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PubMedDate not supplied

Increased invasion and expression of MMP-9 in human colorectal cell lines by a CD44-dependent mechanism.

BACKGROUND: In order to investigate the interactions between MMPs and CD44 we stably transfected a non-invasive colon cell line, SW480 with the cDNA for MMP-9 and investigated the effect on CD44 expression and in vitro invasion and migration. MATERIALS AND METHODS: In vitro invasion and migration assays were carried out using Biocoat matrigel invasion chambers. MMP and CD44 expression was determined using zymography, Western blot analysis and RT-PCR. RESULTS: Transfection of the parental SW480 cells with the cDNA for MMP-9 (SW480M9) caused increased invasion and migration. MMP-9 expression increased when the SW480M9 cells were grown on HA and collagen and cultured in the presence of a CD44-activating antibody. Treatment of the cells with HA and a CD44-activating antibody also resulted in increased invasion, migration and attachment. CONCLUSION: These results demonstrated that CD44 and MMP interactions are important in controlling tumour cell invasion and migration.

Adenocarcinoma↗
PubMed2004

CD44 expression in human meningiomas: an immunohistochemical analysis.

CD44 molecules play an important role in cell adhesion, interaction between cells and extracellular matrix and cellular invasive growth potential. The aim of the study was to evaluate CD44 expression in atypical and benign meningiomas. The tumor specimens were obtained from 61 patients (27 males and 34 females; aged 19 - 78). The analysed material included 10 atypical meningiomas (G2), and following subtypes of benign meningiomas (G1): 21 transitional, 17 meningothelial and 13 fibroplastic. Paraffin tissue sections were immunostained using CD44 antibody (DAKO). The expression of CD44 was multifocal and diffuse. The strong expression was observed in atypical meningiomas, no expression in fibroplastic meningiomas and moderate expression in the other subtypes of benign meningiomas. Statistically significant differences were revealed between the expression of CD44 in G2 and G1 tumors. The results of the study support the thesis on the role of mutated CD44 molecule in the invasive growth potential of neoplastic cells.

Adult↗
PubMed2004

Hyaluronan and CD44: modulators of chondrocyte metabolism.

Stability of cell-matrix interactions promotes tissue homeostasis, and matrix receptors provide for the assembly and retention of matrix as well as the linkage to the signal transduction pathways activated in response to changes within the extracellular matrix. Therefore, changes in cell-matrix interactions may influence cell responses to cytokines and cell survival and may facilitate tissue remodeling. Matrix components sequester or present soluble morphogens to their signaling receptors. Another layer of complexity would be the establishment of new or uncoupling of cell-matrix interactions, leading to altered cellular response to morphogens. The hyaluronan receptor CD44 serves as the critical link for the retention of hyaluronan-proteoglycan aggregates to the chondrocyte cell surface. As we continue to define functional chondrocyte CD44, future studies will need to include analysis of the variant CD44 isoform expression, phosphorylation, cytoskeletal interactions, occupancy, and turnover. Disruption of chondrocyte CD44:hyaluronan interaction will induce a cascade of events resulting in the activation of both catabolic as well as anabolic gene products. Fragments of hyaluronan produced in free radical processes have the potential to augment the production of nitric oxide in a CD44-dependent mechanism. Data also support an emerging paradigm that CD44-mediated signaling affects both chondrocyte survival pathways as well as apoptotic pathways.

Animals↗
PubMedDate not supplied

Paracrine calcitonin in prostate cancer is linked to CD44 variant expression and invasion.

BACKGROUND: Calcitonin (CT) exerts an autocrine/paracrine influence on prostatic tumor invasion through coupling to transduction protein Gsalpha. Cell adhesion glycoprotein CD44 variant v7-v10 also faciliates invasion, but its modulation by the CT-Gsalpha system was unexplored. MATERIALS AND METHODS: LnCaP, PC-3 and metastasis-derived PC-3M cell lines were studied, including cells modified therefrom: Gsalpha-QL, expressing mutant constitutively active Gsalpha protein, and CT+, overexpressing CT. CD44 variant expression was evaluated in vivo after orthotopic implantion into nude mice, and in vitro by real-time RT-PCR and Western blotting. RESULTS: Both mRNA and protein levels of the CD44 variant were minimal in PC-3M tumor implants, but elevated in Gsalpha-QL. Exogenous CT stimulated invasion into Matrigel strongly in LnCaP and CT+, and less in PC-3 and Gsalpha-QL. By Western blot analysis, untreated Gsalpha-QL and CT+ cells overexpressed CD44 variant compared with LnCaP or PC-3. By quantitative RT-PCR, exogenous CT dose-dependently increased CD44 variant mRNA to seven-fold. Pharmacologic agents that stimulated or inhibited Gsalpha activity or stimulated adenylyl cyclase produced proportionate dose-dependent effects on both CD44 variant expression and Matrigel invasion. CONCLUSION: This paracrine factor, acting though cyclic AMP, regulates the expression of CD44v7-10, which modulates the tumor phenotype.

