Biomedical subjects

Minoru Fukuda

Publications and source records attributed to Minoru Fukuda.

At least 19 recordsLinked to original sources

PubMed2006

Inflammatory pseudotumor of the lung: clinicopathological analysis in seven adult patients.

BACKGROUND: As the origin and pathology of inflammatory pseudotumor is not clearly understood, there has recently been some confusion regarding the diagnosis of inflammatory pseudotumor. METHODS: We performed clinicopathological analyses in seven patients with inflammatory pseudotumors of the lung histologically diagnosed after surgical resection. The seven patients, selected from patients admitted to Kawasaki Medical School Hospital between April 1989 and December 2005, consisted of four men and three women (average age, 60.4 years). The detection method was from clinical symptoms in two patients and from health examinations in five patients. RESULTS: Five patients had a solitary nodular shadow on chest radiographs and the other two patients had multiple shadows. Because it was difficult to distinguish pseudotumor from lung cancer by chest computed tomography in the five patients showing a solitary nodular shadow, the final diagnosis was obtained by surgical resection. In the other two patients, with multiple shadows, one of whom had nodular shadows with cavitary lesions, surgical resection was performed to distinguish the pseudotumor from metastatic lung cancer. The histological types according to the criteria of Matsubara were fibrous histiocytic in five patients, organizing pneumonia in one, and lymphoplasmocytic in one. The histological types according to the World Health Organization criteria were compact spindle-cell pattern in six patients and hypocellular fibrous pattern in one. CONCLUSION: Because it is difficult to make a preoperative diagnosis of inflammatory pseudotumor by radiological findings or histological findings using specimens obtained by transbronchial lung biopsy, surgical resection, such as video-assisted thoracic surgery or open lung biopsy, is required to differentiate inflammatory pseudotumors from primary or metastatic lung cancers.

Adult↗

PubMed2006

Significant decrease in alpha1,3-linked fucose in association with increase in 6-sulfated N-acetylglucosamine in peripheral lymph node addressin of FucT-VII-deficient mice exhibiting diminished lymphocyte homing.

Lymphocyte homing is mediated by binding of L-selectin on lymphocytes with L-selectin ligands present on high-endothelial venules (HEV) of peripheral and mesenteric lymph nodes. L-selectin ligands are specific O-linked carbohydrates, 6-sulfo sialyl Lewis X, composed of sialylated, fucosylated, and sulfated glycans. Abrogation of fucosyltransferase-VII (FucT-VII) results in almost complete loss of lymphocyte homing, but structural analysis of carbohydrates has not been carried out on FucT-VII null mice. To determine whether functional losses seen in FucT-VII null mice are caused by structural changes in carbohydrates, we elucidated the carbohydrate structure of GlyCAM-1, a major L-selectin counter-receptor. Our results show that most alpha1,3-fucosylated structures in 6-sulfo sialyl Lewis X are absent and 6-sulfo N-acetyllactosamine is increased in the mutant mice. Surprisingly, the amount of 6'-sulfated galactose (Gal) that bound to Sumbucus nigra agglutinin column was also increased. We found that structures of those oligosaccharides containing 6'-sulfated Gal are almost identical to those synthesized by keratan sulfate sulfotransferase (KSST). We then showed that overexpression of KSST suppresses the expression of sialyl Lewis X on Chinese hamster ovary (CHO) cells engineered to express sialyl Lewis X. Moreover, KSST expression in those cells suppressed lymphocyte rolling compared with mock-transfected CHO cells expressing 6-sulfo sialyl Lewis X. 6'-Sulfo sialyl Lewis X can neither be found in GlyCAM-1 from CHO cells expressing both KSST and FucT-VII nor be found in GlyCAM-1 from HEV of mice. These results combined together suggest that KSST competes with FucT-VII for the same acceptor substrate and downregulates the synthesis of L-selectin ligand by inhibiting alpha1,3-fucosylation.

Acetylglucosamine↗

PubMed2006

Evaluation of serological tests detecting Chlamydophila pneumoniae-specific immunoglobulin M antibody.

