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Article: On the origin of cancer metastasis.

Seyfried, Thomas N / Huysentruyt, Leanne C

2012 Volume 18, Issue 1-2, Page(s) 43–73

Abstract: Metastasis involves the spread of cancer cells from the primary tumor to surrounding tissues and to distant organs and is the primary cause of cancer morbidity and mortality. In order to complete the metastatic cascade, cancer cells must detach from the ... ...

Abstract	Metastasis involves the spread of cancer cells from the primary tumor to surrounding tissues and to distant organs and is the primary cause of cancer morbidity and mortality. In order to complete the metastatic cascade, cancer cells must detach from the primary tumor, intravasate into the circulatory and lymphatic systems, evade immune attack, extravasate at distant capillary beds, and invade and proliferate in distant organs. Currently, several hypotheses have been advanced to explain the origin of cancer metastasis. These involve an epithelial mesenchymal transition, an accumulation of mutations in stem cells, a macrophage facilitation process, and a macrophage origin involving either transformation or fusion hybridization with neoplastic cells. Many of the properties of metastatic cancer cells are also seen in normal macrophages. A macrophage origin of metastasis can also explain the long-standing "seed and soil" hypothesis and the absence of metastasis in plant cancers. The view of metastasis as a macrophage metabolic disease can provide novel insight for therapeutic management.
MeSH term(s)	Cell Adhesion/genetics ; Cell Transformation, Neoplastic/genetics ; Epithelial-Mesenchymal Transition/genetics ; Humans ; Macrophages/physiology ; Mutation ; Neoplasm Metastasis/genetics ; Neoplasm Metastasis/physiopathology ; Neoplasms/genetics ; Neoplasms/physiopathology
Language	English
Publishing date	2012-12-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1036388-9
ISSN	0893-9675
ISSN	0893-9675
DOI	10.1615/critrevoncog.v18.i1-2.40
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Zs.A 2587: Show issues

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Article ; Online: Perspectives on the mesenchymal origin of metastatic cancer.

Huysentruyt, Leanne C / Seyfried, Thomas N

Cancer metastasis reviews

2010 Volume 29, Issue 4, Page(s) 695–707

Abstract: Emerging evidence suggests that many metastatic cancers arise from cells of the myeloid/macrophage lineage regardless of the primary tissue of origin. A myeloid origin of metastatic cancer stands apart from origins involving clonal evolution or ... ...

Abstract	Emerging evidence suggests that many metastatic cancers arise from cells of the myeloid/macrophage lineage regardless of the primary tissue of origin. A myeloid origin of metastatic cancer stands apart from origins involving clonal evolution or epithelial-mesenchymal transitions. Evidence is reviewed demonstrating that numerous human cancers express multiple properties of macrophages including phagocytosis, fusogenicity, and gene/protein expression. It is unlikely that the macrophage properties expressed in metastatic cancers arise from sporadic random mutations in epithelial cells, but rather from damage to an already existing mesenchymal cell, e.g., a myeloid/macrophage-type cell. Such cells would naturally embody the capacity to express the multiple behaviors of metastatic cells. The view of metastasis as a myeloid/macrophage disease will impact future cancer research and anti-metastatic therapies.
MeSH term(s)	Animals ; Epithelial-Mesenchymal Transition ; Humans ; Macrophages/pathology ; Mesenchymal Stem Cells/pathology ; Neoplasm Metastasis ; Neoplasms/pathology ; Phagocytosis
Language	English
Publishing date	2010-03-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604857-2
ISSN	1573-7233 ; 0167-7659
ISSN (online)	1573-7233
ISSN	0167-7659
DOI	10.1007/s10555-010-9254-z
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Zs.A 1812: Show issues

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Article ; Online: Hypothesis: are neoplastic macrophages/microglia present in glioblastoma multiforme?

Huysentruyt, Leanne C / Akgoc, Zeynep / Seyfried, Thomas N

ASN neuro

2011 Volume 3, Issue 4

Abstract: Most malignant brain tumours contain various numbers of cells with characteristics of activated or dysmorphic macrophages/microglia. These cells are generally considered part of the tumour stroma and are often described as TAM (tumour-associated ... ...