Adenylyl Cyclases↗
PubMed2005

[Regulation of leucocyte adhesion molecule CD11b, CD44 by Qichou decoction in the rats with largely partial nephrectomy].

OBJECTIVE: To study on the regulation of leucocyte adhesion molecule CD11b, CD44 (CD11b, CD44) induced by Qichou decoction in the rats with kidney cut off largely. METHOD: The animal model was established by excising five sixth of kidney bilaterally. The rats were randomly divided into sham-operation group, model group with kidney cut off largely, the group treated by aldehyde oxygen amylum, the group treated with Shenshuaining and groups treated by high, moderate and low doses of Qichou decoction. The animals in the sham-operation group and model group were given with equated physiological brine. The dosages of aldehyde oxygen amylum and Shenshuaining were 0.9 g x kg(-1) and 0.37 g x kg(-1) respectively. The high, moderate and low dosages of Qichou decoction were 53.1, 26.6 g x kg(-1) and 13.3 g x kg(-1) respectively. The contents of leucocyte adhesion molecules including CD11b and CD44 in microserum were labeled by fluorescein and measured by flow Cytometry. Tumor necrosis factor (TNF-alpha)was detected by Dot-ELISA assay. RESULT: The expression of CD11b, CD44 and obviously in the model group as compared with sham-operation group. The weights of left kidney, the ratio of left kidney TNF-alpha was increased weight/body weight. BUN and Scr were also increased obviously. After the treatment with Qichou decoction, the contents of CD11b, CD44, TNF-a, BUN and Scr in the rats with kidney cut off largely were reduced significantly. Similarly, the weight of left kidney and the ratio of the left kidney weight/body weight were also decreased obviously. CONCLUSION: Leucocyte adhesion molecules including CD11b and CD44 in the rats with largely partial nephrectomy were significantly regulated by Qichou decoction. Qichou decoction can prevent immersion of the cells and inflammation, inhibit compensatory glomerular hypertrophy of the rest kidney, prevent the glomerular interstitial fibrosis, and protect the kidney in the rats with kidney cut off largely from further impairment.

Animals↗
PubMed2006

Dynamics of hyaluronan, CD44, and inflammatory cells in the rat kidney after ischemia/reperfusion injury.

Ischemia/reperfusion (I/R) injury in the kidney involves hemodynamic and cellular dysfunctions as well as leukocyte infiltration. Functional recovery occurs via cell proliferation and/or migration. To determine the roles of hyaluronan (HA) and its main receptor CD44 in renal postischemic processes, we compared their localization and expression with that of neutrophils, macrophages, and PCNA-positive (regenerative) cells as characterized by immunohistochemistry, up to 28 days after I/R in uninephrectomized rats. Observations covered all kidney zones, i.e. cortex (C), outer and inner stripes of outer medulla (OSOM, ISOM), and inner medulla (IM). In controls, HA was localized to the interstitium of IM and ISOM, and CD44 was mostly present on the basolateral membranes of collecting ducts in ISOM, the thin descending limb of Henle's loop and macula densa cells. After I/R, HA and CD44 staining appeared in C and OSOM at 12 h and persisted throughout the regenerative period, i.e. until day 7. Thereafter, they regressed but remained associated with remodeling areas. CD44 expression was found de novo on the apical pole of regenerating, not fully differentiated tubular cells and on some interstitial cells. It was prominent on all infiltrating neutrophils, as soon as 2 h post-I/R, and on 30% of the macrophages, including those in late HA-rich inflammatory granulomas. CD44 is probably involved in early leukocyte infiltration, in tubular regeneration, and in macrophage activity, while HA modifies the physico-chemical environment of interstitial and migrating cells. Based on its presence in remodeling areas, the HA-CD44 pair may be implicated in persistent postichemic inflammation as observed in chronic allograft nephropathy.