OBJECT: To evaluate a newly developed enzyme-linked immunosorbent assay (ELISA) (Hitazyme C. pneumoniae) detecting Chlamydophila pneumoniae-specific immunoglobulin M (IgM) antibody, we compared the assay with culturing, immunoblotting and the microimmunofluorescence (MIF) test. PATIENTS AND METHODS: Two hundred five patients with stable chronic lung diseases without acute respiratory tract infections (ARTIs) and 116 healthy volunteers without ARTIs were enrolled in this study. Nasopharyngeal swab specimens and sera were obtained from all subjects for isolation and serological testing of C. pneumoniae. RESULTS: C. pneumoniae IgM-positive results were observed in 16.5% of patients with stable chronic lung diseases and in 8.6% of asymptomatic healthy subjects. However, there were no positive cases with cell culture, immunoblot or MIF test. In addition, no cases with a significant increase in IgA or IgG antibody titer for the ELISA kit and MIF test between paired sera were observed in the followed-up groups. IgM-positive cases were more frequent among patients with chronic obstructive pulmonary disease (p=0.1566), collagen disease-associated interstitial lung disease (p<0.0001) and cryptogenic organizing pneumonia (p=0.0199) than among the healthy subjects. CONCLUSION: Our results indicate that IgM-positive results with the ELISA kit do not always reflect acute C. pneumoniae infections. Further studies are needed, to determine an appropriate cut-off level and the possible causes of the false-positive results in the ELISA kit, such as other underlying conditions.

Adult↗

PubMed2006

Clinical reevaluation of the QuantiFERON TB-2G test as a diagnostic method for differentiating active tuberculosis from nontuberculous mycobacteriosis.

INTRODUCTION: We reevaluated the usefulness of a whole-blood interferon-gamma enzyme-linked immunosorbent assay (QuantiFERON TB-2G [QFT-TB]; Cellestis) in obtaining a differential diagnosis between active tuberculosis (TB) and nontuberculous mycobacteriosis (NTM). METHODS: The subjects were 50 healthy volunteers, 50 patients with active TB, and 100 patients with NTM who satisfied the diagnostic guidelines of the American Thoracic Society from April 2005 through June 2006. The tuberculin skin test (TST) and the QFT-TB test were performed for all subjects. The QFT-TB test was performed every 2 months. RESULTS: Of the healthy volunteers, 64% had a negative TST result and 94% had a negative QFT-TB test result. Of the patients with active TB, 64% had a positive TST result and 4% had a negative QFT-TB test result. Of the patients with pulmonary Mycobacterium avium complex disease, 60% had a positive TST result and 7% had a positive QFT-TB test result. The QFT-TB test had a mean sensitivity of 86% and a mean specificity of 94%. The QFT-TB test results for patients with active TB transiently decreased during treatment involving antituberculous drugs. The rate of positive QFT-TB test results was 86% at the initiation of treatment, 48% 6 months later, and 33% 12 months later. CONCLUSIONS: We confirmed that the QFT-TB test is a useful diagnostic method for differentiating active pulmonary TB from NTM, compared with the TST. However, because it is possible that the effect of the QFT-TB test may be long lasting after treatment and may not be resolved over time, even with treatment, as in this study, it may not provide any level of certainty regarding cure of infection.

Adult↗

PubMed2006

A distinctive set of genes is upregulated during the inflammation-carcinoma sequence in mouse stomach infected by Helicobacter felis.

Helicobacter pylori infects over half the population worldwide and is a leading cause of chronic gastritis and gastric cancer. However, the mechanism by which this organism induces inflammation and carcinogenesis is not fully understood. In the present study we used insulin-gastrin (INS-GAS) transgenic mice that fully develop gastric adenocarcinoma after infection of H. pylori-related Helicobacter felis. Histological examination revealed that more than half of those mice developed invasive adenocarcinoma after 8 months of infection. These carcinomas were stained by NCC-ST-439 and HECA-452 that recognize 6-sulfated and non-sulfated sialyl Lewis X. Lymphocytic infiltration predominantly to submucosa was observed in most H. felis-infected mice, and this was associated with the formation of peripheral lymph node addressin (PNAd) on high endothelial venule (HEV)-like vessels detected by MECA-79. Time-course analysis of gene expression by using gene microarray revealed upregulation of several inflammation-associated genes including chemokines, adhesion molecules, surfactant protein D (SP-D), and CD74 in the infected stomach. Immunohistochemical analysis demonstrated that SP-D is expressed in hyperplasia and adenocarcinoma whereas CD74 is expressed in adenocarcinoma in situ and invasive carcinoma. These results as a whole indicate that H. felis induces HEV-like vessels and inflammation-associated chemokines and chemokine receptors, followed by adenocarcinoma formation.

