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A 39-year-old man had been treated for rectal cancer 6 years ago by lower anterior resection of the rectum and perioperative radiochemotherapy. Since then follow-up had been unremarkable but now the patient presented with unspecific lower abdominal pain. The cause of the pain was identified as paraneoplastic retroperitoneal fibrosis secondary to metachronous pulmonary metastases of the rectal cancer.

A 39-year-old man had been treated for rectal cancer 6 years ago by lower anterior resection of the rectum and perioperative radiochemotherapy. Since then follow-up had been unremarkable but now the patient presented with unspecific lower abdominal pain. The cause of the pain was identified as paraneoplastic retroperitoneal fibrosis secondary to metachronous pulmonary metastases of the rectal cancer.

Eine angeborene Hiatushernie stellt einen Risikofaktor fur die Ausbildung einer Refluxosophagitis und damit einer Barrett-Schleimhaut dar, die auch nach fruher operativer Korrektur dieses Defekts fortbestehen kann. Auf diesem Boden entwickelte sich bei unserem Patienten ein gering differenziertes Adenokarzinom, das wir im Rahmen einer Osophagusresektion mit Magenschlauchbildung und Lymphadenektomie erfolgreich behandeln konnten.

We report about a 40 year old patient presenting a severe anemia caused by a folate deficiency combined with chronic alcohol abuse and probable liver cirrhosis. Besides pathophysiology and etiology of folate deficiency the correlation of malnutrition and liver cirrhosis (in particular caused by alcohol abuse) is discussed. As a conclusion for clinical practice the necessity of an extensive investigation for causes of an existing anemia, even in cases, which very much seem to be caused by an acute bleeding event, shall be demonstrated. Furthermore this report shows the importance of a consistent nutrition counseling of patients with liver cirrhosis.

Bei lang anhaltender, ausgepragter Stuhlinkontinenz muss immer auch an einen Tumor gedacht werden. Auch wenn beispielsweise rund 90% der Malignome des Analtrakts Karzinome sind, sollte weiter diagnostisch differenziert werden, da die therapeutischen Konsequenzen von Fall zu Fall erheblich voneinander abweichen konnen. In unserem Fall handelt es sich um ein in dieser anatomischen Region sehr seltenes, spezielles Non-Hodgkin-Lymphom, das prognostisch als infaust einzustufen ist.

Leiomyome der Glans penis sind als primare nichtepitheliale Tumoren des Urogenitaltrakts sehr selten und in der Literatur bislang 4mal beschrieben. Es wird uber einen 12 jahrigen Jungen mit eben dieser Lokalisation eines Leiomyoms der Glans penis berichtet. Bei unserem Patienten imponierte eine leicht erhabene gelbliche Induration an der Glans rechts lateral distal des Sulcus coronarius. Symptome wie Schmerzen, Jucken oder eine Blutung wurden nicht berichtet. Eine Probeexzision aus diesem Areal ergab histologisch das Vorliegen eines Leiomyoms in der Subcutis der Glans penis, fur Malignitat ergaben sich aufgrund des Fehlens von Atypien, Mitosen oder Nekrosen keine Anhaltspunkte. Auf eine vollstandige Resektion im Gesunden wurde verzichtet. In keinem der in der Literatur berichteten Falle ist ein Rezidiv oder eine maligne Entartung beschrieben. Unter regelmasigen Kontrollen (klinisch wie sonographisch) zeigt der Tumor eine Regression. Der Patient ist bis heute (18 Monate postoperativ) beschwerdefrei. Wenn auch das Leiomyom dieser Lokalisation sehr selten ist, mus es in die Differentialdiagnose der Weichteiltumore der Glans penis miteinbezogen werden.

We report about a 40 year old patient presenting a severe anemia caused by a folate deficiency combined with chronic alcohol abuse and probable liver cirrhosis. Besides pathophysiology and etiology of folate deficiency the correlation of malnutrition and liver cirrhosis (in particular caused by alcohol abuse) is discussed. As a conclusion for clinical practice the necessity of an extensive investigation for causes of an existing anemia, even in cases, which very much seem to be caused by an acute bleeding event, shall be demonstrated. Furthermore this report shows the importance of a consistent nutrition counseling of patients with liver cirrhosis.

