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At least 433 records · Page 24Linked to original sources
PubMed2003

[Atypical hyperplasia of endometrium and hysteroscopy].

OBJECTIVE: To evaluate the risk of discovering an endometrial cancer when atypical hyperplasia was diagnosed by either endometrial samples using the pipelle device or hysteroscopic resection products. PATIENTS AND METHODS: A retrospective monocentric study from january 1990 to july 2000. Twenty-three patients with atypical hyperplasia were included. Initial endometrial status was provided by endometrial biopsyduring diagnosis hysteroscopy (12 cases) or by operative hysteroscopic resection products (11 cases). For 23 patients, operative hysteroscopy and analyse of products resected were performed. For all patients, there was no hysteroscopical aspect evocative of adenocarcinoma. For 23 patients, histopathological analysis of the hysterectomy piece precised the final diagnosis. RESULTS: Among the 23 hysterectomy pieces, 7 adenocarcinomas were diagnosed (30.4%). Risk for discovering adenocarcinoma when atypical hyperplasia was diagnosed by means of the pipelle biopsy device was 50% (6/12). Risk for discovering adenocarcinoma when atypical hyperplasia was diagnosed by means of operative hysteroscopy resection products was 5.9 % (1/17). DISCUSSION AND CONCLUSION: Atypical endometrial hyperplasia evidenced by pipelle biopsy device is often associated with adenocarcinoma. Diagnosis hysteroscopy however does not show evident pathological aspect of adenocarcinoma in such cases. Operative hysteroscopy allows in most cases correction of endometrial status. Risk of omitting adenocarcinoma when atypical hyperplasia is discovered on hysteroscopic resection pieces is low.

Adenocarcinoma↗
PubMed2006

Central obesity as a risk factor for prostatic hyperplasia.

OBJECTIVE: Obesity-related metabolic diseases may influence prostatic hyperplasia. This study examined the impact of obesity on prostate volume in men without overt obesity-related metabolic diseases. RESEARCH METHODS AND PROCEDURES: We recruited 146 men over the age of 40 years who did not have overt obesity-related diseases, such as diabetes, impaired fasting glucose, hypertension, or dyslipidemia. Transrectal ultrasonography was performed on all subjects. The subjects were divided into three groups according to their BMI: normal (18.5 to 22.9 kg/m2), overweight (23 to 24.9 kg/m2), and obese (> or = 25 kg/m2), and two groups according to their waist circumference: normal waist (< or = 90 cm) and central obesity (> 90 cm). The classification of the subgroups was based on the Asia-Pacific criteria of obesity. We compared the prostate volume among subgroups and assessed factors related to prostatic hyperplasia. RESULTS: Mean prostate volume was 18.8 +/- 5.0, 21.8 +/- 7.2, and 21.8 +/- 5.6 mL in the normal, overweight, and obese groups, respectively, and was 20.0 +/- 5.9 and 23.7 +/- 5.3 mL in the normal waist and central obesity group, respectively. Prostate volume was significantly greater in the obese group than in the normal group (P = 0.03) and in the central obesity group compared with the normal waist group (P = 0.002). Prostate volume was positively correlated with BMI and waist circumference after adjustment for age. After adjusting for confounding factors, central obesity was an independent factor affecting prostatic hyperplasia, which was defined as a prostate volume > 20 mL (odds ratio = 3.37, p = 0.037). Relative to men with both low BMI (18.5 to 22.9 kg/m2) and normal waist circumference, those with high BMI (> or = 25 kg/m2) and central obesity were at significantly increased risk of prostatic hyperplasia (odds ratio = 4.88, p = 0.008). However, those with high BMI (> or = 25 kg/m2) and normal waist circumference were not at significantly increased risk. DISCUSSION: Prostate volume was greater in the obese and central obesity groups than in the normal group after patients with overt obesity-related metabolic diseases were excluded. Although both BMI and waist circumference were positively correlated with prostate volume, central obesity was the only independent factor affecting prostate hyperplasia. We suggest that central obesity is an important risk factor for prostatic hyperplasia.

Abdominal Fat↗
PubMed2006

Retinoid-induced epidermal hyperplasia is mediated by epidermal growth factor receptor activation via specific induction of its ligands heparin-binding EGF and amphiregulin in human skin in vivo.

