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Manfred Schmitt

Publications and source records attributed to Manfred Schmitt.

At least 37 records · Page 2Linked to original sources
PubMed2005

A meta-analysis on the correlation between the implicit association test and explicit self-report measures.

Theoretically, low correlations between implicit and explicit measures can be due to (a) motivational biases in explicit self reports, (b) lack of introspective access to implicitly assessed representations, (c) factors influencing the retrieval of information from memory, (d) method-related characteristics of the two measures, or (e) complete independence of the underlying constructs. The present study addressed these questions from a meta-analytic perspective, investigating the correlation between the Implicit Association Test (IAT) and explicit self-report measures. Based on a sample of 126 studies, the mean effect size was .24, with approximately half of the variability across correlations attributable to moderator variables. Correlations systematically increased as a function of (a) increasing spontaneity of self-reports and (b) increasing conceptual correspondence between measures. These results suggest that implicit and explicit measures are generally related but that higher order inferences and lack of conceptual correspondence can reduce the influence of automatic associations on explicit self-reports.

Association↗
PubMed2005

Effect of high hydrostatic pressure on biological properties of extracellular bone matrix proteins.

In orthopedic surgery, sterilization of bone used for reconstruction of osteoarticular defects caused by malignant tumors is carried out in various ways. At present, to devitalize tumor-bearing osteochondral segments, extracorporal irradiation or autoclaving is mainly used but both methods have substantial disadvantages, for instance, loss of biomechanical and biological integrity of the bone. In particular, after reimplantation, integration of the implant at the autograft-host junction is often impaired due to alteration of osteoinductivity as a result of its irradiation or autoclaving. As an alternative approach, high hydrostatic pressure (HHP) treatment of bone is suggested, a new technology which is in the preclinical testing stage, with the aim to inactivate tumor cells but leaving the biomechanical properties of bone, cartilage, and tendons intact. We investigated the influence of HHP on the major extracellular matrix (ECM) proteins, fibronectin (FN), vitronectin (VN), and type I collagen (Col-I), present in bone tissue, which are accountable for the biological properties within the bone. FN, VN, and Col-I were subjected to HHP < or = 600 MPa prior to coating of cell culture plates with these matrix proteins. Thereafter, the capacity of HHP-pretreated FN, VN, and Col-I to affect cell proliferation, cell adherence, and spreading of human primary osteoblast-like cells and the human osteosarcoma cell line Saos-2, was tested. Interestingly, even at HHP < or = 600 MPa, all three ECM proteins retained their biological properties because no significant changes were observed between HHP-treated and non-treated FN, VN, and Col-I regarding their biological properties to affect cell adherence, spreading, and proliferation. These data encourage further exploration of the potential of HHP to sterilize tumor-affected bone segments prior to reimplantation. While during this treatment eukaryotic cells including tumor cells will be irreversibly impaired, the bone's biomechanical properties and the biological properties of the ECM proteins FN, VN, and Col-I, respectively, are preserved.

Bone Matrix↗
PubMed2005

Ex vivo detection of apoptotic trophoblast cells applying flow cytofluorometry and immunocytochemistry using M30 antibody directed to the cytokeratin 18 neo-epitope.

Apoptosis of placental trophoblast cells has become the subject of intensive research. Recently, a monoclonal antibody (M30) directed against a neo-epitope of cytokeratin 18, that is formed after cleavage of this cytoskeletal protein by caspases, was shown to be of advantage over other tests for the detection of trophoblast cell apoptosis. In the present study, we describe a method for the enrichment of highly pure villous trophoblast cells based on the proteolytic digestion of placental tissue, density gradient separation of dissected cells, and immunoelimination of contaminating, non-trophoblast cells employing an antibody to the HLA class I antigen. The high purity (94-99%) of the trophoblast cell preparation was shown by antibody staining for cytokeratin 7 and absence of vimentin. Furthermore, we demonstrate that after a simple permeabilization and fixation step with 90% methanol and using the M30 CytoDeath, FITC-conjugated antibody, apoptotic trophoblast cells could be distinguished from non-apoptotic cells by flow cytofluorometry in a highly quantitative and sensitive fashion. Our protocol is an improvement over previously used methods such as immunocytochemistry as it allows to differentiate rapidly between competent and apoptotic trophoblast cells by the quantitative method of flow cytofluorometry.