Animals↗
PubMed1990

Adhesion molecules in the prognosis of diffuse large-cell lymphoma: expression of a lymphocyte homing receptor (CD44), LFA-1 (CD11a/18), and ICAM-1 (CD54).

Adhesive interactions between lymphocyte cell-surface receptors and components of the vascular endothelium and the extracellular matrix play an important role in the control of lymphocyte migration and homing. To investigate whether lymphocyte adhesion molecules involved in the migration of normal lymphocytes, i.e., CD44 homing receptor, LFA-1 (CD11a/18), and ICAM-1 (CD54), also play a role in the spread and hence in the disease course of non-Hodgkin's lymphomas (NHL), expression of these molecules was examined in 78 cases of diffuse large-cell lymphoma. Other potential risk factors considered in this study were sex, age, primary tumor localization, lineage (T cell vs. B cell), and histopathological subtype. 27 of 53 (51%) patients with a lymphoma having a high CD44 antigen expression showed tumor spread beyond stage II at diagnosis while this was the case in only three of 25 (12%) patients with lymphomas that were CD44 low/negative (chi-square 25.4, p less than 0.001). Similarly, poor response to treatment, i.e., absence of remission or relapse, and or death from lymphoma, was more common among patients with lymphomas expressing high levels of CD44; actuarial survival among patients with CD44 high and low lymphomas was 47% and 91%, respectively (Mantel-Cox 6.1, p = 0.02). Neither LFA-1 nor ICAM-1 expression showed a significant correlation to lymphoma dissemination or disease course. Of the other factors considered, T cell phenotype was associated with an unfavorable prognosis while nodal localization was a risk factor for dissemination. Taken together, our findings suggest that CD44 antigen expression plays an important role in the dissemination of NHL and via this mechanism exerts an unfavorable prognostic influence.

Antigens, CD↗
PubMed1990

An antibody that facilitates hematopoietic engraftment recognizes CD44.

Pretreatment of recipients with the monoclonal antibody (MoAb) S5 facilitates engraftment of bone marrow from mismatched, unrelated donors in the canine transplantation model. In the direct comparisons reported here, the S5 glycoprotein (gp) was found to have structural homology to CD44 that in humans has been implicated in adhesive interactions of one type of effector cell, the lymphocyte. The S5 antigen and gp90Hermes-1 exhibited codistribution on canine peripheral blood cells. Both S5 and Hermes-1 (anti-CD44) MoAbs recognized 90-Kd species in radioimmune precipitations of 125I surface-labeled canine peripheral blood lymphocytes and bone marrow cells. Competitive antibody binding experiments showed that the epitope detected by S5 was distinct from that bound by Hermes-1 but overlapped with those defined by two other known anti-CD44 reagents, IM7 and Hutch-1. Sequential immunoprecipitation with S5 and Hermes-1 indicated that the two antibodies recognize the same or overlapping subsets of membrane gps. Tryptic digestion of S5 and anti-CD44 immunoprecipitates generated two major iodinated peptides of 27 and 35 Kd in both cases, a further indication of structural homology. Similarly, after N-glycanase digestion, S5 and CD44 immunoprecipitates were resolved to a single 68-Kd species. These findings suggest that CD44-mediated adhesive events may affect the fate of transplanted hematopoietic cells. The previous implications of this gp in T-lymphocyte activation and lymphocyte adhesion to endothelium thus provide useful paradigms to analyze its function in the bone marrow transplant setting.

Amino Acids↗
PubMed1989

CD44 contributes to T cell activation.