Abstract	Most malignant brain tumours contain various numbers of cells with characteristics of activated or dysmorphic macrophages/microglia. These cells are generally considered part of the tumour stroma and are often described as TAM (tumour-associated macrophages). These types of cells are thought to either enhance or inhibit brain tumour progression. Recent evidence indicates that neoplastic cells with macrophage characteristics are found in numerous metastatic cancers of non-CNS (central nervous system) origin. Evidence is presented here suggesting that subpopulations of cells within human gliomas, specifically GBM (glioblastoma multiforme), are neoplastic macrophages/microglia. These cells are thought to arise following mitochondrial damage in fusion hybrids between neoplastic stem cells and macrophages/microglia.
MeSH term(s)	Brain Neoplasms/pathology ; Glioblastoma/pathology ; Humans ; Macrophages/pathology ; Microglia/pathology
Language	English
Publishing date	2011-09-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2485467-0
ISSN	1759-0914 ; 1759-0914
ISSN (online)	1759-0914
ISSN	1759-0914
DOI	10.1042/AN20110011
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Article ; Online: Glutamine targeting inhibits systemic metastasis in the VM-M3 murine tumor model.

Shelton, Laura M / Huysentruyt, Leanne C / Seyfried, Thomas N

International journal of cancer

2010 Volume 127, Issue 10, Page(s) 2478–2485

Abstract: Metastatic cancer is a major cause of morbidity and mortality. Current therapeutic options consist of chemotherapy, radiation or targeted therapies. However, these therapies are often toxic, effective over a small range of cancer types or result in drug ... ...

Abstract	Metastatic cancer is a major cause of morbidity and mortality. Current therapeutic options consist of chemotherapy, radiation or targeted therapies. However, these therapies are often toxic, effective over a small range of cancer types or result in drug resistance. Therefore, a more global, less toxic strategy for the management of metastatic cancer is required. Although most cancers display increased glucose metabolism, glutamine is also a major energy substrate for many cancers. We evaluated the antimetastatic potential of 6-diazo-5-oxo-L-norleucine (DON), a glutamine analog, using the new VM mouse model of systemic metastasis. We found that primary tumor growth was ∼20-fold less in DON-treated mice than in untreated control mice. We also found that DON treatment inhibited metastasis to liver, lung and kidney as detected by bioluminescence imaging and histology. Our findings provide proof of concept that metabolic therapies targeting glutamine metabolism can manage systemic metastatic cancer.
MeSH term(s)	Animals ; Antimetabolites, Antineoplastic/pharmacology ; Blood Glucose/metabolism ; Body Weight ; Brain Neoplasms/drug therapy ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Caloric Restriction ; Cell Growth Processes/drug effects ; Cell Line, Tumor ; Cerebrum/metabolism ; Cerebrum/pathology ; Diazooxonorleucine/pharmacology ; Drug Delivery Systems ; Female ; Glucose/deficiency ; Glucose/metabolism ; Glutamine/deficiency ; Glutamine/metabolism ; Male ; Mice ; Neoplasm Metastasis
Chemical Substances	Antimetabolites, Antineoplastic ; Blood Glucose ; Diazooxonorleucine (03J0H273KZ) ; Glutamine (0RH81L854J) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2010-04-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.25431
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Zs.A 478: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 576: Show issues

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Article ; Online: Influence of methotrexate and cisplatin on tumor progression and survival in the VM mouse model of systemic metastatic cancer.

Huysentruyt, Leanne C / Shelton, Laura M / Seyfried, Thomas N

International journal of cancer

2010 Volume 126, Issue 1, Page(s) 65–72

Abstract: We recently identified a new tumor (VM-M3), which arose spontaneously in the brain of an inbred VM mouse. When grown outside the brain, the VM-M3 tumor expresses all major biological processes of metastasis to include local invasion, intravasation, ... ...

Abstract	We recently identified a new tumor (VM-M3), which arose spontaneously in the brain of an inbred VM mouse. When grown outside the brain, the VM-M3 tumor expresses all major biological processes of metastasis to include local invasion, intravasation, immune system survival, extravasation, and secondary tumor formation involving lung, liver, kidney, spleen and brain. The VM-M3 tumor also expresses multiple properties of macrophage-like cells similar to those described previously in numerous human metastatic cancers suggesting that the VM-M3 model will be useful for studying most types of metastatic cancer, regardless of tissue origin. VM-M3 tumor cells, expressing firefly luciferase (VM-M3/Fluc), were grown subcutaneously in the immunocompetent and syngeneic VM mouse host. The antimetastatic effects of methotrexate (MTX; 25 mg/kg) and cisplatin (10-15 mg/kg) were evaluated following i.p. injections administered once/wk for 3 weeks. Bioluminescent imaging was used to measure VM-M3/Fluc growth and metastasis. All (12/12) control mice developed systemic cancer within 21 days of subcutaneous VM-M3/Fluc implantation. Although methotrexate did not inhibit VM-M3/Fluc primary tumor growth, it reduced lung and liver metastasis by 50% and completely inhibited metastasis to kidneys, spleen and brain. Cisplatin significantly reduced primary tumor growth, blocked metastasis to lung, liver, kidneys, spleen and brain, and significantly increased survival in all treated animals. Our findings show that the response of the VM-M3/Fluc tumor to MTX and cisplatin is similar to that reported in humans with metastatic disease. These findings indicate that the VM-M3/Fluc tumor is a reliable preclinical model for evaluating antimetastatic cancer therapies and underlying control pathways.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Cisplatin/pharmacology ; Disease Models, Animal ; Disease Progression ; Methotrexate/pharmacology ; Mice ; Mice, Inbred Strains ; Neoplasm Metastasis/pathology ; Survival Analysis
Chemical Substances	Antineoplastic Agents ; Cisplatin (Q20Q21Q62J) ; Methotrexate (YL5FZ2Y5U1)
Language	English
Publishing date	2010-01-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.24649
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Zs.A 478: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 576: Show issues