Retinoids are widely used in the treatment of photoaging to stimulate dermal repair. However, retinoids also induce epidermal hyperplasia, which can lead to excessive scaling. Scaling is the major deterrent to topical retinoid therapy. Keratinocyte growth is strongly stimulated via ligand activation of EGFR. We examined regulation of EGFR ligands by retinoids and the role of EGFR in retinoid-induced hyperplasia in human skin in vivo. Topical treatment of human skin with all-trans retinoic acid (tRA) induces EGFR ligands heparin-binding (HB)-EGF and amphiregulin (AR), and reduces betacellulin mRNA levels. Laser capture microdissection-coupled real-time reverse transcription-PCR reveals that tRA increases HB-EGF mRNA throughout the epidermis, whereas AR induction is limited to basal keratinocytes. Topical tRA activates extracellular signal-regulated kinase 1/2 (Erk1/2) downstream EGFR effectors in human skin in vivo. tRA increases the soluble forms of AR and HB-EGF proteins, and induces epidermal hyperplasia, in human skin organ culture. Neutralization of HB-EGF or AR with specific antibodies strongly reduces tRA-induced epidermal hyperplasia. Finally, inhibition of EGFR activation by genistein reduces epidermal hyperplasia caused by topical retinoid treatment. These data demonstrate the central role of EGFR activation in retinoid-induced epidermal hyperplasia, and suggest that EGFR inhibitors can mitigate retinoid-induced scaling.

Amphiregulin↗
PubMed2001

Serum chromogranin A as a screening test for gastric enterochromaffin-like cell hyperplasia during acid-suppressive therapy.

BACKGROUND: Serum chromogranin A (CgA), a marker of neuroendocrine neoplasia, increases during profound gastric acid inhibition, possibly reflecting the trophic effect of gastrin on the enterochromaffin-like (ECL) cells. AIMS: This study investigated the clinical value of serum CgA as a screening test for gastric fundic enterochromaffin-like (ECL) cell hyperplasia during acid-suppressive therapy. METHOD: A consecutive series of 230 dyspeptic patients referred for upper gastrointestinal endoscopy was investigated in a cross-sectional design. They were 154 patients on continuous medium-term (6 weeks to one year) or long-term (longer than one year) acid inhibition with either proton pump inhibitors (PPIs, n = 117) or histamine2-receptor antagonists (H2RAs, n = 37) for gastro-oesophageal reflux disease, and 76 nontreated subjects, with normal endoscopic findings (control group). Fasting blood samples were analysed for gastrin and CgA. Gastric biopsy specimens (oxyntic mucosa) were examined for histological evaluation of gastritis (Sydney classification) and of ECL cell hyperplasia (Solcia classification). RESULTS: Serum CgA levels correlated positively with serum gastrin, following a quadratic function (r = 0.78, P < 0.0001). Elevated serum CgA values during long-term acid inhibition correlated with the presence and severity of fundic ECL cell hyperplasia. Multivariate analysis identified hypergastrinaemia (P < 0.0001), duration of acid inhibition (P < 0.0001), H. pylori infection (P = 0.008), ECL cell hyperplasia (P = 0.012), and body gland atrophy (P = 0.043) as independent predictors of elevated serum CgA. In subjects on long-term acid inhibition (n = 123), serum CgA was equally sensitive but more specific than serum gastrin for the detection of ECL cell hyperplasia (sensitivity, 91.3% for both; specificity, 73% vs. 43%, P < 0.0001). CONCLUSIONS: During long-term gastric acid inhibition, serum CgA levels reflect the presence and severity of fundic ECL cell hyperplasia. Serum CgA is therefore a useful screening test for gastric ECL cell proliferative changes within this context.

Adult↗
PubMed1996

Immunolocalization of oestrogen and progesterone receptors in prostatic hyperplasia and carcinoma.