We demonstrate here that the CD44 molecule, which mediates lymphocyte adhesion to high endothelial venules (HEV), is also involved in the delivery of an activation signal to the T cell. We have produced a CD44 mAb (H90) which is able to block the binding of lymphocytes to high endothelial venules. H90 had no effect on [3H]TdR incorporation of whole PBL stimulated by lectins, allogeneic cells, or CD3 mAb in the soluble phase; in contrast, it strongly increased [3H]TdR incorporation of PBL stimulated by CD2 pairs of mAb or by CD3 mAb linked to the plastic culture plates, when purified T cells were used, H90 mAb could efficiently induce them to proliferate after a primary signal of activation delivered via cross-linked CD3 or via CD2, an effect mediated by Il-2 synthesis and Il-2R expression. Thus, the effect of H90 mAb resembles the mitogenic effect of CD28 "9.3" mAb. However, several results show that CD28 and CD44 mediate different signals to the T cells: i) in contrast to CD28 mAb, CD44 mAb cannot complement the signal delivered by a soluble CD3 mAb, lectins, or PMA; ii) CD44 mAb, at the difference of CD28 mAb, cannot induce CD3+ thymocytes to proliferate in conjunction with a first signal provided via cross-linked CD3 or via CD2; iii) F(ab) fragments of H90 were efficient, whereas divalent fragments of CD29 9.3 mAb are required to produce activation signals; and iv) CD44 and CD28 mAb produce a very strong synergistic effect on T cell proliferation. These results fit with previous ones showing that endothelial cells can play the role of accessory cell in T cell activation and that a hierarchy of signaling can be delivered to T cells via CD3 and CD2.

Adjuvants, Immunologic↗
PubMed1994

CD44 mediates hyaluronan binding by human myeloid KG1A and KG1 cells.

Hyaluronan-binding function of the CD44 molecule has not been so far detected in myeloid cells. To study pure populations of primitive myeloid cells, we investigated the hyaluronan-binding function of the CD44 molecule from three myeloid cell lines: KG1a, KG1, and HL60. Both KG1a and KG1 cells express the CD34 antigen characteristic of the hematopoietic stem cells and HL60 cells do not; accordingly, KG1a and KG1 cells are generally considered as the most primitive and HL60 cells as the most mature of these cell lines. Measurement of cell adhesion to hyaluronan-coated surfaces (using 51Cr-labeled cells) and of aggregate formation in hyaluronan-containing solutions, showed that 45% of KG1 cells and 22% to 24% of KG1a spontaneously bind to hyaluronan, whereas HL60 cells do not either spontaneously or after treatment with a phorbol ester. Hyaluronan binding by KG1a and KG1 cells is mediated by CD44, because it is specifically abolished by monoclonal antibodies (MoAbs) to this molecule. The binding might require phosphorylation by protein kinase C and perhaps also by protein kinase A, because it is prevented by staurosporine, which inhibits these enzymes. 12-O-tetradecanoylphorbol-13-acetate (TPA) which activates protein kinase C, rises to 80% the proportion of KG1 and KG1a cells that bind hyaluronan; this activation is dependent on protein synthesis, for it is abrogated by cyclophosphamide, a protein synthesis inhibitor. Binding of TPA-treated cells to hyaluronan is only partly inhibited by MoAb to CD44: this suggests that TPA may induce synthesis of a hyaluronan-binding protein distinct from CD44. Considering the abundance of hyaluronan in human bone marrow, these results suggest that CD44 may be involved in mediating precursor-stroma interaction.

Alkaloids↗
PubMed1994

Role of CD44 in the development of natural killer cells from precursors in long-term cultures of mouse bone marrow.

The role of the adhesion molecule CD44 in the development of NK cells was analyzed in a mouse long-term bone marrow culture system. After 4 wk of culture (day 0), recombinant human IL-2 was added and 13 days later the cells generated were shown to have substantial cytotoxic activity against YAC-1 and to be enriched for NK cells, as assessed for NK-1.1 phenotype by flow cytometric analysis. Physical separation between stroma and precursors partially inhibited proliferation and, consequently, a lower number of cytotoxic cells were produced. Similar results were obtained when an anti-CD44 mAb was added together with IL-2 at day 0. The disruption of hyaluronic acid (HA), one of the ligands of CD44, by hyaluronidase or the competition for the binding of CD44 by soluble HA added with IL-2 on day 0 inhibited both proliferation and development of cytotoxicity to a greater degree than did anti-CD44. These results indicate that interaction of CD44 with HA plays an important role in the development of pre-NK cells into cytotoxic effector cells.

Animals↗
PubMed1995

Adhesion molecules on intermediate TCR cells. I. Unique expression of adhesion molecules, CD44+ L-selectin-, on intermediate TCR cells in the liver and the modulation of their adhesion by hyaluronic acid.

