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At least 163 records · Page 9Linked to original sources
PubMed2006

Imaging steps of lymphatic metastasis reveals that vascular endothelial growth factor-C increases metastasis by increasing delivery of cancer cells to lymph nodes: therapeutic implications.

Preclinical and clinical studies positively correlate the expression of vascular endothelial growth factor (VEGF)-C in tumors and the incidence of lymph node metastases. However, how VEGF-C regulates individual steps in the transport of tumor cells from the primary tumor to the draining lymph nodes is poorly understood. Here, we image and quantify these steps in tumors growing in the tip of the mouse ear using intravital microscopy of the draining lymphatic vessels and lymph node, which receives spontaneously shed tumor cells. We show that VEGF-C overexpression in cancer cells induces hyperplasia in peritumor lymphatic vessels and increases the volumetric flow rate in lymphatics at the base of the ear by 40%. The increases in lymph flow rate and peritumor lymphatic surface area enhance the rate of tumor cell delivery to lymph nodes, leading to a 200-fold increase in cancer cell accumulation in the lymph node and a 4-fold increase in lymph node metastasis. In our model, VEGF-C overexpression does not confer any survival or growth advantage on cancer cells. We also show that an anti-VEGF receptor (VEGFR)-3 antibody reduces both lymphatic hyperplasia and the delivery of tumor cells to the draining lymph node, leading to a reduction in lymph node metastasis. However, this treatment is unable to prevent the growth of tumor cells already seeded in lymph nodes. Collectively, our results indicate that VEGF-C facilitates lymphatic metastasis by increasing the delivery of cancer cells to lymph nodes and therapies directed against VEGF-C/VEGFR-3 signaling target the initial steps of lymphatic metastasis.

Animals↗
PubMed1984

Natural cytotoxicity in lymphatic metastasis. I. In vitro studies using the rat tumor BSp73 and its variants.

Serial transplantation of primary BSp73 ascites cells to a subcutaneous (SC) site gave rise to the appearance of two solid variants differing in their capacity to metastasize via the lymphatics. Tissue cultures derived from variant AS (nonmetastasizing) showed epithelioid morphology, while cultures derived from variant ASML (metastatic) showed spherical morphology. Upon cloning, both variants proved to be operationally homogeneous. Susceptibility of cultured BSp73 cells to NK and macrophage-mediated cytotoxicity was closely correlated to morphology, inasmuch as epithelioid cells were susceptible, while spherical cells were resistant, to lysis. With stimulated effector cells a general increase in cytotoxicity was observed, but epithelioid cells still showed a higher susceptibility level. Resistance of ASML-type cells to natural cytotoxicity was not due to the lack of recognition structures or to a general increase in the mechanical stability of spherical cells. This was concluded from cold target inhibition and from hypotonic shock treatment experiments, respectively.

Animals↗
PubMed1976

An experimental model for lymphatic metastasis in rats.

An experimental model was described for inducing spontaneous lymph node metastasis, in which tumor cells of the rat ascites hepatoma AH-109A were transplanted into the subcutaneous tissue of the penis, which is rich of lymph plexus. Growth of tumor at the site of transplantation was measured serially and metastasis was recognized by palpation in the inguinal lymph nodes initially, and then in the axillary and lumbar nodes. When animals were sacrificed 12 days after transplantation, these lymph nodes were weighed and high percentage of metastasis was confirmed by histological examination. As an experimental model of lymph node metastasis, the usefulness of this method was discussed.

Animals↗
PubMed2001

[PET studies of recurrent rectal carcinoma. Fundamental aspects of lymphatic metastasis of visceral and somatic carcinomas].

We have shown previously that the bodies of vertebrates are made of a somatic and a visceral component, separated by thin fascial sheets (Chirurg 66: 1230). We postulated that advanced visceral cancers are confined in their pattern of lymphatic spread to one or a few distinct metastatic pathways. In this they are fundamentally different from somatic cancers. To investigate this hypothesis in vivo, we evaluated positive lymph nodes (LNs) on PET scan series of 58 consecutive patients with rectum cancers (RC) compared to breast cancers (BC). We conclude that in RC, a visceral cancer spreads mostly along only one caudocranial pathway (regional, para-aortic, mediastinal, supraclavicular LNs) and never affects somatic LNs. In contrast, BC and urogenital carcinomas, as somatic cancers spread to regional somatic LNs, but do not affect visceral LNs.

Breast Neoplasms↗