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Article ; Online: Hypothesis

Thomas N Seyfried / Leanne C Huysentruyt / Zeynep Akgoc

ASN Neuro, Vol 3, Iss 4, p e

are neoplastic macrophages/microglia present in glioblastoma multiforme?

2011 Volume 00064

Abstract	Most malignant brain tumours contain various numbers of cells with characteristics of activated or dysmorphic macrophages/microglia. These cells are generally considered part of the tumour stroma and are often described as TAM (tumour-associated macrophages). These types of cells are thought to either enhance or inhibit brain tumour progression. Recent evidence indicates that neoplastic cells with macrophage characteristics are found in numerous metastatic cancers of non-CNS (central nervous system) origin. Evidence is presented here suggesting that subpopulations of cells within human gliomas, specifically GBM (glioblastoma multiforme), are neoplastic macrophages/microglia. These cells are thought to arise following mitochondrial damage in fusion hybrids between neoplastic stem cells and macrophages/microglia.
Keywords	fusion ; glioblastoma multiforme ; glioma ; macrophage ; microglia ; phagocytosis ; Physiology ; QP1-981 ; Science ; Q ; DOAJ:Physiology ; DOAJ:Biology ; DOAJ:Biology and Life Sciences ; Neurosciences. Biological psychiatry. Neuropsychiatry ; RC321-571
Language	English
Publishing date	2011-09-01T00:00:00Z
Publisher	SAGE Publishing
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The prevalence of HIV-1 DNA in AIDS-related lymphoma and Kaposi Sarcoma throughout the AIDS epidemic

Huysentruyt Leanne C / Lamers Susanna / McGrath Michael S

Infectious Agents and Cancer, Vol 7, Iss Suppl 1, p P

2012 Volume 43

Keywords	Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Language	English
Publishing date	2012-04-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The role of macrophages in the development and progression of AIDS-related non-Hodgkin lymphoma.

Huysentruyt, Leanne C / McGrath, Michael S

Journal of leukocyte biology

2009 Volume 87, Issue 4, Page(s) 627–632

Abstract: Despite HAART, patients infected with HIV develop NHL at a significantly higher level than the noninfected population. The primary difference between lymphoma in non-HIV-infected individuals and those with ARL is that ARL is consistently high-grade and ... ...

Abstract	Despite HAART, patients infected with HIV develop NHL at a significantly higher level than the noninfected population. The primary difference between lymphoma in non-HIV-infected individuals and those with ARL is that ARL is consistently high-grade and metastatic. The emergence of ARL is associated with the presence of macrophage viral reservoirs, similar to what has been observed for HAD. HIV-infected macrophages, as seen by histology and HIV p24 staining, are present in approximately half of ARLs. Macrophage reservoirs recruit additional immune cells, including monocytes/macrophages, through the release of chemoattractants. Additionally, TAM are known to promote tumor progression for most cancer types, including lymphomas. This review will highlight and discuss the role of macrophage viral reservoirs in the development and progression of ARLs and hopefully, shed light on this new and interesting field.
MeSH term(s)	Animals ; Chemotactic Factors/immunology ; HIV/immunology ; HIV Core Protein p24/immunology ; HIV Infections/complications ; HIV Infections/immunology ; HIV Infections/pathology ; Humans ; Lymphoma, AIDS-Related/etiology ; Lymphoma, AIDS-Related/immunology ; Lymphoma, AIDS-Related/pathology ; Macrophages/immunology ; Macrophages/pathology ; Macrophages/virology ; Neoplasm Metastasis
Chemical Substances	Chemotactic Factors ; HIV Core Protein p24
Language	English
Publishing date	2009-12-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1189/jlb.0809564
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Zs.A 603: Show issues

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Article ; Online: Calorie restriction as an anti-invasive therapy for malignant brain cancer in the VM mouse.