Oestrogen receptors and progesterone receptors were immunolocalized in 19 patients with benign prostatic hyperplasia and in 26 patients with prostatic carcinoma. Immunohistochemistry was performed on tissue that had been fixed in 8% paraformaldehyde and then paraffin-embedded, using microwave irradiation for antigen retrieval. Oestrogen receptor expression was observed exclusively in the stromal cells of six out of 26 (23%) patients with prostatic carcinoma, but in none of the cells of patients with benign prostatic hyperplasia. Progesterone receptor expression was detected in 16 of 19 (84%) and 17 of 19 (89%) of the epithelial cells and stromal cells of patients with benign prostatic hyperplasia, respectively. In patients with prostatic carcinoma, progesterone receptor immunoreactivity was observed in 12 of 20 (46%) and 20 of 26 (77%) of the carcinoma and stromal cells of prostatic carcinoma, respectively. The ratio of epithelial cells with progesterone receptor immunoreactivity corresponded well with that of stromal cells with immunoreactivity in patients with benign prostatic hyperplasia. However, the ratio of stromal cells with progesterone receptor immunoreactivity was much higher than that in carcinoma cells in patients with prostatic carcinoma. Immunolocalization patterns or the ratio of the cells with progesterone receptor immunoreactivity did not significantly correlate with histological differentiation or patient's age in carcinoma cases. However, patients with advanced surgical stages of disease demonstrated a significantly smaller number of carcinoma and stromal cells with progesterone immunoreactivity in patients with prostatic carcinoma. These results suggest that oestrogens do not have a direct effect on the biological behaviour of benign prostatic hyperplasia and prostatic carcinoma, but that progesterone appears to play a role in the pathogenesis of benign prostatic hyperplasia and prostatic carcinoma.

Aged↗
PubMed2001

Genetic analysis of pancreatic duct hyperplasia in Otsuka Long-Evans Tokushima Fatty rats: possible association with a region on rat chromosome 14 that includes the disrupted cholecystokinin-A receptor gene.

An Otsuka Long-Evans Tokushima Fatty (OLETF) strain of rat spontaneously developed hyperglycemia, hyperinsulinemia, insulin resistance and mild obesity, which had been studied as animal model for type II diabetes mellitus (T2DM). Recently, we observed that this strain coincidentally developed atypical hyperplasia of the choledocho-pancreatic ductal epithelium with a complete incidence. In an effort to locate genes responsible for this hyperplasia, we prepared 288 backcross progeny from a mating between OLETF rats and BN rats (which do not develop hyperplasia), and performed a genome-wide scan using 207 polymorphic genetic markers. We observed a prominent association of hyperplasia with a region involving a marker locus D14Mit4 (P = 0.00020, Fisher's exact test) and Cckar (the cholecystokinin-A receptor gene; P = 0.00025, Fisher's exact test) which is known to be disrupted in an OLETF strain. Our findings indicated that epithelial hyperplasia of the choledocho-pancreatic duct is associated with a region on rat chromosome 14 around the Cckar gene in an additive fashion with another two susceptible loci, each on chromosome 9 and 7. This implied the possibility that Cckar deficiency could result in a predisposition towards pancreatic duct hyperplasia.

Animals↗
PubMed2002

Aggressive venous neointimal hyperplasia in a pig model of arteriovenous graft stenosis.

BACKGROUND: Vascular access dysfunction is the most important cause of morbidity and hospitalization in the hemodialysis population in the United States at a cost of well over one billion dollars per annum. Venous neointimal hyperplasia characterized by stenosis and subsequent thrombosis, is the major cause of polytetrafluoroethylene (PTFE) dialysis graft failure. Despite the magnitude of the problem, there are currently no effective therapies for the prevention or treatment of venous neointimal hyperplasia in PTFE dialysis grafts. We believe that this is partly due to the lack of a validated large animal model of arteriovenous stenosis that could be used to test out novel interventions. METHODS: Seven-centimeter PTFE loop grafts were placed between the femoral artery and vein of domestic pigs. The grafts were removed at 2, 4, 7, 14 and 28 days after surgery and subjected to a detailed histological and immunohistochemical examination. RESULTS: Significant neointimal hyperplasia and venous stenosis developed by 28 days at the graft-vein anastomosis. There was minimal neointimal hyperplasia at the graft-artery anastomosis. Venous neointimal hyperplasia (VNH) was characterized by (a) the presence of smooth muscle cells/myofibroblasts; (b) angiogenesis within both the neointima and adventitia; and (c) the presence of an active macrophage cell layer lining the PTFE graft material. These results are very similar to the human lesion previously described by us in dialysis patients. CONCLUSIONS: We have developed and validated a pig model of venous neointimal hyperplasia that is very similar to the human lesion. We believe that this is an ideal model in which to test out novel interventions for the prevention and treatment of clinical hemodialysis vascular access dysfunction.

Animals↗
PubMedDate not supplied

Cancer history and loss of MSH2 and MLH1 protein expression in patients with endometrial hyperplasia.