In addition to thymus-derived T cells, it was demonstrated recently that extrathymically differentiated T cells exist in the liver and other immune organs of mice. Since such extrathymic T cells have T-cell receptors (TCR) of intermediate intensity (i.e. intermediate TCR cells) and constitutively express IL-2 receptor beta-chain (IL-2R beta) similar to natural killer (NK) cells, they are easily distinguished from thymus-derived T cells with a TCR-bright+ IL-2R beta- phenotype (i.e. bright TCR cells). In the present study, the expression of adhesion molecules CD44 and L-selectin was compared between these T-cell subsets. Intermediate TCR cells in the liver and other organs were found to be CD44+ L-selectin- and, inversely, bright TCR cells were CD44- L-selectin+. CD3- IL-2R beta+ NK cells were also estimated to be CD44+ L-selectin-. Hyaluronic acid, which is known to adhere to a CD44 ligand, bound to intermediate TCR cells, but not to bright TCR cells. Among many extracellular matrices, hyaluronic acid induced a prominent decrease in the numbers and proportions of intermediate TCR cells and NK cells in the liver from 6 to 24 hr after in vivo administration. The half-life span of injected hyaluronic acid was approximately 7 hr in the plasma. These results suggest that the CD44 molecule, which is uniquely expressed on intermediate TCR cells and NK cells, is eventually associated with their adhesion to the sinusoidal walls in the liver.

Animals↗
PubMed1995

Lymph node (but not spleen) invasion by murine lymphoma is both CD44- and hyaluronate-dependent.

Similar to activated T cells, LB T cell lymphoma expresses the CD44 cell surface Ag. In addition, the vast majority of LB cells also express the beta 2 (CD18) and alpha L (CD11a) chains of LFA-1 integrin. In view of the finding that anti-CD18 mAb blocked spleen, but not lymph node invasion by LB cells inoculated s.c. into BALB/c mice, we tested the ability of anti-CD44 mAb (IM 7.8.1) to block the infiltration of LB cells into the lymph nodes. We found that, as opposed to anti-CD18 mAb, anti-CD44 mAb, as well as its F(ab')2 or Fab fragment, prevented lymph node infiltration but had no effect on spleen invasion. This conclusion was based on histologic examination and [3H]thymidine incorporation into proliferating LB cells invading the lymphoid organs. Histologic analysis further demonstrated that LB cells invade the lymph node via the afferent lymphatics. The surface expression of CD44 molecules on LB cells was enhanced after PMA activation. PMA activation also enabled in vitro binding of the lymphoma to hyaluronic acid (HA), a known ligand of CD44. Because anti-CD44 mAb, its F(ab')2 or Fab fragment, and hyaluronidase blocked this binding, we also tested the ability of the enzyme to inhibit lymph node invasion by LB cells. We established through histologic examination and [3H]thymidine incorporation that hyaluronidase protected the lymph node, but not the spleen, from invasion by the lymphoma.

Animals↗
PubMed1995

Expression of CD44 in human hepatocellular carcinoma cell lines.

CD44 is a glycosylated cell surface adhesion molecule expressed on a diverse range of cells and has several variant forms, some of which are involved in metastasis of cancer cells. Because little is known about CD44 in human hepatocellular carcinoma (HCC), we investigated its expression in tissue specimens from primary lesions (12 cases), in smear specimens from peritoneal effusions (2 cases), and in cell lines (HCC cell lines, KIM-1, KYN-1, KYN-2, KYN-3, HAK-1A, and HAK-1B; combined hepatocholangiocarcinoma cell lines, KMCH-1 and KMCH-2; and bile duct carcinoma cell lines, KMC-1 and KMBC). Immunohistochemical studies using monoclonal antibody recognizing epitope Group 1 of human CD44 molecule showed that HCC cells in all tissue specimens, including the original tumors of one smear specimen and HAK-1A, were negative for CD44; whereas, HCC cells in two-smear specimens, KIM-1, KYN-2, KYN-3, HAK-1A, HAK-1B, KMCH-1, KMC-1, and KMBC, showed positive reactions on the cell membrane. Immunostain-positive cell lines showed a positive cell rate of 51.9% to 99.8% by flow cytometric analysis. Western blotting detected CD44 protein of hemopoietic type in KIM-1, KYN-3, HAK-1A, and HAK-B and epithelial type in KMC-1 and KMBC. Southern blotting of complementary DNA amplified after reverse transcriptase-polymerase chain reaction (RT-PCR) detected hemopoietic type and some variant forms with longer insertion in all cell lines but KMCH-2, whereas hemopoietic type and variants with minor insertion were only detectable in tissue specimens. These findings suggest that HCC cells in ascites and in culture often express CD44, but those in tissue do not at protein level.

