Clinicopathological observations on metastasis in man studied in patients treated with peritoneovenous shunts.

Tarin, David; Price, Janet E.; Kettlewell, M. G. W.; Souter, R G; Vass, A; Crossley, Beryl

doi:10.1136/bmj.288.6419.749

Cited by 74 publications

(26 citation statements)

References 9 publications

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“…Some of these sequential steps include invasion through extracellular matrix, intravasation, survival in the circulation, extravasation into a distant site, and progressive growth at that site. Consistent with the multistep nature, there is experimental and clinical evidence to suggest that metastasis is an inefficient process whereby the vast majority of circulating tumor cells are not able to progressively grow at distant sites (3)(4)(5)(6). Related to this is the observation that metastatic cells exhibit tissue tropism, preferring to grow in certain organs in a way that cannot be explained by circulatory patterns alone.…”

Section: Introductionmentioning

confidence: 95%

Distinct organ-specific metastatic potential of individual breast cancer cells and primary tumors

Minn¹,

Kang²,

Serganova³

et al. 2005

J. Clin. Invest.

203

219

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We used bioluminescence imaging to reveal patterns of metastasis formation by human breast cancer cells in immunodeficient mice. Individual cells from a population established in culture from the pleural effusion of a breast cancer patient showed distinct patterns of organ-specific metastasis. Single-cell progenies derived from this population exhibited markedly different abilities to metastasize to the bone, lung, or adrenal medulla, which suggests that metastases to different organs have different requirements. Transcriptomic profiling revealed that these different single-cell progenies similarly express a previously described "poor-prognosis" gene expression signature. Unsupervised classification using the transcriptomic data set supported the hypothesis that organ-specific metastasis by breast cancer cells is controlled by metastasis-specific genes that are separate from a general poor-prognosis gene expression signature. Furthermore, by using a gene expression signature associated with the ability of these cells to metastasize to bone, we were able to distinguish primary breast carcinomas that preferentially metastasized to bone from those that preferentially metastasized elsewhere. These results suggest that the bone-specific metastatic phenotypes and gene expression signature identified in a mouse model may be clinically relevant.

show abstract

Section: Introductionmentioning

confidence: 95%

Distinct organ-specific metastatic potential of individual breast cancer cells and primary tumors

Minn¹,

Kang²,

Serganova³

et al. 2005

J. Clin. Invest.

203

219

View full text Add to dashboard Cite

show abstract

“…As early as 1889, Paget proposed that the growth of metastasis is due to the speci®c interaction of tumor cells with particular organ environments (Paget, 1889). This hypothesis has been supported both experimentally and clinically (Hart et al, 1981;Tarin et al, 1984). Multiple cellular properties are involved in the ability of tumor cells to colonize distant organ.…”

Section: Introductionmentioning

confidence: 89%

Modification of PDGFα receptor expression or function alters the metastatic phenotype of 3LL cells

Fitzer‐Attas

Feigelson

et al. 1997

Oncogene

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Functional PDGFa receptors are selectively expressed on highly lung-metastasizing clones of the 3LL Lewis lung carcinoma, but not on low-mestastatic clones. The highly metastatic clones are also growth induced in vitro by PDGF and lung conditioned medium. To investigate whether modi®cation of PDGFa receptor expression or function can a ect metastatic capability, we transfected cells of a low-metastatic 3LL clone with a full length PDGFa receptor gene and cells of a highly-metastatic clone with a truncated kinase domain PDGFa receptor gene. Introduction of the full length PDGFa receptor conferred upon low-metastatic cells the ability to grow in vitro in the presence of PDGF-AA and to colonize the lung in experimental and spontaneous metastases assays. Conversely, introduction of a truncated version of the PDGFa receptor into highly metastatic cells reduced their metastatic load to control levels. Accordingly, their responses to PDGF-AA, including growth stimulation and receptor autophosphorylation, were reduced. These results demonstrate that PDGFa receptor expression and function can control the capacity of tumor cells to generate metastases in the lung. The response of this receptor to lung-derived PDGF-like factors may de®ne a paracrine mode of metastatic cell growth in the target organ.

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“…Similar findings have being documented in different cancer patients, patients with malignant ascites, breast cancer (Braun et al, 2005, Riethdorf et al, 2008, and liver cancer. In the case of cancer patients with malignant ascites who have implantation of peritoneo as procedure which help alleviate abdominal distention, but also has the unavoidable effect of shunting huge number of tumor cells into systemic circulation, disseminated cancer is a rare event (Campioni et al, 1986, Tarin et al, 1984. A related clinical example is the recognition that viable breast cancer cells have been found in the bone marrow of a large percentage of patients.…”

Section: Evidences That Not All Cancer Cells Are Tumorigenicmentioning

confidence: 99%

The New Model of Carcinogenesis: The Cancer Stem Cell Hypothesis

Loaiza¹,

Rojas²,

Valverde³

2012

Carcinogen

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Clinicopathological observations on metastasis in man studied in patients treated with peritoneovenous shunts.

Cited by 74 publications

References 9 publications

Distinct organ-specific metastatic potential of individual breast cancer cells and primary tumors

Distinct organ-specific metastatic potential of individual breast cancer cells and primary tumors

Modification of PDGFα receptor expression or function alters the metastatic phenotype of 3LL cells

The New Model of Carcinogenesis: The Cancer Stem Cell Hypothesis

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