In order to evaluate the hereditary background of endometrial hyperplasia patients in relation to protein expression of DNA mismatch repair genes, we evaluated 69 patients with endometrial hyperplasia and 18 patients with normal endometrium having both a personal and family history of cancer (two hereditary nonpolypoid colorectal cancer (HNPCC) patients). We obtained personal and family histories of cancer for all patients. MSH2 and MLH1 protein expression was investigated by immunohistochemical methods. In the endometrial hyperplasia patients, 11 had personal histories and 40 had family histories of cancer. Among the 11 endometrial hyperplasia patients with a personal history of cancer, most cancers were breast or colorectal cancers (82%). In the 40 patients with a family history of cancer, colorectal cancer (33%) was the most frequent. The incidence of loss of expression of MSH2 and/or MLH1 protein in endometrial hyperplasia patients with personal (64%) or family (40%) histories was significantly higher than that in patients without such history (no personal: 21% and no family: 10%; P = 0.0035 and 0.0065). No protein loss was detected in any of the cases with normal endometrium having either a personal or family history of cancer. Our results suggest that a portion of endometrial hyperplasia cases having a personal or family history of cancer may belong to HNPCC, and that in these cases, abnormality of the mismatch repair system may be an early event in endometrial carcinogenesis.

Adaptor Proteins, Signal Transducing↗
PubMed2002

Reduction of non-endothelial cell contamination of microvascular endothelial cell seeded grafts decreases thrombogenicity and intimal hyperplasia.

INTRODUCTION: fat derived microvascular endothelial cells (MVEC) seeded on prosthetic vascular grafts, improve patency in animals. Results in humans were disappointing, due to thrombogenicity and progressive intimal hyperplasia. Also in animals intimal hyperplasia was found. We postulate that contaminating cells present in the transplant are involved in the intimal hyperplasia. We developed a method to further purify human MVEC from 40-90%. Here we tested the effects of enrichment upon thrombogenicity and seeding-related intimal hyperplasia. METHODS: liposuction fat was enzymatically digested and centrifuged. To enrich MVEC, contaminating macrophages and fibroblasts were removed with dynabeads coated with macrophage- and fibroblast-specific antibodies. Thrombogenicity was assessed by measuring tissue factor and thrombomodulin activity, presence of endothelial nitric oxide synthase and via perfusion of the cells with whole blood. To investigate seeding-related intimal hyperplasia, PTFE grafts were seeded with the cells and cultured for 3 weeks. RESULTS: tissue factor activity of purified cells was reduced compared to nonpurified cells. Purified cells showed thrombomodulin activity and eNOS expression. Fragment 1+2 and Fibrinopeptide A generation after perfusion of purified cells were significantly lower than after perfusion of nonpurified cells, and only nonpurified cells were covered with platelets and fibrin. Prostheses seeded with nonpurified cells showed an EC monolayer above a multilayer of myofibroblasts, prostheses seeded with purified cells only showed a single EC monolayer. Mixing experiments with human umbilical cord EC (HUVEC) and fibroblasts showed that when more than 25% HUVEC were present a confluent EC layer was formed. When the amount of fibroblasts was 25% or less, no development of a subendothelial multilayer of myofibroblasts was found within 3 weeks. CONCLUSION: reduction of non-endothelial cell contamination of microvascular endothelial cell seeded grafts decreases thrombogenicity and might prevent seeding-related intimal hyperplasia.

Cell Separation↗
PubMed1997

Role of T helper 2 cells in intestinal goblet cell hyperplasia in mice infected with Trichinella spiralis.

BACKGROUND & AIMS: The four principal types of intestinal epithelial cells are derived from multipotent stem cells. Currently, there is no information on factors that regulate commitment of stem cells to differentiate along one lineage vs. another. The aim of our study was to investigate the role of T cells in the regulation of small intestinal goblet cell hyperplasia in mice infected with the parasite Trichinella spiralis. METHODS: NIH mice were infected with T. spiralis, and intestinal goblet cells and cytokine response were studied. Interferon gamma and interleukin 5 were used as candidate T helper (Th)1 and Th2 cytokines, respectively. Adoptive transfer experiments were also performed. RESULTS: Small intestinal goblet cell hyperplasia occurred 8 days after infection with T. spiralis. Th1-type cells were predominant in the mesenteric lymph nodes early in the course of infection, with a switch to Th2-predominant cells around the time of goblet cell hyperplasia. Transfer of Th2-enriched mesenteric lymph node cells further enhanced goblet cell hyperplasia in recipient mice. Neutralization of interleukin 5 activity did not affect T. spiralis-induced goblet cell hyperplasia. CONCLUSIONS: Small intestinal goblet cell hyperplasia in T. spiralis-infected mice is probably regulated by Th2 cells. We postulate that Th2-derived factors (other than interleukin 5) induce stem cells to differentiate preferentially along the goblet cell lineage.