Adenocarcinoma↗

PubMed2006

Galectin-1 binds different CD43 glycoforms to cluster CD43 and regulate T cell death.

Galectin-1 kills immature thymocytes and activated peripheral T cells by binding to glycans on T cell glycoproteins including CD7, CD45, and CD43. Although roles for CD7 and CD45 in regulating galectin-1-induced death have been described, the requirement for CD43 remains unknown. We describe a novel role for CD43 in galectin-1-induced death, and the effects of O-glycan modification on galectin-1 binding to CD43. Loss of CD43 expression reduced galectin-1 death of murine thymocytes and human T lymphoblastoid cells, indicating that CD43 is required for maximal T cell susceptibility to galectin-1. CD43, which is heavily O-glycosylated, contributes a significant fraction of galectin-1 binding sites on T cells, as T cells lacking CD43 bound approximately 50% less galectin-1 than T cells expressing CD43. Although core 2 modification of O-glycans on other glycoprotein receptors is critical for galectin-1-induced cross-linking and T cell death, galectin-1 bound to CD43 fusion proteins modified with either unbranched core 1 or branched core 2 O-glycans and expression of core 2 O-glycans did not enhance galectin-1 binding to CD43 on T cells. Moreover, galectin-1 binding clustered CD43 modified with either core 1 or core 2 O-glycans on the T cell surface. Thus, CD43 bearing either core 1 or core 2 O-glycans can positively regulate T cell susceptibility to galectin-1, identifying a novel function for CD43 in controlling cell death. In addition, these studies demonstrate that different T cell glycoproteins on the same cell have distinct requirements for glycan modifications that allow recognition and cross-linking by galectin-1.

Animals↗

PubMed2006

Expression cloning of cholesterol alpha-glucosyltransferase, a unique enzyme that can be inhibited by natural antibiotic gastric mucin O-glycans, from Helicobacter pylori.

Helicobacter pylori infects over half the world's population, but only 3% of those infected develop peptic ulcer, gastric cancer, and mucosa-associated lymphoid tissue (MALT) lymphoma. In H. pylori, alpha-glucosyl cholesterol constitutes more than 25% of cell wall lipids, and it has been suggested that alpha-glucosyl cholesterol is essential for H. pylori viability. Here, we identified cholesterol alpha-glucosyltransferase (CHLalphaGcT) using an expression cloning strategy and showed that this enzyme is distinctively inhibited by mucin-type O-glycans similar to those present in deeper portions of the gastric mucosa. Moreover, inactivation of CHLalphaGcT by homologous recombination led to H. pylori lethality. These results indicate that H. pylori CHLalphaGcT is a unique enzyme targeted by a natural antibiotic mucin and constitutes an excellent therapeutic target to prevent H. pylori-induced peptic ulcer, gastric carcinoma, and MALT lymphoma.

Amino Acid Sequence↗

PubMed2006

Haploinsufficiency of C2GnT-I glycosyltransferase renders T lymphoma cells resistant to cell death.

Neoplastic T cells in mycosis fungoides (MF) are resistant to apoptotic agents, including galectin-1 that is abundant in skin. Although MF cells are typically CD7-, and thus galectin-1 resistant, CD7+ HH cells, derived from a patient with MF, were also resistant to galectin-1. HH cells demonstrate altered cell surface glycosylation, with loss of core 2 O-glycan ligands for galectin-1 created by core 2 beta1,6-N-acetylglucosaminyltransferase (C2GnT-I). Loss of core 2 O-glycans on tumor cells was also seen in primary CD7+ MF lesions. Surprisingly, HH cells are heterozygous for a C2GnT-I point mutation, yet this mutation resulted in a dramatic reduction in cellular glycosyltransferase activity. Expression of wild-type C2GnT-I in human HH cells, or murine lymphoma cells that lack C2GnT-I, restored core 2 O-glycan expression and susceptibility to galectin-1, whereas mutant enzyme lacked activity and did not restore core 2 O-glycan expression or susceptibility to galectin-1. Mutant enzyme did not have a dominant negative effect by affecting dimerization or activity of wild-type enzyme; rather, C2GnT-I haploinsufficiency is sufficient for loss of core 2 O-glycan expression and galectin-1 resistance. Thus, glycosyltransferase haploinsufficiency results in altered cellular glycosylation and resistance to cell death, identifying a new survival mechanism for T-lymphoma cells.