Shelton, Laura M / Huysentruyt, Leanne C / Mukherjee, Purna / Seyfried, Thomas N

ASN neuro

2010 Volume 2, Issue 3, Page(s) e00038

Abstract: GBM (glioblastoma multiforme) is the most aggressive and invasive form of primary human brain cancer. We recently developed a novel brain cancer model in the inbred VM mouse strain that shares several characteristics with human GBM. Using bioluminescence ...

Abstract	GBM (glioblastoma multiforme) is the most aggressive and invasive form of primary human brain cancer. We recently developed a novel brain cancer model in the inbred VM mouse strain that shares several characteristics with human GBM. Using bioluminescence imaging, we tested the efficacy of CR (calorie restriction) for its ability to reduce tumour size and invasion. CR targets glycolysis and rapid tumour cell growth in part by lowering circulating glucose levels. The VM-M3 tumour cells were implanted intracerebrally in the syngeneic VM mouse host. Approx. 12-15 days post-implantation, brains were removed and both ipsilateral and contralateral hemispheres were imaged to measure bioluminescence of invading tumour cells. CR significantly reduced the invasion of tumour cells from the implanted ipsilateral hemisphere into the contralateral hemisphere. The total percentage of Ki-67-stained cells within the primary tumour and the total number of blood vessels was also significantly lower in the CR-treated mice than in the mice fed ad libitum, suggesting that CR is anti-proliferative and anti-angiogenic. Our findings indicate that the VM-M3 GBM model is a valuable tool for studying brain tumour cell invasion and for evaluating potential therapeutic approaches for managing invasive brain cancer. In addition, we show that CR can be effective in reducing malignant brain tumour growth and invasion.
MeSH term(s)	Animals ; Brain Neoplasms/diet therapy ; Brain Neoplasms/pathology ; Brain Neoplasms/prevention & control ; Caloric Restriction/methods ; Disease Models, Animal ; Glioblastoma/diet therapy ; Glioblastoma/pathology ; Glioblastoma/prevention & control ; Male ; Mice ; Mice, Inbred Strains ; Neoplasm Invasiveness/pathology ; Neoplasm Invasiveness/prevention & control
Language	English
Publishing date	2010-07-23
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2485467-0
ISSN	1759-0914 ; 1759-0914
ISSN (online)	1759-0914
ISSN	1759-0914
DOI	10.1042/AN20100002
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Article ; Online: Is the restricted ketogenic diet a viable alternative to the standard of care for managing malignant brain cancer?

Seyfried, Thomas N / Marsh, Jeremy / Shelton, Laura M / Huysentruyt, Leanne C / Mukherjee, Purna

Epilepsy research

2012 Volume 100, Issue 3, Page(s) 310–326

Abstract: Malignant brain cancer persists as a major disease of morbidity and mortality. The failure to recognize brain cancer as a disease of energy metabolism has contributed in large part to the failure in management. As long as brain tumor cells have access to ...

Abstract	Malignant brain cancer persists as a major disease of morbidity and mortality. The failure to recognize brain cancer as a disease of energy metabolism has contributed in large part to the failure in management. As long as brain tumor cells have access to glucose and glutamine, the disease will progress. The current standard of care provides brain tumors with access to glucose and glutamine. The high fat low carbohydrate ketogenic diet (KD) will target glucose availability and possibly that of glutamine when administered in carefully restricted amounts to reduce total caloric intake and circulating levels of glucose. The restricted KD (RKD) targets major signaling pathways associated with glucose and glutamine metabolism including the IGF-1/PI3K/Akt/Hif pathway. The RKD is anti-angiogenic, anti-invasive, anti-inflammatory, and pro-apoptotic when evaluated in mice with malignant brain cancer. The therapeutic efficacy of the restricted KD can be enhanced when combined with drugs that also target glucose and glutamine. Therapeutic efficacy of the RKD was also seen against malignant gliomas in human case reports. Hence, the RKD can be an effective non-toxic therapeutic option to the current standard of care for inhibiting the growth and invasive properties of malignant brain cancer.
MeSH term(s)	Animals ; Brain Neoplasms/diet therapy ; Caloric Restriction ; Diet, Ketogenic ; Energy Metabolism/drug effects ; Glioblastoma/diet therapy ; Glucose/metabolism ; Humans
Chemical Substances	Glucose (IY9XDZ35W2)
Language	English
Publishing date	2012-07
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632939-1
ISSN	1872-6844 ; 0920-1211
ISSN (online)	1872-6844
ISSN	0920-1211
DOI	10.1016/j.eplepsyres.2011.06.017
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