Animals↗
PubMed2001

G-protein expression and intimal hyperplasia after arterial injury: a role for Galpha(i) proteins.

PURPOSE: Guanine nucleotide binding protein (G-protein) coupled receptors are involved in smooth muscle cell proliferation, but the role of G-proteins in arterial intimal hyperplasia has not been defined. This study examines the expression of G-proteins in the developing intimal hyperplasia after balloon injury of the rat carotid artery and specifically tests the hypothesis that the pertussis toxin sensitive G(i) G-protein subunit plays a role in the initiation of intimal hyperplasia. METHODS: In vitro responses to serum stimulation (10% fetal bovine serum) were examined in the presence and absence of pertussis toxin (PTx). After a standard balloon injury in male Sprague-Dawley rats, the expression of G-protein subunits (alpha(o), alpha(i), alpha(q), alpha(s), and betagamma) was determined by means of Western blotting in the first 28 days. Thereafter, a second set of animals was allocated to control and PTx-treated (a Galpha(i) inhibitor; 500 ng/mL in an externally applied 30% pluronic gel) groups. Smooth muscle cell proliferation was estimated by means of thymidine analogue 5-bromo-2' deoxyuridine incorporation 2 days after injury, and vessel dimensions were determined by means of videomorphometry 14 days after injury. RESULTS: There was inhibition of DNA synthesis and smooth muscle cell proliferation in response to serum with an IC(50) of 100 ng/mL. Three days after balloon injury, there was an increase in Galpha(i3) expression, which decreased at days 7, 14, and 28, compared with the uninjured carotid. Galpha(q) expression increased in a time-dependent manner. There was a marked time-dependent increase in Gbetagamma in the 28 days. Galpha(i2) and Galpha(s) isoforms (45 and 52 kDa) did not change significantly with time. There was no major change in Galpha(i1) and Galpha(o) in the study period. At 14 days, PTx treatment reduced intimal hyperplasia by 52% (63 +/- 4 microm vs. 30 +/- 5 microm, control vs. PTx; P <.001). Medial smooth muscle cell proliferation at day 2 was decreased in the PTx group, compared with that in the gel-coated group (15% +/- 2% and 26% +/- 3%; P = .02). CONCLUSION: After balloon injury, there is a time-dependent increase in G-protein expression, which is subunit specific. Activation of PTx sensitive G-proteins (Galpha(i)) is involved during the initiation of intimal hyperplasia after arterial injury, and their inhibition results in a decrease in early medial cell proliferation. This acute interruption of G(i) signaling produces a long-term decrease in intimal hyperplasia.

Animals↗
PubMedDate not supplied

Ultrastructural changes in prostate cells during hormone-induced canine prostatic hyperplasia.

Benign prostatic hyperplasia is a prevalent disease that has received relatively little attention in spite of its morbidity and remarkable social impact. There are few animal models of prostatic hyperplasia. The dog is the only species, along with humans, in which prostatic hyperplasia develops spontaneously and almost universally with age. The aim of the present study has been to compare the ultrastructural findings in a model of experimentally induced canine prostatic hyperplasia with those of the spontaneously developed changes in untreated dogs. An experimental group of 5 male beagle dogs were castrated and treated with combined steroids (3 weekly doses for over 30 weeks). Prostate samples were surgically obtained every 42 days (experimental stages 0 through 6). The control group consisted of 3 noncastrated dogs that were treated with vehicle and in which samples were taken only at stages 0, 1, 4, and 6. Changes in the control groups were similar but of lower intensity compared to those of the experimental groups. In luminal cells, crowding with papillary projections, prominent, branching microvilli, and abundant, often compartmentalized granules were observed. The most striking change was the previously unreported finding of caveolae in basal cells. They were mostly located in the basal aspect of basal cells and were more prominent in the experimental group and in advanced stages of treatment. These ultrastructural findings have not been previously reported in canine or human prostatic hyperplasia and merit further research. The model of experimentally induced canine prostatic hyperplasia provides an adequate setting for the understanding of this disease.