Diabetes mellitus is commonly associated with reproductive neuroendocrinopathy in both humans and animal models for the disease. Diabetes-associated reproductive failure in the male is a result of multilevel dysfunction within the hypothalamo-pituitary-testicular axis. In view of the known effects of diabetes on hypothalamic gonadotropin-releasing hormone (GnRH) and gonadotropins in chemically-induced animal models for diabetes, we examined hypothalamic aminergic activities (important to the regulation of GnRH release), circulating gonadotropin levels and testicular morphology in the infertile, genetically diabetic (C57BL/KsJ-db/db) male mouse. Groups of 2–5 month old (average age: 3.4 months) and 6–11 month old (average age: 8.8 months) diabetic mice were compared with age-matched non-diabetic (C57BL/KsL-+/?) male mice. Diabetic mice in both age groups were markedly obese and hyperglycemic. Hypothalamic serotonin synthesis was inhibited in the preoptic area-anterior hypothalamus (POA-AH) in both 2–5 month old and 6–11 month old diabetic mice as well as in the mediobasal hypothalamus-median eminence (MBH-ME) of 6–11 month old diabetic mice. Catecholamine synthesis (norepinephrine and dopamine) was reduced in the POA-AH of 2–5 month old diabetic mice and in the MBH-ME of 6–11 month old mice. These aminergic changes were associated in 2–5 month old diabetic mice with reduced circulating levels of LH and in 6–11 month old diabetic mice, of both LH and FSH. In 6–11 month old diabetic mice, testes were characterized by a thickened tunica albuginea, numerous Sertoli cells and the near absence of any spermatogenic cells. The epididymis from these diabetic mice was devoid of spermatozoa. In considering the central role played by these hypothalamic amine systems in regulating GnRH release and thus reproductive function, these results suggest, at least in part, an explanation for the infertility associated with the genetically diabetic male mouse.

A 75 year old patient was admitted to hospital due to painless jaundice and fatigue. Patient's history was not remarkable for chronic viral hepatitis, autoimmune hepatitis, hereditary metabolic disorders or a hepatotoxic damage. Laboratory tests revealed significant elevation of the parameters of cholestasis and aminotransferase activity, a significantly elevated titer of both antinuclear (ANA) and antimitochondrial (AMA) antibodies. Abdominal ultrasound and computertomography showed no mechanic cholestasis nor tumorous process but a situs inversus abdominalis of the abdominal parenchymatous organs. Portal and periportal inflammation, consistent with autoimmune hepatitis, was diagnosed histologically after performing laparoscopic liver biopsy. Regarding the significantly elevated cholestatic parameters and the positive AMA-autoantibodies AIH-PBC overlap syndrome was highly probable so medical treatment including both ursodeoxycholic acid and immunosuppressive therapy with corticosteroids and azathioprine was started resulting in a continous downward tendency of liver enzymes and an improvement of the patient's clinical condition. Finding the correct diagnosis and therapy of autoimmune liver disease is not always easy and unproblematic. Regarding its sometimes fatal progression and good response towards medical treatment prompt diagnosis and institution of autoimmune hepatitis--alone or combined as PBC/AIH overlap syndrome--should not be deferred. Laparoscopic liver biopsy should be the method of choice in patients's with situs inversus abdominalis regading the variable anatomy.

The scientific investigation of mummies and skeletons provides considerable data for the reconstruction of the living conditions and diseases of past populations. We describe the data on four completely analyzed tomb complexes from the huge necropolis of Thebes-West in Upper Egypt dating to different time periods. A total of 211 individuals from the so-called "Middle Kingdom" (MK, c. 2050-1750 BC) were compared to 273 individuals from the "New Kingdom" (NK) to "Late Period" (LP, in total 1550-500 BC). The age at death and the sex ratio were comparable between both groups. There was a high rate of early death with a maximum between the 2nd and 3rd decade of life but infant/adolescent burials were comparably rare. This early death is assumed to be due to an elevated prevalence of various infectious diseases. Likewise, a high rate of tuberculosis infections was seen in those individuals regardless of which time period they came from. Metabolic disorders with osseous manifestations, such as scurvy, osteomalacia and chronic anemia (cribra orbitalia, porotic hyperostosis) were found with a high frequency in the MK populations but significantly less in the NK-LP populations. On the other hand signs of trauma were comparably high, and lesions due to degenerative joint and vertebral diseases were significantly higher in LP than in MK or NK individuals suggesting a higher mechanical load in the later populations. Cases of malignant (secondary) bone tumors and various soft tissue/organ diseases indicate that "civilization" disorders were present when the living conditions assured survival into advanced age. In summary, we provide circumstantial evidence that the systematic and concise analysis of mummy and skeletal remains can allow a reconstruction of major aspects of life and disease in historic populations, although a complete reconstruction is not possible.