Antigens, CD7↗

PubMed2006

Nepmucin, a novel HEV sialomucin, mediates L-selectin-dependent lymphocyte rolling and promotes lymphocyte adhesion under flow.

Lymphocyte trafficking to lymph nodes (LNs) is initiated by the interaction between lymphocyte L-selectin and certain sialomucins, collectively termed peripheral node addressin (PNAd), carrying specific carbohydrates expressed by LN high endothelial venules (HEVs). Here, we identified a novel HEV-associated sialomucin, nepmucin (mucin not expressed in Peyer's patches [PPs]), that is expressed in LN HEVs but not detectable in PP HEVs at the protein level. Unlike conventional sialomucins, nepmucin contains a single V-type immunoglobulin (Ig) domain and a mucin-like domain. Using materials affinity-purified from LN lysates with soluble L-selectin, we found that two higher molecular weight species of nepmucin (75 and 95 kD) were decorated with oligosaccharides that bind L-selectin as well as an HEV-specific MECA-79 monoclonal antibody. Electron microscopic analysis showed that nepmucin accumulates in the extended luminal microvillus processes of LN HEVs. Upon appropriate glycosylation, nepmucin supported lymphocyte rolling via its mucin-like domain under physiological flow conditions. Furthermore, unlike most other sialomucins, nepmucin bound lymphocytes via its Ig domain, apparently independently of lymphocyte function-associated antigen 1 and very late antigen 4, and promoted shear-resistant lymphocyte binding in combination with intercellular adhesion molecule 1. Collectively, these results suggest that nepmucin may serve as a dual-functioning PNAd in LN HEVs, mediating both lymphocyte rolling and binding via different functional domains.

Amino Acid Sequence↗

PubMed2006

Synchronus presentation of early-stage small cell carcinoma and adenocarcinoma in the same lung lobe.

A 73-year-old man with no symptoms was admitted to our hospital with a nodular shadow (>2 cm) in the left upper lung field on chest X-ray. A histological diagnosis (small cell carcinoma) was obtained by bronchoscopic examination including a transbronchial lung biopsy (TBLB). The preoperative clinical staging was T1N0M0 (StageIA). After preoperative chemotherapy (CDDP + CPT11) was carried out, a nodule in the left S(1+2) diminished remarkably, but a smaller nodule in the left S3 (>8 mm) remained unchanged. While the nodule in the left S(1+2) (small cell carcinoma) had become completely necrotic by the time the final diagnosis was made after resection of the left upper lobe, histological diagnosis of the nodule in the left S3 revealed a well differentiated adenocarcinoma. Synchronous presentation of early-stage lung cancer consisting of small cell carcinoma and adenocarcinoma was identified in the same left upper division of the lung. Because there have been the few previous reports regarding cases of synchronous presentation of early-stage lung cancer in the same lung lobe, we also report on the clinical characteristics, thus adding this case to the five previously reported cases.

Adenocarcinoma↗

PubMed2006

BCRP/ABCG2 levels account for the resistance to topoisomerase I inhibitors and reversal effects by gefitinib in non-small cell lung cancer.

PURPOSE: Breast cancer resistance protein (BCRP) confers resistance against topoisomerase I inhibitors in cancer cells. Very recently, we reported that gefitinib reverses BCRP-mediated drug resistance by direct inhibition. However, it remains undetermined how much BCRP contributes to the resistance to topoisomerase I inhibitors in non-small cell lung cancer (NSCLC). The present study was designed to examine whether BCRP levels in NSCLC cells are correlated with the resistance to topoisomerase I inhibitors and the reversal effect by gefitinib. METHODS: BCRP levels and its function were evaluated by Western blotting and flowcytometry, respectively. Gefitinib-insensitive NSCLC cells expressed various levels of BCRP, which were closely correlated not only with the IC50 values of SN-38 (r=0.874, P<0.05) and those of topotecan (r=0.968, P<0.001), but also with the reversal effects of 1 microM gefitinib on SN-38 resistance (r=0.956, P<0.001) and topotecan resistance (r=0.977, P=0.0001). RESULTS: BCRP levels accounted for between 80 and 90% of the variation in the resistance to topoisomerase I inhibitors and the reversal effects by gefitinib. Also, gefitinib increased intracellular topotecan accumulation in proportion to the BCRP levels. CONCLUSIONS: These findings suggest that BCRP is the most important molecule responsible for topoisomerase I inhibitor resistance, and that the development of BCRP inhibitors is an effective approach for overcoming this resistance. In addition, the examination of BCRP levels in NSCLC tissues may identify an optimal patient population for treatment with topoisomerase I inhibitors alone or in combination with BCRP inhibitors.