Androstane-3,17-diol↗
PubMed2006

Nasopharyngeal lymphoid hyperplasia after therapy for childhood lymphomas.

Although diffuse thymic hyperplasia after therapy has been reported in lymphomas, no report is found in the medical literature about hyperplasia of other lymphoid tissues following chemotherapy in malignancies as far as we could reach. So, we planned to investigate the nasopharyngeal region of the lymphoma cases during their follow-up while at remission. Children who were in follow-up after cessation of oncological therapy with the diagnosis of lymphoma were evaluated for their nasopharyngeal lymphoid tissues by means of computed tomography. When a mass lesion was diagnosed, biopsies were taken. Among 23 lymphoma cases in follow-up, at a median of eight months (range 1-13 months), eight patients (six Hodgkin's and two Non-Hodgkin's malignant lymphoma) developed nasopharyngeal lymphoid hyperplasia (34.78%) that were proven to be benign by means of biopsies. Two of the patients also developed thymic hyperplasia. Nasopharyngeal hyperplasia regressed in four patients at a median of four months. Nasopharyngeal lymphoid hyperplasia may be diagnosed after the cessation of therapy in lymphomas and whatever the cause, it seems to be a benign process.

Adolescent↗
PubMed1983

Basal cell hyperplasia of the prostate.

Basal cell hyperplasia of the prostate is a rare, benign lesion that often has been misdiagnosed as adenocarcinoma. Thirteen cases of basal cell hyperplasia were reviewed. All of the patients were over 60 years of age (range 63-83) and all had benign prostatic hypertrophy in addition to basal cell hyperplasia. Histologic features consisted of nests of uniform small cells with scant cytoplasm forming solid nests and acinar structures. Some foci had nodular configurations and most were located within larger nodules of "typical" glandular hyperplasia. In some instances there was a merging of the two types of hyperplasia. There was neither nuclear atypia nor pleomorphism, and the adjacent stroma was hyperplastic. Small elongated cells with desmosomes and nonspecific, dense bodies were seen on electron microscopic studies of formalin-fixed material. The architectural and cytologic features of the basal cell proliferations were not those of carcinoma. However, synchronously, two patients demonstrated foci of prostate carcinoma unrelated to the basal cell hyperplasia.

Adenocarcinoma↗
PubMed1993

Comparison of 12-O-tetradecanoylphorbol-13-acetate and teleocidin for induction of epidermal hyperplasia, activation of epidermal PKC isozymes and skin tumor promotion in SENCAR and C57BL/6 mice.

The present study compared the ability of 12-O-tetradecanoylphorbol-13-acetate (TPA) and teleocidin to induce sustained epidermal hyperplasia, activate partially purified epidermal protein kinase C (PKC) isozymes and promote skin tumors in SENCAR and C57BL/6 mice. Teleocidin was less effective than TPA on a molar basis for inducing sustained epidermal hyperplasia, promoting skin tumors and activating partially purified epidermal PKC isozymes in vitro when examined using SENCAR mice. In contrast, teleocidin was more effective than TPA on a molar basis for inducing sustained epidermal hyperplasia, approximately equi-effective for promoting skin tumors and significantly less effective for activating PKC isozymes in vitro when examined using C57BL/6 mice. Despite the differences in response of C57BL/6 mice to TPA and teleocidin, this mouse strain was still highly resistant to skin tumor promotion by both types of promoters when compared with SENCAR mice. The current results, when considered in light of our recent studies (Cancer Res., 51, 1398-1405, 1991), indicate that C57BL/6 are generally resistant to a variety of classes of skin tumor promoters, including the teleocidins. In addition, except for the phorbol esters, the induction of sustained epidermal hyperplasia does not appear to be as good a marker for overall promotion responsiveness between SENCAR and C57BL/6 mice with other classes of tumor promoters; although the induction of a significant sustained hyperplasia in the latter mouse strain did yield a weak tumor response. Taken together, the current data suggest that factors in addition to the induction of sustained epidermal hyperplasia, control responsiveness of C57BL/6 mice to skin tumor promotion by diverse promoting stimuli.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1995

Tyrosine phosphorylation in mouse mammary hyperplasias.

