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Inflammation and tumor microenvironment in lymph node metastasis.

Wu X, Takekoshi T, Sullivan A, Hwang ST - Cancers (Basel) (2011)

Bottom Line: In nearly all human cancers, the presence of lymph node (LN) metastasis increases clinical staging and portends worse prognosis (compared to patients without LN metastasis).Many of the newly identified genes that appear to influence LN metastasis facilitate general motility, chemotactic, or invasive properties that also increase the ability of cancer cells to disseminate and survive at distant organ sites.These new biomarkers will help predict clinical outcome and point to novel future therapies in metastatic melanoma as well as other cancers.

View Article: PubMed Central - PubMed

Affiliation: Department of Dermatology, Medical College of Wisconsin, Milwaukee, WI 53226, USA. sthwang@mcw.edu.

ABSTRACT
In nearly all human cancers, the presence of lymph node (LN) metastasis increases clinical staging and portends worse prognosis (compared to patients without LN metastasis). Herein, principally reviewing experimental and clinical data related to malignant melanoma, we discuss diverse factors that are mechanistically involved in LN metastasis. We highlight recent data that link tumor microenvironment, including inflammation (at the cellular and cytokine levels) and tumor-induced lymphangiogenesis, with nodal metastasis. Many of the newly identified genes that appear to influence LN metastasis facilitate general motility, chemotactic, or invasive properties that also increase the ability of cancer cells to disseminate and survive at distant organ sites. These new biomarkers will help predict clinical outcome and point to novel future therapies in metastatic melanoma as well as other cancers.

No MeSH data available.


Related in: MedlinePlus

Model of melanoma cell metastasis to regional LNs. The process of inflammation-mediated metastasis of melanoma cells from primary sites to regional LNs. (1). Tumor cells induce an inflammatory microenvironment (i.e., infiltration of tumor-associated macrophages (TAMs) and neutrophils; production of cytokines and chemokines); (2). Facilitated by matrix-metallo proteases, tumor cells invade basement membrane and degrade extracellular matrix; (3). Tumor cells undergo epithelial to mesenchymal transition (EMT), which increases the propensity of metastasis; (4). Increased numbers of lymphatic vessels around or with tumors increase probability of invading lymphatic system; (5). Tumor cells passively flow within lymphatic vessels into draining LNs; (6). Metastatic cells survive and form focal metastases within LN.
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f3-cancers-03-00927: Model of melanoma cell metastasis to regional LNs. The process of inflammation-mediated metastasis of melanoma cells from primary sites to regional LNs. (1). Tumor cells induce an inflammatory microenvironment (i.e., infiltration of tumor-associated macrophages (TAMs) and neutrophils; production of cytokines and chemokines); (2). Facilitated by matrix-metallo proteases, tumor cells invade basement membrane and degrade extracellular matrix; (3). Tumor cells undergo epithelial to mesenchymal transition (EMT), which increases the propensity of metastasis; (4). Increased numbers of lymphatic vessels around or with tumors increase probability of invading lymphatic system; (5). Tumor cells passively flow within lymphatic vessels into draining LNs; (6). Metastatic cells survive and form focal metastases within LN.

Mentions: In summary, diverse biological processes, including inflammation, EMT, and lymphangiogenesis, influence nodal metastasis. Pre-existing or tumor-elicited inflammation assists the tumor metastasis at almost every step necessary for LN metastasis (i.e., malignant cell expansion, invasion, EMT, migration, and microenvironment modulation) (Figure 3). Many of the newly identified genes that appear to influence LN metastasis facilitate general motility or invasion properties that promote growth of tumors, encourage transition to a more motile phenotype, or increase the ability of a cancer cell to survive at distant metastatic sites. Already, the identification of such biomarkers allows physicians to better predict patient survival. Investigators are beginning to understand that certain receptors such as CCR7 not only promote LN metastasis but may also profoundly affect tumorigenesis. The development of CCR7 antagonists will allow investigators to determine whether such agents can potentially be beneficial to cancer therapy.