Glans penis leiomyomas are uncommon as primary nonepithelial tumors of the urogenital tract. Only 4 cases are described until today. We saw an other case of an 12 years old boy with a leiomyoma of the glans penis. Clinically the lesion presented as a yellow induration with no symptoms as pain, pruritus or bleeding. The biopsy revealed histological a leiomyoma in the subcutis of the glans penis with no symptoms of malignancy. Because of suspected functional and cosmetic deficiency a total resection was not performed. None of the cases described in the literature showed in the follow up malignancy or recurrency. 18 months postoperatively our patient is furthermore well and without symptoms. Nevertheless the leiomyoma of that localization is rare, this tumor should be included in the differential diagnosis of the neoplasms of the glans penis.

The molecular mechanisms leading to prostate cancer progression are poorly understood. In particular, those changes which are responsible for androgen-independent growth and metastatic spread in prostate cancer are an issue of current investigations.To gain more insight into these processes, paired microdissected samples from both untreated, locally advanced primary tumors (n = 20) and recurrences (n = 20) after conventional androgen-deprivation therapy (ADT) were analyzed retrospectively for microsatellite instability (MSI) and loss of heterozygosity (LOH) at nine loci on chromosomes 8, 18, and X by polymerase chain reaction. In parallel, 12 prostatic carcinomas treated by radical prostatectomy and nine corresponding lymph-node metastases were analyzed in the same way.The group treated with ADT showed a total of 10 MSI in 7 of the primary tumors (35%): 4 of these (20%) at one locus, and 3 of these (15%) at two loci. In the recurrences, MSI was observed in 4 cases (20%): 3 of these at one locus (15%), and 1 of these (5%) at two loci. LOH was found in 8 cases (40%) before as well as after ADT. In the radically resected carcinomas, MSI could be detected at two chromosomal loci in one of the primary tumors (8%) and in one of the metastases (11%); LOH was found in 2 primaries (16%) and 3 metastases (33%).Although MSI can be found in advanced prostatic carcinomas, it apparently does not play a major role in the progression of prostate cancer regarding androgen-independent growth or lymphogenous spread.

Defects of the respiratory chain are a typical feature of mitochondrial diseases and occur also during normal aging where they have been described in postmitotic tissues. The present study addresses the question of defect expression in the normal and cirrhotic liver. Randomly distributed defects of complex III (ubiquinone-cytochrome-c-oxidoreductase) and of complex IV (cytochrome-c-oxidase) of the respiratory chain have been detected with age-related increasing frequency both in normal and cirrhotic livers. No defects were present for complex II (succinate-dehydrogenase) and complex V (adenosine triphosphate-synthase) and in liver cell carcinomas. Sixty-one of 107 normal livers (57%) showed defects of the respiratory chain. The defects occurred in advanced age (over 50 years) in 87%. In contrast 50 of 64 cirrhotic livers (78%) had defects and approximately 60% occurred after age 50. The defects were caused by a loss of enzyme protein involving both nuclearly and mitochondrially coded subunits. Ninety-four percent of the defects (n = 275) involved complex IV selectively. In 4% selective defects of complex III were found and combined defects of both complexes occurred in only 2%. In situ hybridization and polymerase chain reaction (PCR) studies for the detection of the common deletion (4.977 bp) and of various point mutations of mitochondrial DNA (mtDNA) revealed no consistent molecular genetic abnormalities in microdissected respiratory chain defective liver cell areas. Single point mutations at nt 3243 and/or 5692 were found only in 7 of 18 microdissected probes from 6 patients. The results show that defects of the respiratory chain occur already in normal livers most probably during cell aging and at a higher rate in cirrhosis. The random defect pattern favors a stochastic process, e.g., free radical damage. However, the role of mutations of mtDNA remains to be established.