Tyrosine phosphorylation status was investigated during mouse mammary tumor development using non-tumorigenic and tumorigenic hyperplastic outgrowth lines. These outgrowth lines were compared with normal mammary glands from pregnant mice and with their corresponding tumors. The levels of total tyrosine phosphorylation in proteins of hyperplastic and neoplastic tissues were 4.7- and 3.4-fold higher than in the normal gland respectively. These results indicate that increases in tyrosine phosphorylation occur in the earliest stages of neoplastic development and are not restricted to neoplastic cells per se. These results led to the identification of the specific proteins showing high levels of tyrosine phosphorylation. Of the eight molecular weight bands of proteins exhibiting detectable levels of tyrosine phosphorylation, the only proteins exhibiting consistently different degrees of phosphorylation between hyperplasias and tumors were of approximately 34 kDa. In a series of six different hyperplasias with tumorigenic potentials ranging from 0 to 93%, the extent of tyrosine phosphorylation of 34 kDa proteins correlated inversely with tumorigenic potential. The levels of p34cdc2 and p33cdk2 proteins were examined, using antibodies specific for the cdc2 and cdk2 proteins. The amounts of p34cdc2 and p33cdk2 proteins were low in non-tumorigenic (TM3 and TM2L) compared to tumorigenic hyperplasias and correlated inversely with tyrosine phosphorylation of 34 kDa proteins during tumor development. Thus in the non-tumorigenic hyperplasias (TM2L and TM3) the majority of p34cdc2 was phosphorylated on tyrosine, in contrast to the p34cdc2 in tumorigenic (TM2H) hyperplasias and tumors. Two-dimensional PAGE analysis of mammary tumor samples with antibodies specific to cdc2, cdk2 and phosphorylated tyrosine revealed one p34cdc2 form, two p33cdk2 isoforms and two phosphotyrosine isoforms of about 33-34 kDa. The results suggest that the high levels of tyrosine phosphorylation in cdc2 and cdk2 reflect the low tumorigenic potential of a subset of mammary preneoplastic hyperplasias. This interpretation is in accord with current concepts on the role of tyrosine phosphorylation in the regulation of the cyclin-dependent kinases.

Animals↗
PubMed1988

Pseudocarcinomatous hyperplasia.

Pseudocarcinomatous hyperplasia is not fundamentally a hyperplasia of epidermal epithelium, but rather a hyperplasia of adnexal epithelia, namely, of follicular infundibula and eccrine ducts. All examples of pseudocarcinomatous hyperplasia are responses to an underlying inflammatory or neoplastic process. That process can usually be discerned beneath the pseudocarcinomatous hyperplasia in the biopsy specimen. Application of criteria that pertain mostly to architectural pattern (silhouette) enables pseudocarcinomatous hyperplasia to be differentiated histopathologically from squamous cell carcinoma.

Carcinoma, Squamous Cell↗
PubMed2003

Massive pseudoepitheliomatous hyperplasia: an unusual reaction to a tattoo.

We document an unusual tattoo reaction presenting as verrucous plaques, which on histopathologic examination showed marked pseudoepitheliomatous epidermal hyperplasia. The patient is a 27-year-old female who presented to her dermatologist complaining of itchy overgrowth of her tattoo. Her symptoms began 2 months after tattoo placement approximately 1 year ago. Physical examination revealed verrucous plaques in the purple areas of the tattoo, suggesting a clinical diagnosis of a granulomatous tattoo reaction. A superficial biopsy showed epidermal hyperplasia somewhat reminiscent of a regressing keratoacanthoma. No tattoo was identified. A repeat shave biopsy demonstrated marked epidermal hyperplasia with focal keratin filled cystic dilatations, and local mild reactive keratinocytic atypia. In the surrounding dermis, there was dense chronic inflammation, fibrosis, and granules of dark red pigment. These findings suggest marked pseudoepitheliomatous hyperplasia secondary to the tattoo. Different reaction patterns have been described in association with tattoos, such as granulomatous and/or perivascular lymphocytic inflammation. However, there have been few cases reported of pseudoepitheliomatous hyperplasia arising at a tattoo site. Therefore, we encourage physicians to consider massive epidermal hyperplasia in the differential diagnosis of a verrucous tattoo reaction.

Adult↗