Antibodies, Monoclonal↗
PubMed2004

Isolation and characterization of Rac1 pseudogenes (psi1Rac1-psi4Rac1) in the human genome.

Ras-related C3 toxin substrate 1 (Rac1) is a small Rho-GTPase with important functions in fundamental cellular processes such as cytoskeleton rearrangements, signal transduction, cell cycle progression and malignant transformation. Using Rac1 primer, we identified a 5.5-kb DNA sequence on chromosome 4 (Chr. 4) in the human genome, containing the intronless protein coding sequence of Rac1. Sequence analysis revealed features of a processed pseudogene, which we named psi1Rac1, that could be detected by Southern blot and polymerase chain reaction (PCR) on genomic DNA. A psi1Rac1 pseudogene transcript was not detected by reverse transcription-polymerase chain reaction (RT-PCR), nor had the psi1Rac1 promoter any transcriptional activity. In addition, three other intronless pseudogenes of Rac1 on chromosomes 4, 13 and X were identified (psi1Rac1-psi4Rac1) sharing an 86-96% sequence similarity with Rac1. Neither RT-PCR with pseudogene specific restriction enzymes, nor the sequencing of 130 cDNA clones from benign and malignant breast tissue and cell lines, detected the transcription of any of the Rac1 pseudogenes (psi2Rac1-psi4Rac1). Existence of Rac1 pseudogenes should be taken into consideration when analyzing genomic alterations of the human Rac1 gene.

Amino Acid Sequence↗
PubMed2004

Urokinase-type plasminogen activator system in breast cancer: association with tamoxifen therapy in recurrent disease.

The prognostic value of components of the urokinase-type plasminogen activator (uPA) system, its receptor uPAR (CD87), and plasminogen activator inhibitors PAI-1 and PAI-2 is well established. We studied the predictive value of these proteolytic factors by evaluating the association of their tumor expression level and the efficacy of tamoxifen therapy in patients with recurrent breast cancer. The antigen levels of the four factors were determined by ELISA in cytosols prepared from estrogen receptor-positive primary breast tumors of 691 hormone-naive breast cancer patients with recurrent disease and treated with tamoxifen as first-line systemic therapy. High tumor levels of uPA (P < 0.001), uPAR (P < 0.01), and PAI-1 (P = 0.01) were associated with a lower efficacy of tamoxifen therapy. In the multivariable analysis, uPA (P < 0.001) provided additional information independent of the traditional predictive factors to predict benefit from tamoxifen therapy. High levels of uPA, uPAR, and PAI-1 predicted a shorter progression-free survival (PFS) on tamoxifen in an analysis of the first 9 months of therapy. However in the analysis during the total follow-up period, high PAI-2 levels (P = 0.01) showed a longer response to tamoxifen. In conclusion, uPA, uPAR, and PAI-1, components of the urokinase system, are predictive for the efficacy of tamoxifen therapy in patients treated for recurrent breast cancer. Knowledge of their tumor expression levels might be helpful for future individualized therapy protocols, including possible new-targeted therapies based on the interference in the urokinase system.

Adult↗
PubMed2004

Biomolecular features of clinical relevance in breast cancer.

Breast cancer is a heterogeneous disease and its consequent complexity is a major challenge for physicians and biologists. Notwithstanding its potential curability due to the availability of treatment modalities which are effective in the presence of favourable clinical or pathobiological features, there is still a great deal of controversy over its clinical management. In recent decades, tumour biomarkers that are indicative of or related to cell traits characterising malignancy--that is self-sufficiency in proliferative growth signals, insensitivity to growth inhibitory signals, evasion of apoptosis, limitless replicative potential, and activation of pathways leading to neo-angiogenesis, invasion and metastasis--have provided information that has been proven to be associated with disease progression. However, when these biomarkers have been analysed individually, their prognostic relevance has been found to be modest, the only remaining clinically useful biomarkers being cell proliferation and plasminogen activation-related factors for prognosis, and steroid hormone receptors and the oncogene HER2/neu for prediction of response to hormonal therapy or to the novel targeted anti-HER2/neu therapy. It therefore remains necessary to reduce the intrinsic complexity of breast cancer in order to improve its clinical outcome. One way to achieve this objective derives directly from the concept that cancer is a genetic disease at the somatic level and from the recent availability of high-throughput post-genomic analytical tools such as gene and protein expression techniques for global gene expression analysis. Following these novel approaches, a number of recent studies have produced gene expression profiles in breast cancer that are markedly associated with disease progression and directed to answer different clinical and biological questions. However, the outcome of these novel studies still needs to be validated, which will entail cooperation between different specialists and integration of all the different skills involved in translational research in oncology.