In this study, photochemotherapy (PCT) was used for adjunct immunosuppression in the first six months after heart transplantation (HTx). Fifteen patients after orthotopic HTx were included in the study; all received standard triple-drug immunosuppression including cyclosporine, azathioprine and glucocorticoids, but no adjunct therapy with mono- or polyclonal antibodies. The patients were divided into three groups: group I served as control with no additional treatment; group II received adjunct treatment with 10 courses of PCT (single-day treatments); and group III received 20 PCT courses since it was given each time on two consecutive days. PCT was started in both groups on day one after HTx; it was applied with a higher frequency in the early postoperative period and thereafter continued at four-week intervals for a total of 6 months. The photopheresis method for PCT included extracorporeal UVA irradiation of mononuclear cells that were treated with the photosensitive drug 8-methoxypsoralen (8-MOP) and subsequently retransfused to the patient. A new liquid form of 8-MOP was added directly to the buffy coat, resulting in reliable and sufficient drug levels in the cell suspension during the irradiation period; problems caused by oral application due to unpredictable variations in gastrointestinal absorption were thus prevented. Analysis of the total numbers of acute rejection episodes (AREs) within the first four weeks after HTx revealed a more impressive decrease by double PCT (group III, 3 AREs) than by single PCT (group II, 5 AREs) in comparison with the control (group I, 6 AREs). Over the total observation time (mean: 9.6 months), however, both PCT schedules reduced the total number of AREs observed in the control group (20 AREs) equally by more than 50% (9 AREs each in groups II and III) (P = 0.007). Furthermore, PCT treated patients had significantly fewer infections (6 infections in each group) than control group patients (15 infections) (P = 0.026); this, however, may be accounted for by the higher number of acute rejections in the control group and consequent increase in unspecific immunosuppression treatment. Our results suggest that PCT is a safe and effective method of adjunct immunosuppression that can be applied early in the postoperative period; it reduces the number of rejection episodes and does not increase the risk of infections.

Polycystic kidney disease (PKD) is a life-threatening disease characterized by focal dilatations or cysts in certain kidney tubules. Changes (i. e. thickening) in the support structure for these tubules, the basement membrane, have been related to the development of the cysts. Analysis of changes in basement membranes of humans with PKD is difficult, however, due to the restricted amount of material available for study. Several genetic and induced animal models, including diphenylamine-treated rats, have been employed to study the effects of PKD on basement membrane synthesis. While all these studies agree that PKD has a significant influence on basement membranes, no clear understanding as to how PKD effects basement membrane composition has emerged. Here, we report our findings of the effect of diphenylamine treatment on the composition of the basement membrane. Our immunohistological studies indicate that bamin, a recently described glycoprotein associated with glomerular basement membranes (Robinson et al., 1989), is not present in the glomerular basement membranes of diphenylaminetreated mice. This finding was confirmed by analysis of the composition of the basement membrane matrix synthesized by EHS tumors grown in control and diphenylamine-treated mice. The possible role of bamin in the pathogenesis of renal cysts is discussed.

11 This additional skeletogenic potential of the cranial neural crest makes it qualitatively different from trunk neural crest and, in some ways, similar to mesodermal tissue. One skeletal derivative of the cranial neural crest is Meckel's cartilage. Meckel's cartilage is a central rod of cartilage that runs the length of the developing mandible.11 ~14 Initially, the mandibular skeleton consists only of Meckel's cartilage, which presumably functions developmentally as a skeletal element. Later, Meckel's cartilage becomes surrounded by six membranous bones.1113 In birds this cartilage persists into adult life,1115 but in mammals it is only a temporary structure that disappears within the body of the mandible.1116 The role of Meckel's cartilage in mammalian mandibular bone formation and even basic information on the migratory patterns and differentiative fates of mammalian neural crest cells are not well understood.

In diabetes, certain basement membranes become thicker yet more porous than normal. To identify possible changes in the basement membrane, we have grown the Engelbreth-Holm-Swarm tumor, a tissue that produces quantities of basement membrane in normal mice and in streptozotocin-treated, insulin-deficient, diabetic mice. The level of laminin, a basement membrane-specific glycoprotein, and the level of total protein were slightly elevated in the diabetic tissue. In contrast, the level of the basement membrane specific heparan sulfate proteoglycan was only 20% of control. The synthesis of this proteoglycan was also reduced in the diabetic animals, while the synthesis of other proteoglycans by tissues such as cartilage was normal. The synthesis of the heparan sulfate proteoglycan in diabetic animals was inversely related to plasma glucose levels showing an abrupt decrease above the normal range of plasma glucose. Insulin restored synthesis to normal but this required doses of insulin that maintained plasma glucose at normal levels for several hours. Since the heparan sulfate proteoglycan in the basement membrane restricts passage of proteins, its absence could account for the increased porosity of basement membrane in diabetes. A compensatory synthesis of other components could lead to their increased deposition and the accumulation of basement membrane in diabetes.