Base Sequence↗
PubMedDate not supplied

Expression of CD44 in prostate cancer cells: association with cell proliferation and invasive potential.

High level expression of the cell surface adhesion molecule CD44 standard form and its splice variants, have been causally linked to tumor metastasis. In this study, we investigated the significance of CD44 expression in human prostatic carcinoma cells. Immunocytochemistry showed high level expression of CD44 in cells from a high grade prostate tumor, and two androgen-independent, invasive prostatic carcinoma lines, PC-3 and TSU-Pr1. Normal prostatic epithelial cells and LNCaP, a low metastatic, androgen sensitive cell line, expressed none to a very low level of CD44, although mRNA transcripts were detected in all cell lines. Immunoprecipitation detected two proteins of M(r) approximately 140 kDa and 210 kDa in PC-3, and predominantly the M(r) approximately 95 kDa protein in TSU Pr1, but none in LNCaP. Most importantly, a neutralizing antibody to CD44 inhibited cell proliferation and basement membrane invasive activity, suggesting a definitive role of CD44 in prostate tumor growth and metastasis.

Antibodies, Monoclonal↗
PubMed1995

Are CD44 variant isoforms involved in human tumour progression?

The transmembrane glycoprotein CD44 exists in a variety of isoforms generated by alternative splicing of the pre-mRNA. In a rat metastasis model, certain variant isoforms (containing exon 6v) are causally involved in lung metastasis formation. We have summarized the data obtained to date on the expression of CD44 variant isoforms in human tumour progression. In non-Hodgkin lymphomas, expression of exon 6v containing isoforms is an independent prognostic factor indicating an adverse prognosis. Upregulation of exon 9v containing isoforms in gastric and renal cell carcinomas relates to a poor prognosis of patients. In colorectal carcinomas, CD44-9v isoforms are strongly expressed already in early adenomas; CD44-6v isoforms are upregulated in late adenomas along with ras and TP53 mutations. No expression of variant isoforms has been detectable in neuroblastomas, but significant downregulation of CD44s correlates inversely with tumour progression and N-myc amplification. Only in breast carcinoma has no correlation of CD44 expression with survival or any other prognostic marker been established. Evaluation of CD44 isoform expression by immunohistochemistry in cases of non-Hodgkin lymphoma, gastric, colon and renal cell carcinomas, as well as neuroblastomas, may be a useful diagnostic parameter indicating invasive processes.

Breast Neoplasms↗
PubMed1995

[Expression of CD44 metastatic variant mRNA in colorectal carcinomas and its role in tumor metastasis and invasion].

The expression of CD44 molecules was investigated in colorectal carcinomas by RT-PCR and Southern Blot Analysis. There were significant differences between neoplastic and non-neoplastic colonic mucosa in the expression of CD44 metastatic variant mRNA. The CD44 metastatic variant mRNA was found to be increased in the neoplastic mucosa. However, we could not find metastasis-specific transcript in primary colorectal carcinomas. Our study suggests that the neoplastic transformation of colonic mucosa increases the expression of CD44 molecules, including the variant forms, which modulate the behavior of the tumor cells. The measurement of serum CD44 is useful in the estimation of tumor mass and its regression by treatment. Further investigation is needed to clearly understand the role of CD44 molecules in tumor metastasis and invasion.

Colorectal Neoplasms↗
PubMed1995

[Expression of CD44 in endometrial cancer and metastasis].

We have examined expression of CD44 in 17 normal endometria and 58 endometrial carcinomas by reverse transcription and polymerase chain reaction (RT-PCR) and by immunohistochemistry using antibodies to CD44. CD44 variants were expressed in 13 out of 17 (76.5%) normal endometria, whereas 11 out of 58 (19.0%) endometrial carcinomas. Furthermore, lymph-vascular space involvement of cancer cells was observed to be statistically significant in the CD44 negative group as opposed to the positive group. Immunohistochemical examination revealed that intense staining in normal endometria was seen on the gland cells at the basement membrane side. CD44 may have a role in the function of normal endometrium such as implantation, and CD44 might be related with metastasis of endometrial cancer cells through lymph-vascular space.

Endometrial Neoplasms↗