ATP Binding Cassette Transporter, Subfamily G, Mem↗

PubMed2006

A phase I trial of carboplatin and etoposide for elderly (>or=75 year-old) patients with small-cell lung cancer.

PURPOSE: The combination of carboplatin and etoposide is currently considered the most appropriate regimen for treating elderly patients with small-cell lung cancer (SCLC). Previous reports on elderly patients, 70 years or older, found that the recommended dose was close to that of younger patients. Then, we conducted a phase I study of carboplatin and etoposide in elderly patients, 75 years or older, with SCLC. This study aimed to determine the maximum tolerated dose (MTD) and dose-limiting toxicity (DLT). METHODS: Twenty-six patients fulfilling the eligibility criteria, chemotherapy-naive, performance status (PS) of 0-2, age>or=75, and adequate organ functions were enrolled. Patients' characteristics were: male/female=21/5; PS 0/1/2=9/11/6; median age (range)=78 (75-82); and limited/extensive stage=16/10. The patients intravenously received carboplatin with a target AUC of 4 or 5 mg min/ml (Chatelut formula) on day 1 and etoposide at 80-120 mg/m2 on days 1, 2 and 3. Therapy was repeated four times in every 4 weeks. RESULTS: The MTD of carboplatin/etoposide was AUC=5/80, 4/110, and 4/120. The DLTs were thrombocytopenia, neutropenia, leukopenia, and febrile neutropenia. Overall, grade 4 thrombocytopenia, neutropenia (>or=4 days), leukopenia (>or=4 days), and febrile neutropenia occurred in 27, 20, 7, and 13% of cases at MTD levels, respectively, and 0% at other levels. Twenty of 26 patients showed objective responses (2CR, 18PR; RR=77%). CONCLUSION: A dose of carboplatin of AUC=4 and etoposide of 100 mg/m2 was recommended in this regimen.

Aged↗

PubMed2006

Pulmonary Mycobacterium intracellulare disease with a solitary pulmonary nodule detected at the onset of pneumothorax.

A 61-year-old man with a past history of pulmonary emphysema 6 years earlier was admitted to the emergency department at our hospital because of cough and dyspnea. Left pneumothorax was recognized on a chest radiograph. After his admission to the emergency department, chest drainage was inserted and the left lung was expanded. Afterwards, a nodular shadow (>1.5 cm) was found in the left upper lobe, and differentiation from pulmonary adenocarcinoma was required. As a definite diagnosis could not be made by bronchoscopy, video-assisted thoracoscopic surgery was performed, and a solitary nodule in the left upper lobe was resected. Histologically, a caseating epitheloid granuloma with acid-fast bacilli was found. Regarding the causative pathogen, Mycobacterium intracellulare was identified from the surgically resected specimen. We have reported a peculiar case of pulmonary M. intracellulare disease, detected at the onset of left secondary pneumothorax caused by pulmonary emphysema, which required differentiation from pulmonary adenocarcinoma.

Adenocarcinoma↗

PubMed2006

Assay of human gastric mucin as a natural antibiotic against Helicobacter pylori.

Helicobacter pylori infects more than half of the world's population and is considered a leading cause of peptic ulcer and gastric carcinoma. Although a large number of persons are infected with H. pylori, only a limited number of those infected (approximately 3%) develop peptic ulcers and gastric carcinoma. The progression of the disease is restricted by deeper portion of the gastric mucosa, and in many persons glandular atrophy appears to be prevented by mucins secreted in the deeper portion of the mucosa. Recent studies have shown that this inhibitory activity is at least partly due to the expression of alpha1,4-N-acetylglucosamine residues attached to the mucin (MUC6) in the deeper portion of the mucosa. alpha1,4-N-acetylglucosamine residues inhibit cholesterol alpha-glucosyltransferase, the product of which constitutes a major component of H. pylori cell wall. This inhibitory activity is thus regarded as a natural antibiotic function. This chapter describes the assay for antibiotic activity of MUC6 mucin against H. pylori infection and growth as well as inhibition by alpha1,4-N-acetylglucosamine-capped mucin-type oligosaccharides.