A previously undescribed protein has been isolated and purified from the extracellular matrix of the Engelbreth-Holm-Swarm (EHS) tumor, a murine tumor that synthesizes an extensive matrix composed of basement membrane molecules. Molecular characterization of the molecule determined that it is a glycoprotein with internal disulfide bonds and an isoelectric point of 6.0. Electrophoretic mobility on sodium dodecyl sulfate-polyacrylamide gel electrophoresis indicated that the glycoprotein migrated as a diffuse band with a molecular weight of approximately 72,000-80,000. The amino acid composition was significantly different from known basement membrane components. Polyclonal antibodies that specifically recognize the glycoprotein localized it to the kidney glomerular basement membrane. These antibodies did not cross-react with either known basement membrane components (laminin, type IV collagen, and heparan sulfate proteoglycan), with 70K "culture shock" protein or with components of normal mouse serum (including mouse transferrin, albumin, or alpha-fetoprotein), when analyzed by "Western" immunoblots. Our data indicate that the glycoprotein is synthesized by the EHS tumor cells and is present at relatively high levels in the EHS tumor matrix.

The fibronectin produced by clonal murine-human hybrid cell lines containing various complements of human chromosomes was measured. Human and murine fibronectins were assayed by specific immunoassay, and the production of human fibronectin was correlated with karyology and isozyme markers for specific human chromosomes. The data show a 100% concordance between the expression of human fibronectin and glutathione reductase, a marker for human chromosome 8, indicating that chromosome 8 codes for the fibronectin polypeptide.

We have grown the EHS (Engelbreth-Holm, Swarm) tumor in normal and genetically diabetic mice (db/db) and measured some components of basement membrane produced in the tumor. These studies showed similar amounts of total protein in control and diabetic tissue and similar patterns of proteins on SDS gel electrophoresis of extracts of the tissue. Laminin, a basement membrane specific glycoprotein utilized as an attachment factor by epithelial cells, was present in increased amounts in diabetic tissue. In contrast, the amount of BM-1 (heparan sulfate) proteoglycan was reduced. Less 35S-sulfate was incorporated into this proteoglycan, and the proteoglycan, but not its component glycosaminoglycans, was heterogeneous in size. The data indicate that either the synthesis of proteoglycan was decreased or its degradation was increased in diabetic tissue. Since the heparan sulfate proteoglycan serves to block the passage of anionic macromolecules through the basement membrane, decreased levels could account for the increased porosity of diabetic basement membrane. Compensatory synthesis of the basement membrane components to restore normal permeability could account for the thickened basement membranes observed in diabetes.

Somatic cell hybrids between mouse and human corneal stroma fibroblasts have been used to identify the human chromosome responsible for the synthesis of human corneal type I procollagen. Twenty-six separate hybrid clones and subclones from three separate hybridization events were isolated in hypoxanthine-aminopterin-thymidine (HAT) selection medium and were used to assay for the production of human type I procollagen. Human and mouse chromosomes were identified in each hybrid clone by alkaline Giemsa staining of metaphase chromosomes spread and by isozyme analysis. We have found that human type I procollagen production segregates concordantly with human chromosome 7 and with beta-glucuronidase, another human chromosome 7 marker. The pro-alpha 1 gene and possibly the pro-alpha 2 gene appear to be encoded on human chromosome 7. Because we have previously assigned the gene for human skin type I procollagen to chromosome 17, our present data indicate that separate genes and control mechanisms must exist for skin and corneal type I procollagen.

The glycoprotein laminin appears to function in the attachment of various epithelial cells to basement membranes. We examined whether its putative cell-adhesive activity could be analyzed in a simple, one-component model system--the agglutination of erythrocytes. Laminin is a potent agglutinin of aldehyde-fixed sheep and human erythrocytes, with half-maximal agglutination at 0.8 micrograms/ml in a standard hemagglutination assay. Inhibitors of this hemagglutinating activity include gangliosides and certain charged phospholipids. The spectrum of molecules is similar but not identical to inhibitors of the hemagglutinating activity of the adhesive glycoprotein fibronectin. Laminin is much less biologically active in three other assays for fibronectin biological activity involving cell spreading on tissue culture substrates, attachment of fibroblastic cells to type I collagen, and restoration of normal morphology to transformed fibroblasts. The adhesive glycoproteins laminin and fibronectin therefore differ markedly in biological activities in several specific adhesion assays; however, they resemble one another in binding to heparin, collagen, and cell surfaces and in their agglutinin activity.

