JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. Ecological Society of America is collaborating with JSTOR to digitize, preserve and extend access to Ecology.Abstract. In western parts of its native range, the small Indian mongoose (Herpestes javanicus) is sympatric with one or both of two slightly larger congeners. In the eastern part of its range, these species are absent. The small Indian mongoose was introduced, about a century ago, to the West Indies, the Hawaiian islands, Mauritius, the Fijian islands, and Okinawa. All introductions except possibly that to Mauritius were from the region of Calcutta and Bangladesh, where it is sympatric with both congeners. No other mongoose is present on any of these islands. In each instance, the introduced population derived from a small propagule. We examined size variation in the maximum diameter of the upper canine tooth (the prey-killing organ) and skull length. In the eastern (allopatric) part of its native range, males of the small Indian mongoose are much larger in both traits than in the western (sympatric) regions, approaching the size of the smaller of its absent two congeners, Herpestes edwardsii. Females from the allopatric part of the range are also larger than those of the source region. The species is more sexually dimorphic in the region of allopatry. On all islands to which it has been introduced, in 100-200 generations the small Indian mongoose has increased in male size and in sexual dimorphism; changes in female size have been slight and inconsistent. In general, sizes of island individuals are approximately intermediate in size between those in the region of origin (where they are sympatric and small) and those in the region of allopatry. Sexual dimorphism is greatest for canine diameter. Thus, H. javanicus shows variation consistent with ecological release from competition with its congeners. There is no evidence on whether this variation is genetic, nor on what dietary items might be partitioned between species and between sexes. However, morphological variation is consistently smaller for both traits and both sexes on the islands of introduction than in any part of the native range, consistent with idea of a genetic bottleneck imposed by the small propagule size. Neither of the two congeneric mongooses shows morphological variation consistent with ecological release from competition with H. javanicus in the southern part of their ranges, where the latter species is absent.

In western parts of its native range, the small Indian mongoose (Herpestes javanicus) is sympatric with one or both of two slightly larger congeners. In the eastern part of its range, these species are absent. The small Indian mongoose was introduced, about a century ago, to the West Indies, the Hawaiian islands, Mauritius, the Fijian islands, and Okinawa. All introductions except possibly that to Mauritius were from the region of Calcutta and Bangladesh, where it is sympatric with both congeners. No other mongoose is present on any of these islands. In each instance, the introduced population derived from a small propagule. We examined size variation in the maximum diameter of the upper canine tooth (the prey‐killing organ) and skull length. In the eastern (allopatric) part of its native range, males of the small Indian mongoose are much larger in both traits than in the western (sympatric) regions, approaching the size of the smaller of its absent two congeners, Herpestes edwardsii. Females from the allopatric part of the range are also larger than those of the source region. The species is more sexually dimorphic in the region of allopatry. On all islands to which it has been introduced, in 100–200 generations the small Indian mongoose has increased in male size and in sexual dimorphism; changes in female size have been slight and inconsistent. In general, sizes of island individuals are approximately intermediate in size between those in the region of origin (where they are sympatric and small) and those in the region of allopatry. Sexual dimorphism is greatest for canine diameter. Thus, H. javanicus shows variation consistent with ecological release from competition with its congeners. There is no evidence on whether this variation is genetic, nor on what dietary items might be partitioned between species and between sexes. However, morphological variation is consistently smaller for both traits and both sexes on the islands of introduction than in any part of the native range, consistent with idea of a genetic bottleneck imposed by the small propagule size. Neither of the two congeneric mongooses shows morphological variation consistent with ecological release from competition with H. javanicus in the southern part of their ranges, where the latter species is absent.

Background: We have previously described an alternative invasion-independent pathway of cancer metastasis in a murine mammary tumor model. This pathway is initiated by intravasation of tumor nests enveloped by endothelial cells of sinusoidal vasculature within the tumor. In this study, we examined whether evidence for the invasion-independent pathway of metastasis is present in human cancers.

An invasion-independent pathway has been proposed as a novel mechanism in blood-borne metastasis, where tumour cells enveloped by sinusoidal tumour vessels enter the circulation without vascular invasion. We previously identified the secretory leukocyte protease inhibitor (SLPI) as a candidate gene responsible for this pathway. In this study, the functional role of SLPI in metastatic dissemination was investigated. We transfected the SLPI gene into a poorly metastatic clone of the MCH66 mouse mammary tumour cell line. Over-expression of SLPI promoted in vivo growth and spontaneous metastasis to the lung, whereas it suppressed invasive activity in vitro. The inoculated tumours of SLPI-transfectants exclusively induced a sinusoidal vasculature and subsequently produced endothelial-coated tumour emboli, which are morphological indices of the invasion-independent pathway. In addition, exogenous SLPI inhibited the migration activity through Matrigel of both tumour cells and human umbilical vein endothelial cells (HUVECs). In vivo angiogenesis assays also demonstrated that SLPI suppressed the migration of newly formed blood vessels. These results suggest that an anti-migratory effect of SLPI on tumour-associated endothelial cells may induce vascular remodelling to form a sinusoidal architecture, and consequently promote invasion-independent metastasis. This study provides a new model for metastasis, based on the mechanism regulated by anti-invasive factors, such as SLPI.

Hepatocellular carcinoma (HCC) has a tendency for intravascular dissemination leading to a poor prognosis. The importance of the sinusoidal structure of the tumor vasculature in HCC has been implicated in the metastasis formation. To clarify the role of tumor angiogenesis in HCC metastasis, we morphologically investigated the interaction of HCC cells with blood vessels during the sequential process of metastasis. Autopsy specimens of 80 patients with HCC were examined with immunohistochemistry using a specific antibody against CD31, a marker for endothelial cells. The most frequent sites of metastasis were the liver (82.5%) and lung (43.8%). In most cases, the metastatic process was initiated by vascular involvement where tumor nests surrounded by sinusoidal vessels extend into the portal and hepatic veins. Subsequently, these endothelial-coated tumor emboli enter the circulation, embolize at distant organs, proliferate within the blood vessel and ultimately form metastatic foci. These steps are indicative of an invasion-independent pathway. Our findings in animal models and now in human cases suggest that sinusoidal angiogenesis may represent a novel target for therapeutic strategies to limit HCC metastasis. In combination with primary tumor treatment, perturbation of tumor emboli may reduce dissemination of disease.