Biomarkers, Tumor↗
PubMed2004

Human kallikrein 13 protein in ovarian cancer cytosols: a new favorable prognostic marker.

PURPOSE: Human kallikrein 13 (hK13; encoded by the KLK13 gene) is a secreted serine protease expressed in endocrine tissues, including the prostate, testis, breast, and ovary. We have previously reported steroid hormone regulation of the KLK13 gene and its clinical value as a marker of favorable prognosis in breast cancer at the mRNA level. We hypothesized that hK13 may represent a potential biomarker for ovarian carcinomas. PATIENTS AND METHODS: Using a newly developed enzyme-linked immunosorbent assay (ELISA), hK13 levels were quantified in 131 ovarian tumor extracts and correlated with various clinicopathological variables and outcome (progression-free survival [PFS], overall survival [OS]), over a median follow-up period of 42 months. RESULTS: hK13 concentration in ovarian tumor cytosols ranged from 0 to 18.4 ng/mg of total protein. An optimal cutoff value of 0.13 ng/mg (67(th) percentile) was selected, based on the ability of hK13 values to predict the PFS of the study population, to categorize tumors as hK13-positive or negative. Women with hK13-positive tumors most often had early stage (stage I/II) disease, no residual tumor after surgery and optimal debulking success (P <.05). Univariate and multivariate Cox regression analyses revealed that patients with hK13-positive tumors had a significantly longer PFS and OS than hK13-negative patients (P <.05). Kaplan-Meier survival curves further confirmed a reduced risk of relapse and death in women with hK13-positive tumors (P =.007 and P =.002, respectively). CONCLUSION: These results indicate that hK13 is an independent marker of favorable prognosis in ovarian cancer.

Adult↗
PubMed2004

Human kallikrein 11: an indicator of favorable prognosis in ovarian cancer patients.

OBJECTIVES: Human kallikrein 11 (hK11) is a secreted serine protease, highly expressed in hormonally regulated tissues, including the prostate and the ovary. Our preliminary studies indicate that hK11 may represent a diagnostic and prognostic biomarker for ovarian cancer. The aim of the present study was to examine the prognostic value of hK11 expression in ovarian tumors. METHODS: Using our established immunofluorometric assay, hK11 levels were quantified (ng per mg of total protein) in 134 ovarian tumor extracts and correlated with various clinicopathological variables and outcome [progression-free survival (PFS), overall survival (OS)], over a median follow-up period of 42 months. RESULTS: hK11 concentration in ovarian tumor cytosols ranged from 0 to 155 ng/mg of total protein, with a median of 1.45 ng/mg. An optimal cutoff value of 6.3 ng/mg was selected to categorize tumors as hK11-positive or negative. hK11-positive tumors were most often of early stage (Stage I/II) and grade (G1/G2) (P < 0.05). Univariate analysis revealed that patients with hK11-positive tumors had a significantly longer PFS (HR of 0.39, P = 0.005) and OS (HR of 0.44, P = 0.033). Cox multivariate analysis indicated that hK11 was an independent prognostic indicator of PFS (HR of 0.47, P = 0.042). Kaplan-Meier survival curves further confirmed that women with hK11-positive tumors have longer PFS and OS (P = 0.003 and P = 0.028, respectively). Also, a weak positive correlation was found between the expression levels of tissue hK11 and tissue CA125 (rs = 0.508; P < 0.001). CONCLUSIONS: These results further validate our initial findings that hK11 is an independent marker of favorable prognosis in ovarian cancer patients.

Adult↗
PubMed2004

Urokinase-type plasminogen activator (uPA) and its inhibitor PAI-I: novel tumor-derived factors with a high prognostic and predictive impact in breast cancer.