Acetylglucosamine↗

PubMed2006

Expression profiling of glycosyltransferases and related enzymes using in situ hybridization.

In situ hybridization (ISH) is a technique used to detect messenger RNAs (mRNAs) expressed in cells in tissue sections with probes specifically hybridizing to an mRNA of interest. Polysialic acid (PSA) is a unique glycan composed of a linear homopolymer of alpha2,8-linked sialic acid residues and formed by two distinct polysialyltransferases, ST8Sia II and ST8Sia IV. PSA plays an important role in neural development and progression of certain tumors. This chapter describes the use of ISH to detect ST8Sia II and ST8Sia IV mRNAs expressed in human astrocytomas using digoxigenin-labeled RNA probes.

Astrocytoma↗

PubMed2006

Expression of specific carbohydrates by transfection with carbohydrate modifying enzymes.

The identification of cDNAs encoding glycosyltransferases and carbohydrate-modifying enzymes such as sulfotransferases has allowed expression of a given enzyme in cells that lack the enzyme or express it at very low levels. By comparing the function and/or structure of carbohydrates expressed in cells before and after transfection, we can determine the function of the ectopically expressed enzyme. This assay is less time consuming than assaying function by obtaining cells deficient in a given enzyme. Moreover, it is a more definitive method for establishing the function of the enzyme because the result is derived from an enzyme introduced by transfection. Using this method, an enormous amount of knowledge relevant to the structure and function of glycoenzymes has been derived from such studies. In this chapter, we describe methods used to obtain mammalian cells that have acquired new carbohydrate structures and function following transfection of mammalian expression vectors harboring glycoenzymes.

Animals↗

PubMed2006

Roles of mucin-type O-glycans synthesized by core2beta1,6-N-acetylglucosaminyltransferase.

Core 2 branched O-linked oligosaccharides (O-glycans) represent the first example of onco-developmental antigens in mucin-type O-glycans. Core 2 branched O-glycans are expressed in immature T lymphocytes (cortical thymocytes), disappear on mature T lymphocytes (medullary thymocytes) and T lymphocytes in the peripheral blood, and appear again in activated T lymphocytes, leukemic cells, and other cancer cells. Core 2 branched O-linked oligosaccharides are synthesized by Core2beta1,6-N-acetylglucosaminyltransferase (Core2GlcNAcT). The first cloned Core2GlcNAcT-1 has been inactivated in mice through homologous recombination, and mutants show significantly reduced leukocyte rolling on E-, P-, and L-selectin-coated plates. Moreover, mutant mice exhibit an impaired peritoneal inflammatory response associated with reduced neutrophil infusion. By contrast, lymphocyte homing to secondary lymphoid organs is only marginally compromised. These results combined indicate that Core2GlcNAcT-1 plays a major role in leukocyte trafficking and distinguish leukocyte trafficking to inflamed sites from lymphocyte homing to secondary lymphoid organs.

Animals↗

PubMed2006

Cell type-specific roles of carbohydrates in tumor metastasis.

Protein- or lipid-bound glycans have been shown to play important roles in many biological processes; their functional diversity is due primarily to the multiple linkages, branching patterns, and terminal modifications seen in these glycans. Furthermore, one particular glycan may play different roles depending on the biological system. Sialyl Lewis X oligosaccharides, prototypic ligands for E-, L-, and P-selectins, are essential for naive lymphocyte homing to secondary lymphoid organs. They have also been implicated clinically in tumor metastasis and poor prognosis of cancer patients. In this chapter, we describe the protocol for the formation of lung tumor after intravenous injection of B16 melanoma cells. In our study, B16 melanoma cells formed more tumors when the cells were transfected with fucosyltransferase-III to express sialyl Lewis X. In the second experimental protocol, we describe metastatic tumor formation at the draining lymph node after primary tumor was formed at the footpad. In this experimental system, natural killer (NK) cell recruitment to the draining lymph node was found to be critical to suppress tumor metastasis and this tumor suppression is dependent on L-selectin-mediated trafficking of NK cells to the lymph nodes.

Animals↗