The basement membrane is a structure of prime importance for the proper functioning of certain organs such as the lens and the kidney. Its inaccessibility and resistance to extraction, however, make an absolute determination of its composition difficult. The establishment of a cell line that synthesizes authentic basement membrane components in vitro would make basement membrane components more easily obtained, and would provide a controlled situation which could be more easily manipulated. In this report, a Balb/C mouse lens epithelial cell line was investigated. The cells were observed to undergo morphological transformations in vitro depending upon the cell density. As cell-cell contacts became prevalent, stellate cells organized into an epithelioid sheet. Later, elongate cells and lentoid bodies predominated in the culture. Thus, morphologically the cells mimicked the in vivo transition of the lens epithelial cells into lens fiber cells. Furthermore, the collagen(s) synthesized by these cells reacted specifically with affinity purified antibody directed against mouse type IV collagen. These morphological and immunological data lend credence to the concept that this lens epithelial cell line is an authentic replica of the in vivo situation.

In this paper we have examined the growth and differentiation of the embryonal carcinoma cell line, F9, in the defined medium EM-3 at low density. We show that the growth of F9 and their differentiated cells (F9-diff) in EM-3 is strongly density dependent. At low cell densities the growth of both cell types is severely limited and most of the cells do not survive. Although this poses a problem for working with F9 and F9-diff in EM-3, it provides a convenient assay for identifying molecules that support their growth at low density. Using this assay, we have determined that laminin, a newly isolated glycoprotein of basement membranes, significantly improves the growth and short-term survival of both F9 and F9-diff. However, addition of laminin to EM-3 is insufficient to promote the clonal growth of these cell types. Our findings also indicate that laminin promotes the attachment of F9 and F9-diff in defined media. On the basis of our results, we propose an attachment function for laminin during the early stages of mammalian development.

In diabetes, certain basement membranes become thicker yet more porous than normal. To identify possible changes in the basement membrane, we have grown the Engelbreth-Holm-Swarm tumor, a tissue that produces quantities of basement membrane in normal mice and in streptozotocin-treated, insulin-deficient, diabetic mice. The level of laminin, a basement membrane-specific glycoprotein, and the level of total protein were slightly elevated in the diabetic tissue. In contrast, the level of the basement membrane specific heparan sulfate proteoglycan was only 20% of control. The synthesis of this proteoglycan was also reduced in the diabetic animals, while the synthesis of other proteoglycans by tissues such as cartilage was normal. The synthesis of the heparan sulfate proteoglycan in diabetic animals was inversely related to plasma glucose levels showing an abrupt decrease above the normal range of plasma glucose. Insulin restored synthesis to normal but this required doses of insulin that maintained plasma glucose at normal levels for several hours. Since the heparan sulfate proteoglycan in the basement membrane restricts passage of proteins, its absence could account for the increased porosity of basement membrane in diabetes. A compensatory synthesis of other components could lead to their increased deposition and the accumulation of basement membrane in diabetes.

Measurements of the attachment of the PAM 212 line of mouse epithelial cells to various collagen substrates show that these cells adhere preferentially to type IV, basement membrane collagen. Neither serum nor fibronectin stimulated the attachment of these cells (unlike fibroblasts) to type IV collagen. Preincubation of the PAM 212 cells with cycloheximide prevented attachment. Thus these cells do not attach by means of a macromolecule present inserum, but instead synthesize an attachment factor. Extracts of the EHS tumor, which produces an extracellular matrix containing basement membrane components, were tested for their ability to promote attachment to cycloheximide-treated PAM 212 cells. Saline extracts of the tumor stimulated the attachment of the PAM 212 cells to type IV collagen in the presence of cycloheximide. Laminin, a high molecular weight glycoprotein constituent of basement membrane, was purified from the salt extract and was found to be the active species at concentrations as low as 1-5 microgram/ml. When laminin was preincubated on plates coated with either type I, II, III, IV, or V collagen and the plates subsequently washed, high levels of attachment were seen only on type IV collagen-coated plates. Affinity purified antibody directed against laminin inhibited the attachment of PAM 212 cells to a type IV collagen substrate. Laminin appears to be a specific attachment protein for epithelial cells since it did not stimulate the attachment of fibroblasts to type I or to type IV collagen substrates. These data suggest that lamin is produced and utilized by these epithelial cells to attach to basement membrane collagen.