Urokinase-type plasminogen activator (uPA) and its inhibitor, PAI-I, play a key role in tumor invasion and metastasis. They were the first novel tumor biological factors to be validated at the highest level of evidence (LOE I) regarding their clinical utility in breast cancer. Their antigen levels are determined in tumor tissue extracts by standardized, quality-assured immunometric assays (ELISA). Since the late 1980s, numerous independent studies have demonstrated that patients with low levels of uPA and PAI-I in their primary tumor tissue have a significantly better survival than patients with high levels of either factor. These prognostic data have recently been validated by an EORTC (European Organization for Research and Treatment of Cancer) pooled analysis comprising more than 8,000 breast cancer patients. In addition, results from a multicenter prospective randomized therapy trial in node-negative breast cancer ("Chemo N(0)") showed that node-negative breast cancer patients with low levels of uPA and PAI-I in their primary tumor have a very good prognosis, and may thus be candidates for being spared the burden of adjuvant chemotherapy. In contrast, node-negative patients with high uPA/PAI-I are at substantially increased risk of disease recurrence, comparable to that of patients with three or more tumor cell positive axillary lymph nodes. The "Chemo N(0)" trial as well as retrospective data also indicate that these high-risk patients benefit from adjuvant chemotherapy. In conclusion, over a period of about 15 years sufficient evidence has been put forward to demonstrate that determination of uPA and PAI-I in primary breast cancer patients supports risk-adapted individualized therapy decisions, particularily in patients with node-negative disease.

Biomarkers, Tumor↗
PubMed2004

Non-muscle alpha-actinin-4 interacts with plasminogen activator inhibitor type-1 (PAI-1).

PAI-1 modulates many biological processes involving fibrinolysis, cell migration or tissue remodelling. In addition to inhibiting serine proteases (mainly tPA and uPA), PAI-1 interacts with vitronectin (Vn), fibrin or alpha(1)-acid glycoprotein, interactions which are important for PAI-1-mediated effects in inflammation, tumor invasion and metastasis. To further identify proteins interacting with PAI-1, the yeast two-hybrid strategy was employed. Screening of a human placenta cDNA library identified--in addition to the C-terminal region of cytokeratin 18 (CK18(182-430))--a large C-terminal fragment of alpha-actinin-4 (Act-4) as a binding partner for PAI-1. Two different cDNA clones encoding Act-4(287-911) and Act-4(330-911) respectively, were isolated. An Act-4(330-911)/GST-fusion protein, but not GST alone, was immunoprecipitated together with active PAI-1. In solid phase binding assays, active wild-type PAI-1 as well as the PAI-1 variant Q123K (which does not interact with multimeric Vn) was found to bind to Act-4(330-911)/GST. Latent PAI-1, latent Q123K, and the inactive PAI-1 variant Q55P did not display any binding activity. Act-4 is mainly present intracellularly and is involved in cellular motility via interaction with the actin cytoskeleton, thus probably affecting the metastatic potential of tumor cells. However, an extracellular Act-4-derived fragment (mactinin) has previously been identified, which (i) is generated by proteolytic action of uPA, (ii) displays significant chemotactic activity for monocytes, and (iii) promotes monocyte/macrophage maturation. We suggest that PAI-1, via interaction with both Act-4 and uPA, may function as a modulator of this mononuclear phagocyte response, not only in inflammation but also in tumor invasion and metastasis.

Actinin↗
PubMed2004

Effects of objective and subjective account components on forgiving.

The authors explored the effects of the components of a harm-doer's account of her transgression on the victims' emotional reactions to the transgression and to the character traits that she attributes to the harm-doer. Participants were 480 people whom the authors asked to imagine an incident in which they were harmed by the careless behavior of a friend. Subsequently, the authors offered participants an account of the harm-doer. In a 2 x 2 x 2 x 2 x 2 between-subjects design, the authors manipulated 5 account components: Admitting Fault, Admitting Damage, Expressing Remorse, Asking for Pardon, and Offering Compensation. The authors measured the participants' perceptions of these components. Results indicated that (a) the subjective perception of account components occurs schematically so that components are implicitly perceived without being objectively present, (b) objective components affect victims' reactions via subjective perceptions of these components, (c) personality factors (Irreconcilability, Interpersonal Trust, and Trait Anger) affect victims' reactions directly. Finally, certain configurations of account components are more effective than others. Specifically, asking for pardon had an effect on forgiving only when it was combined with an acknowledgment of the damage and a compensation offer. This result suggests that in this situation, the victim perceives a harm-doer's asking for pardon without the other components as an insincere apology.

