Immunobiology of Cancer Metastasis

Killion, Jerald J.; Fidler, Isaiah J.

doi:10.1007/978-1-4471-0201-4_13

Cited by 6 publications

(6 citation statements)

References 63 publications

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“…The presence of circulating melanoma cells might not always result in the formation of metastatic melanoma lesions in distant organs. Formation of metastasis requires multiple biological processes, including implantation of cancer cells on the endothelium, production of matrix metalloproteinases for invasion, movement through vessels and angiogenesis for their growth [30]. Thus, it is essential to examine the relationships among the presence of melanoma cells in peripheral blood, the formation of metastatic lesions and the profiles of gene expression of melanoma cells in the blood and metastatic lesions.…”

Section: Discussionmentioning

confidence: 99%

Detection of tyrosinase and tyrosinase-related protein 1 sequences from peripheral blood of melanoma patients using reverse transcription-polymerase chain reaction

Jin

Yamashita

Minamitsuji

et al. 2003

Journal of Dermatological Science

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Section: Discussionmentioning

confidence: 99%

Detection of tyrosinase and tyrosinase-related protein 1 sequences from peripheral blood of melanoma patients using reverse transcription-polymerase chain reaction

Jin

Yamashita

Minamitsuji

et al. 2003

Journal of Dermatological Science

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“…It is well accepted that intratumoral heterogeneity occurs with respect to a variety of biological, biochemical, and immunological properties (30). These properties determine the ability of particular cancer cell subpopulations to emerge from the primary tumor and establish metastatic growth within distant organs (31). Furthermore, resistance to specific treatments can also be innate in some genetic subclones present in polyclonal colorectal carcinomas (23).…”

Section: Discussionmentioning

confidence: 99%

A Personalized Preclinical Model to Evaluate the Metastatic Potential of Patient-Derived Colon Cancer Initiating Cells

Puig

Chicote

Tenbaum

et al. 2013

Clinical Cancer Research

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Purpose: Within the aim of advancing precision oncology, we have generated a collection of patientderived xenografts (PDX) characterized at the molecular level, and a preclinical model of colon cancer metastasis to evaluate drug-response and tumor progression.Experimental Design: We derived cells from 32 primary colorectal carcinomas and eight liver metastases and generated PDX annotated for their clinical data, gene expression, mutational, and histopathological traits. Six models were injected orthotopically into the cecum wall of NOD-SCID mice in order to evaluate metastasis. Three of them were treated with chemotherapy (oxaliplatin) and three with API2 to target AKT activity. Tumor growth and metastasis progression were analyzed by positron emission tomography (PET).Results: Patient-derived cells generated tumor xenografts that recapitulated the same histopathological and genetic features as the original patients' carcinomas. We show an 87.5% tumor take rate that is one of the highest described for implanted cells derived from colorectal cancer patients. Cecal injection generated primary carcinomas and distant metastases. Oxaliplatin treatment prevented metastasis and API2 reduced tumor growth as evaluated by PET.Conclusions: Our improved protocol for cancer cell engraftment has allowed us to build a rapidly expanding collection of colorectal PDX, annotated for their clinical data, gene expression, mutational, and histopathological statuses. We have also established a mouse model for metastatic colon cancer with patient-derived cells in order to monitor tumor growth, metastasis evolution, and response to treatment by PET. Our PDX models could become the best preclinical approach through which to validate new biomarkers or investigate the metastatic potential and drug-response of individual patients.

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“…A principal barrier to destruction of disseminated cancer is the heterogenous nature of cancer, that is, tumors contain subpopulations of cells that are able to subvert host defenses and recruit infiltrating cells that supply needed growth factors and blood supply. 44,45 Mounting lines of evidence also implicate TAMs in the regulation of metastasis. 34 Wyckoff and his coworkers 46 demonstrated a synergistic relationship between breast tumor cells and macrophages in cell migration and suggested a role for TAMs in metastasis.…”

Section: Role Of Tams In Invasion and Metastasismentioning

confidence: 99%

Tumor Versus Tumor-Associated Macrophages: How Hot is the Link?

Guruvayoorappan

2008

Integr Cancer Ther

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One of the functions of macrophages is to provide a defense mechanism against tumor cells. In contrast, tumor-associated macrophages (TAMs), which represent the major inflammatory component of the stroma of many tumors, are associated with tumor progression and metastasis. TAMs, in contrast with normal macrophages, exhibit the M2 phenotype, and thereby exhibit pro-tumoral functions, including angiogenesis and matrix remodeling. This review will discuss the role of TAMs in tumor progression and provide an overview of their significant part in tumor metastasis and angiogenesis.

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Immunobiology of Cancer Metastasis

Cited by 6 publications

References 63 publications

Detection of tyrosinase and tyrosinase-related protein 1 sequences from peripheral blood of melanoma patients using reverse transcription-polymerase chain reaction

Detection of tyrosinase and tyrosinase-related protein 1 sequences from peripheral blood of melanoma patients using reverse transcription-polymerase chain reaction

A Personalized Preclinical Model to Evaluate the Metastatic Potential of Patient-Derived Colon Cancer Initiating Cells

Tumor Versus Tumor-Associated Macrophages: How Hot is the Link?

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