ReviewCancer metastasis reviews1993
Paracrine and autocrine growth mechanisms in tumor metastasis to specific sites with particular emphasis on brain and lung metastasis.
Review in Cancer metastasis reviews, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 132 citations in OpenAlex.
- A Virus-Inspired Inhalable Liponanogel Induces Potent Antitumor Immunity and Regression in Metastatic Lung Tumors.Cancer research · 2024Article
- Multiple endocrine disorders manifested as gynecomastia in a patient with renal pelvis cancer.Clinical case reports · 2022Article
- Bladder cancer metastasis producing beta-human chorionic gonadotropin, squamous cell carcinoma antigen, granulocyte-colony stimulating factor, and parathyroid hormone-related protein.IJU case reports · 2019Article
- CXCR4/CXCR7/CXCL12 axis promotes an invasive phenotype in medullary thyroid carcinoma.British journal of cancer · 2017Article
- Knockdown of ELMO3 Suppresses Growth, Invasion and Metastasis of Colorectal Cancer.International journal of molecular sciences · 2016Article
- The importance of microenvironment: the role of CCL8 in metastasis formation of melanoma.Oncotarget · 2015Article
- Significance of Trask protein interactions in brain metastatic cohorts of lung cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Dynamic Switch Between Two Adhesion Phenotypes in Colorectal Cancer Cells.Cellular and molecular bioengineering · 2014Article
- Association between Gαi2 and ELMO1/Dock180 connects chemokine signalling with Rac activation and metastasis.Nature communications · 2013Article
- Differences in chemosensitivity between primary and paired metastatic lung cancer tissues: In vitro analysis based on the collagen gel droplet embedded culture drug test (CD-DST).Journal of thoracic disease · 2012Article
- Expression and histopathological correlation of CCR9 and CCL25 in ovarian cancer.International journal of oncology · 2011Article
- Metastasis suppressors and the tumor microenvironment.Seminars in cancer biology · 2011Review
- Hypoxia increases the metastatic ability of breast cancer cells via upregulation of CXCR4.BMC cancer · 2010Article
- Clinical and biological significance of CXCR5 expressed by prostate cancer specimens and cell lines.International journal of cancer · 2009Article
- Serum CXCL13 positively correlates with prostatic disease, prostate-specific antigen and mediates prostate cancer cell invasion, integrin clustering and cell adhesion.Cancer letters · 2009Article
- HIV Nef-M1 Effects on Colorectal Cancer Growth in Tumor-induced Spleens and Hepatic Metastasis.Molecular and cellular pharmacology · 2009Article
- Chemokine CCL2/MCP-1 negatively regulates metastasis in a highly bone marrow-metastatic mouse breast cancer model.Clinical & experimental metastasis · 2009Article
- Strong expression of chemokine receptor CXCR4 by renal cell carcinoma cells correlates with metastasis.Clinical & experimental metastasis · 2009Article
- Metastasis: recent discoveries and novel treatment strategies.Lancet (London, England) · 2007Review
- Expression of chemokine receptor CXCR4 in esophageal squamous cell and adenocarcinoma.BMC cancer · 2006Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Once metastatic cells successfully seed at distant sites, their clinical detection and danger to the host are dependent on growth to form gross metastases. Metastatic tumor cells proliferate in response to local paracrine growth factors and inhibitors, and their growth also depends on production and responses to autocrine growth factors. A major organ-derived (paracrine) growth factor from lung tissue-conditioned medium has been isolated that differentially stimulates the growth of cells metastatic to brain or lung. Characterization of this mitogen demonstrated that it is a transferrin or a transferrin-like glycoprotein. Furthermore, antibodies to transferrin can remove significant growth activity from lung tissue-conditioned medium. Cells that are metastatic to brain or lung express greater numbers of transferrin receptors on their surfaces than cells that are poorly metastatic or metastatic to liver. Growth responses of metastatic cells and organ preferences of colonization appear to change during progression to more malignant states. At early stages of metastatic progression there is a tendency for many common malignancies to metastasize and grow preferentially at particular sites, suggesting that paracrine growth mechanisms may dominate the growth signals at this stage of progression. In contrast, at later stages of metastatic progression widespread dissemination to various tissues and organs occurs, and autocrine growth mechanisms may dominate the growth responses of metastatic cells. Ultimately, the progression of malignant cells to completely autonomous (acrine) states can occur, and at this stage of metastatic progression cell growth may be completely independent of autocrine and paracrine growth factors or inhibitors.
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Registered trials
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