Adolescent↗
PubMed2004

Urokinase-type plasminogen activator and its inhibitor type 1 predict disease outcome and therapy response in primary breast cancer.

Combined determination of urokinase-type plasminogen activator (uPA) and its inhibitor, activator inhibitor type 1 (PAI-1), supports risk-adapted individualized therapy concepts, particularly in node-negative breast cancer. The prognostic impact of both factors in primary breast cancer was substantiated by a pooled analysis of > 8000 patients with breast cancer and a multicenter prospective randomized therapy trial in node-negative breast cancer; findings achieved the highest level of evidence for tumor biomarkers. Patients with node-negative breast cancer with low antigen levels of uPA and PAI-1 in their primary tumor tissue have a very good prognosis and therefore may be spared the burden of adjuvant chemotherapy, whereas those with elevated uPA/PAI-1 antigen levels carry an increased risk of disease recurrence. Recent retrospective analysis of > 3000 patients indicated that patients with breast cancer with high uPA/PAI-1 values derive a significantly greater benefit from adjuvant chemotherapy than patients with low uPA/PAI-1 levels. Similarly, in the multicenter prospective Chemo N0 trial, administration of cyclophosphamide/methotrexate/5-fluorouracil-based chemotherapy led to a substantial reduction in risk of disease recurrence in patients with high uPA/PAI-1. However, benefit from adjuvant endocrine therapy appears to be independent of a patient's uPA/PAI-1 status. In metastatic breast cancer, retrospective studies showed that elevated uPA or PAI-1 present in the primary tumor tissue are associated with a poor response to later palliative endocrine therapy. These findings suggest that high levels of uPA and/or PAI-1 do reflect an aggressive phenotype that may be overcome or suppressed by early systemic therapy in the adjuvant setting but may be too advanced for response to palliative therapy at a later stage.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2004

Protein expression of MMP-13, uPA, and PAI-1 in pseudocapsular and interface tissue around implants of loose artificial hip joints and in osteoarthritis.

Matrix metalloproteinase 13 (MMP-13), urokinase type plasminogen activator (uPA), and plasminogen activator inhibitor type-1 (PAI-1) have been reported to be involved in aseptic loosening of artificial hip joints. This study for the first time presents the protein levels of all of these factors in synovial-like interfaces between bone and prosthesis and in pseudocapsular tissues surrounding the artificial joint in patients with aseptic loosening (n=17) measured by ELISA. No differences were observed in the antigen expression of MMP-13, uPA, and PAI-1, comparing interface and pseudocapsular tissue. Also, no significant correlation between the protein expression of these factors and years from arthroplasty to revision or to type of fixation (cemented vs. cementless) was observed. As control, MMP-13, uPA, and PAI-1 antigen levels were also determined in the synovium of patients with osteoarthritis (n=10). Yet, the antigen levels of MMP-13, uPA, and PAI-1 in tissue specimens from patients with aseptic loosening of artificial hip joints were significantly higher compared to their expression in synovial capsular tissues obtained from patients with osteoarthritis. In conclusion, this study shows that elevated protein levels of uPA, PAI-1, and MMP-13 in periprosthetic pseudocapsular and interface tissues from patients after total hip replacement due to aseptic loosening seem not to be associated with the patient outcome.

Adult↗
PubMed2004

Effect of extracorporal high hydrostatic pressure on tumor cell adherence and viability.

In orthopedic surgery, reconstruction of bone segments afflicted with cancer is done in various ways, including devitalization of the bone or replacement of the bone by artificial bone constructs. To devitalize bone cells, extracorporal irradiation or autoclaving is used although both methods have substantial disadvantages. We now introduce the technique of extracorporal high hydrostatic pressure (HHP) treatment to disintegrate tumor cells in suspension or in their adherent state. The effect of HHP on cell viability, adherence and morphology of four different tumor cell lines (fibrosarcoma HT-1080, osteosarcoma SAOS-2, ovarian cancer OV-MZ-6, breast cancer MCF-7) was investigated. For this, adherently growing (with fibronectin serving as the growth-promoting substrate) or suspended tumor cells were placed into a test vial which was transferred into the pressure chamber of a high hydrostatic pressure device. After pressure treatment, the pressure was relaxed to atmospheric pressure and subsequently cell viability, adherence and morphology assessed. High hydrostatic pressure as high as 350 MPa (10 min, 37 degrees C) did not detach the tumor cells from the fibronectin-coated surface although at these conditions all of the four cell lines tested were irreversibly damaged. Adherently growing tumor cells were considerably more sensitive to HHP than tumor cells detached from the surface and treated by HHP in suspension. HHP-treated tumor cells showed drastic morphological changes, evident by cell membrane ruffling and bleb formation. At 150 MPa adherently growing or suspended tumor cells are irreversibly damaged by short-term treatment with HHP. In another investigation, we experienced that treatment of freshly excised bones or tendons by HHP has no adverse effect on their stability or biomechanical properties. Therefore, we anticipate that in orthopedic surgery HHP could be used as a new gentle way of treating resected cancer-afflicted bones or tendons to inactivate tumor cells before autologous reimplantation.

