wound model was used to manufacture a full-body model of acute inflammation in order to investigate the macro effect between inflammation and tumors. The results show a gradual reduction of tumor volume when the wound was building; the tumor volume reached the minimum at day 7. After day 7, the inhibitory effect of the wound (inflammation) on the tumor down-regulated gradually. The tumor volume of the inflammatory group at day 11 was almost the same as the control group at day 13. This is even higher than the average tumor volume. The tumor growth curve showed two phases: the early phase (before day 7, the inhibition phase) and the latter phase (after day 7 and marked in day 11, the inhibition missing phase). The latter phase presented an increasing proliferation of tumors. (Figure 1A)


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)

A wound model was built in C57BL/B16 tumor-bearing mouse to determine the influence on melanoma by inflammation. When the tumor grew to 0.5 cm3, we created a wound beyond the tumor in the opposite site of the mouse's body. A.) The results show gradual reduction of the tumor volume when the wound was building; the tumor volume reached the minimum at day 7 (shown in black box, p < 0.01). After day 7, the tumor inhibitory effect of the wound (inflammation) weakened gradually. On about day 11 of the inflammatory group compared with the control group, tumor volume almost as same as the control group at day 13 (shown in black box, p > 0.05). B.) The cross-section of the tumor showed that the tumor necrosis with hemorrhage occurred in different proportions of times and groups. On day 7, the group wound tumors were smaller than the control group, and the area with necrotic tissue is greater than the control group (p < 0.01). After 11 days, the tumor volume in the wound group was increased, but in the cross-section area of necrotic tissue rather than in the control group (p > 0.05). The necrotic percentage after day 11 showed the tumor through a mechanism to adapt the wounds caused by inflammation induced necrosis, promoted the emergence of proliferation.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: A wound model was built in C57BL/B16 tumor-bearing mouse to determine the influence on melanoma by inflammation. When the tumor grew to 0.5 cm3, we created a wound beyond the tumor in the opposite site of the mouse's body. A.) The results show gradual reduction of the tumor volume when the wound was building; the tumor volume reached the minimum at day 7 (shown in black box, p < 0.01). After day 7, the tumor inhibitory effect of the wound (inflammation) weakened gradually. On about day 11 of the inflammatory group compared with the control group, tumor volume almost as same as the control group at day 13 (shown in black box, p > 0.05). B.) The cross-section of the tumor showed that the tumor necrosis with hemorrhage occurred in different proportions of times and groups. On day 7, the group wound tumors were smaller than the control group, and the area with necrotic tissue is greater than the control group (p < 0.01). After 11 days, the tumor volume in the wound group was increased, but in the cross-section area of necrotic tissue rather than in the control group (p > 0.05). The necrotic percentage after day 11 showed the tumor through a mechanism to adapt the wounds caused by inflammation induced necrosis, promoted the emergence of proliferation.
Mentions: To determine if inflammation has an inhibitory effect on the melanoma cells, a wound mouse model was built. When the tumor grew to a specific size, we created a wound in the opposite side of the mouse's body. The wound model was used to manufacture a full-body model of acute inflammation in order to investigate the macro effect between inflammation and tumors. The results show a gradual reduction of tumor volume when the wound was building; the tumor volume reached the minimum at day 7. After day 7, the inhibitory effect of the wound (inflammation) on the tumor down-regulated gradually. The tumor volume of the inflammatory group at day 11 was almost the same as the control group at day 13. This is even higher than the average tumor volume. The tumor growth curve showed two phases: the early phase (before day 7, the inhibition phase) and the latter phase (after day 7 and marked in day 11, the inhibition missing phase). The latter phase presented an increasing proliferation of tumors. (Figure 1A)

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