Inflammation and tumor microenvironment in lymph node metastasis.

Wu X, Takekoshi T, Sullivan A, Hwang ST - Cancers (Basel) (2011)

Model of melanoma cell metastasis to regional LNs. The process of inflammation-mediated metastasis of melanoma cells from primary sites to regional LNs. (1). Tumor cells induce an inflammatory microenvironment (i.e., infiltration of tumor-associated macrophages (TAMs) and neutrophils; production of cytokines and chemokines); (2). Facilitated by matrix-metallo proteases, tumor cells invade basement membrane and degrade extracellular matrix; (3). Tumor cells undergo epithelial to mesenchymal transition (EMT), which increases the propensity of metastasis; (4). Increased numbers of lymphatic vessels around or with tumors increase probability of invading lymphatic system; (5). Tumor cells passively flow within lymphatic vessels into draining LNs; (6). Metastatic cells survive and form focal metastases within LN.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3756397&req=5

f3-cancers-03-00927: Model of melanoma cell metastasis to regional LNs. The process of inflammation-mediated metastasis of melanoma cells from primary sites to regional LNs. (1). Tumor cells induce an inflammatory microenvironment (i.e., infiltration of tumor-associated macrophages (TAMs) and neutrophils; production of cytokines and chemokines); (2). Facilitated by matrix-metallo proteases, tumor cells invade basement membrane and degrade extracellular matrix; (3). Tumor cells undergo epithelial to mesenchymal transition (EMT), which increases the propensity of metastasis; (4). Increased numbers of lymphatic vessels around or with tumors increase probability of invading lymphatic system; (5). Tumor cells passively flow within lymphatic vessels into draining LNs; (6). Metastatic cells survive and form focal metastases within LN.
Mentions: In summary, diverse biological processes, including inflammation, EMT, and lymphangiogenesis, influence nodal metastasis. Pre-existing or tumor-elicited inflammation assists the tumor metastasis at almost every step necessary for LN metastasis (i.e., malignant cell expansion, invasion, EMT, migration, and microenvironment modulation) (Figure 3). Many of the newly identified genes that appear to influence LN metastasis facilitate general motility or invasion properties that promote growth of tumors, encourage transition to a more motile phenotype, or increase the ability of a cancer cell to survive at distant metastatic sites. Already, the identification of such biomarkers allows physicians to better predict patient survival. Investigators are beginning to understand that certain receptors such as CCR7 not only promote LN metastasis but may also profoundly affect tumorigenesis. The development of CCR7 antagonists will allow investigators to determine whether such agents can potentially be beneficial to cancer therapy.

Bottom Line: In nearly all human cancers, the presence of lymph node (LN) metastasis increases clinical staging and portends worse prognosis (compared to patients without LN metastasis).Many of the newly identified genes that appear to influence LN metastasis facilitate general motility, chemotactic, or invasive properties that also increase the ability of cancer cells to disseminate and survive at distant organ sites.These new biomarkers will help predict clinical outcome and point to novel future therapies in metastatic melanoma as well as other cancers.

View Article: PubMed Central - PubMed

Affiliation: Department of Dermatology, Medical College of Wisconsin, Milwaukee, WI 53226, USA. sthwang@mcw.edu.

ABSTRACT
In nearly all human cancers, the presence of lymph node (LN) metastasis increases clinical staging and portends worse prognosis (compared to patients without LN metastasis). Herein, principally reviewing experimental and clinical data related to malignant melanoma, we discuss diverse factors that are mechanistically involved in LN metastasis. We highlight recent data that link tumor microenvironment, including inflammation (at the cellular and cytokine levels) and tumor-induced lymphangiogenesis, with nodal metastasis. Many of the newly identified genes that appear to influence LN metastasis facilitate general motility, chemotactic, or invasive properties that also increase the ability of cancer cells to disseminate and survive at distant organ sites. These new biomarkers will help predict clinical outcome and point to novel future therapies in metastatic melanoma as well as other cancers.

No MeSH data available.


Related in: MedlinePlus