Bone and Bones↗
PubMed2004

Identification, validation, and clinical implementation of tumor-associated biomarkers to improve therapy concepts, survival, and quality of life of cancer patients: tasks of the Receptor and Biomarker Group of the European Organization for Research and Treatment of Cancer.

Guiding principles are provided and discussed on how to inform the physician scientist and cancer researcher about quality control systems to enable a consistent assessment of the clinical value of tumor-associated biomarkers. Next to cancer research itself, the Receptor and Biomarker Group of the European Organization for Research and Treatment of Cancer (RBG-EORTC) advises on methodologies, test kits and test reagents utilized for tumor biomarker determination. Tumor-associated biomarkers are important and clinically useful tools which can aid the early diagnosis of cancer, determine prognosis, predict therapy response, and monitor disease. With regard to clinical use of tumor-associated bio-markers, quality assessment and quality assurance programs of the RBG-EORTC are crucially important issues. Test reagents, assays, and procedures for tumor sample collection and handling should be standardized. Furthermore, standard operating procedures (SOPs) should be developed for each type of tumor specimen. Assay formats and the quality of the tumor biomarker assay results have to be monitored by continuous within- and inter-laboratory proficiency testing. With this approach, a major step forward in the knowledge and understanding of the biological role and the clinical utility of tumor-associated biomarkers would be anticipated.

Biomarkers, Tumor↗
PubMed2003

Human kallikrein 5: a potential novel serum biomarker for breast and ovarian cancer.

The kallikrein family is a group of 15 serine protease genes clustered on chromosome 19q13.4. Human kallikrein (hK) gene 5 (KLK5) is a member of this family and encodes for a secreted serine protease (hK5). KLK5 was shown to be differentially expressed at the mRNA level in breast and ovarian cancer. Until now, detection of hK5 protein in either biological fluids or tissues has not been described due to lack of suitable reagents and methods. The aim of this study was to develop immunological reagents and a sensitive and specific fluorometric immunoassay (ELISA) for hK5, to examine the presence of hK5 in human tissues and biological fluids, and to study the possible clinical utility of hK5 as a biomarker for endocrine-related malignancies. Recombinant hK5 protein was produced and purified using a Pichia pastoris yeast expression system. The protein was used as an immunogen to generate mouse and rabbit polyclonal anti-hK5 antibodies. A sandwich-type microplate immunoassay (ELISA) was developed using these antibodies, coupled with a time-resolved fluorometric detection technique. The ELISA assay was then used to measure hK5 in various biological fluids, tissue extracts, and serum samples from normal individuals and patients with various malignancies. The hK5 ELISA immunoassay has a lower detection limit of 0.1 micro g/liter, is specific for hK5, and has no cross-reactivity with other homologous kallikreins. The dynamic range is 0.1-25 micro g/liter, and within-run and between-run coefficients of variation within this range are <10%. hK5 is found in many tissues, with the highest expression levels seen in the skin, breast, salivary gland, and esophagus. hK5 is present at relatively high levels in milk of lactating women. Whereas the levels of hK5 are almost undetectable in serum of normal individuals (male and female) and patients with diverse malignancies, higher concentrations were found in a proportion of patients with ovarian (69%) and breast (49%) cancer. High levels were also detected in ascites fluid from metastatic ovarian cancer patients and in ovarian cancer tissue extracts. In conclusion, we report development of the first immunofluorometric assay for hK5 and describe the distribution of hK5 in biological fluids and tissue extracts. Our preliminary data indicate that hK5 is a potential biomarker in patients with ovarian and breast cancer.

Adult↗