Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metalloproteinases are thought to be important for tumor invasion and metastasis. We used in situ hybridization with 35S-labeled cRNA probes to localize sites of expression for 92-kDa type IV collagenase mRNA in sections of nodular basal cell carcinoma. Positive signal for 92-kDa type IV collagenase mRNA was detected in eosinophilic granulocytes within inflammatory infiltrates surrounding the tumor nodules. Eosinophils, however, were not adjacent to tumor cells, suggesting that metalloenzyme production by these granulocytes in this disease may be targeted more to stromal components than to remodeling or destruction of the basement lamina. The identity of the eosinophils was confirmed by cell morphology and specific histochemical staining. No resident or other migratory cells were positive for enzyme mRNA in these samples. Signal specificity for in situ hybridization was shown by a duplication of the results with complementary oligomeric probes and by a lack of signal in sections hybridized with a sense RNA probe or nonspecific oligomer. No signal for 92-kDa type IV collagenase mRNA was detected in circulating eosinophils or in eosinophils associated with Hodgkin's lymphoma. These data suggest that eosinophils migrate into the dermis and express type IV collagenase in response to basal cell carcinoma and that this process may have a role in tumor growth.
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PMID:Expression of 92-kDa type IV collagenase mRNA by eosinophils associated with basal cell carcinoma. 140 8

The mortality rate of nonmelanoma skin cancer is higher than generally considered. An actual nonmelanoma skin cancer is a risk factor not only for other skin cancers but also for cancers in other organs. The recurrence rate can, according to the method of calculation, yield surprisingly diverging results. Statistical mapping of subclinical tumor growth in basal cell carcinoma supplies the margins for tumor-free excision. An even better but more expensive tool for therapy planning is tumor imaging with magnetic resonance imaging. Psoralen plus ultraviolet light of the A wavelength-treated patients run a dose-dependent risk of developing squamous cell carcinoma of the skin but also cancers in other organs. Human papilloma virus-16 seems not to be associated with squamous cell carcinoma of the skin except for the anogenital region and possibly the finger. The finding of retroviruslike particles in endemic non-acquired immunodeficiency syndrome Kaposi's sarcoma strongly suggests that a virus other than human immunodeficiency virus may play a role in the pathogenesis of this disease.
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PMID:Basal cell and squamous cell carcinoma and Kaposi's sarcoma. 159 11

Basal cell carcinoma is the most common malignancy in humans. Although rarely metastatic, it is capable of significant local destruction and disfigurement. This two-part article reviews the current understanding of basal cell carcinoma biology. Part I examines significant clinical, histologic, and ultrastructural features that relate to invasive potential. Genetic characteristics, including tumor growth rate, chromosomal abnormalities, and oncogene presence, are discussed, and expression of important cell and matrix proteins, including keratin, fibronectin, and HLA antigens, are reviewed. Further topics to be explored in Part II include host immunologic responses, theories of pathogenesis, and valuable second-line therapeutic regimens for treatment of multiple cancers.
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PMID:Biology of basal cell carcinoma (Part I). 199 6

Pathologists frequently need to judge whether basal cell carcinomas have been excised adequately. Traditionally, excision adequacy is assessed by looking for the presence of tumor at the margins of resection. This time-honored activity has questionable value, since it has been demonstrated that the majority of tumors with positive margins do not recur, and a substantial minority of tumors with negative margins do recur. It is proposed that excision adequacy can be evaluated by considering the pattern of tumor growth. Tumors composed of widely dispersed nests need wider margins than tumors that grow as tight clusters of tumor nests, and this assertion can be evaluated statistically. A morphometric study of 28 basal cell carcinomas (BCCs) was performed, in which the distribution of tumor cell nests seen in cross-section was analyzed. The average distance from the center varied greatly (272 to 2273 microns) among these tumors. Standard deviations were calculated from distances between the tumor center to each nest within the tumor, and one-tailed Student's t tests were used to obtain 90%, 95%, and 99% confidence limits for distances beyond which no additional tumor nests are expected. These distances, in tumor radii, ranged from 0.8 to 1.9 and from 1.03 to 4.89, for 90% and 99% confidence limits, respectively. Conventional methods used to determine margin adequacy do not account for the discontinuous appearance of BCC in histologic sections. This theoretical model demonstrates that an alternate way of assessing excision adequacy can be achieved with a statistical analysis of the pattern of tumor growth, rather than looking for absence of tumor at the resection margin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Basal cell carcinoma: importance of histologic discontinuities in the evaluation of resection margins. 178 69

Sclerosing or morphea-like variant of basal cell carcinoma (BCC) is characterized by an extensive connective tissue stroma, and histopathology has suggested that the extracellular matrix is largely composed of collagen. In addition, fibronectin deposition has been proposed to modulate tumor growth in BCC. In this study, we examined the expression of genes coding for type I, III, and IV procollagens, as well as for fibronectin, in tissue from 10 patients with sclerosing BCC. For comparison, tissues from 5 patients with nodular BCC and 4 controls were examined. Total RNA was isolated by CsCl density gradient centrifugation, and messenger RNA (mRNA) steady-state levels were determined by slot-blot hybridizations with human sequence specific complementary DNAs (cDNAs). The abundance of type I procollagen mRNA in sclerosing BCC tissue was increased to 233.6 +/- 36.7% of the controls (mean +/- SEM). The corresponding value for type III procollagen mRNA in sclerosing BCC was 281.8 +/- 54.8% of the controls. Consequently, the steady-state ratio of type I/III procollagen mRNAs in sclerosing BCCs (5.0 +/- 1.2; mean +/- SD) was within the control range. Thus, there is a coordinate increase in type I and type III procollagen mRNA levels in sclerosing BCC. In contrast, the values for type I and type III procollagen mRNAs in nodular BCC were not different from the controls. In addition, type IV procollagen and fibronectin mRNA levels were not different from the controls either in sclerosing or nodular BCCs, attesting to the selectivity of the increase in type I and III procollagen mRNA levels in sclerosing BCC. These observations may relate to the excessive deposition of the extracellular matrix stroma surrounding the tumor cells in sclerosing BCC.
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PMID:Selectively enhanced procollagen gene expression in sclerosing (morphea-like) basal cell carcinoma as reflected by elevated pro alpha 1(I) and pro alpha 1(III) procollagen messenger RNA steady-state levels. 336 Nov 39

Basal cell carcinomas (BCCs) obtained from 22 subjects undergoing microscopically controlled surgery were transplanted to 40 athymic (nude) mice. With no further immunosuppression of the mice, no tumor growth was noted in the first 14 attempts. When mice were further immunosuppressed with anti-lymphocyte serum (ALS) injections and by splenectomy, successful tumor growth was achieved in 15 of 22 mice by a subcutaneous implantation technique and in 1 of 4 by a superficial grafting technique. Transplanted BCC retained the morphology and basement membrane proteins typical of human BCC. As determined by autoradiography, 3H-thymidine was incorporated primarily in the peripheral palisaded cells of the transplanted tumor. Successful use of the athymic mouse model for study of human BCC requires use of mice further immunosuppressed by splenectomy and ALS, and the use of a subcutaneous implantation technique. With the use of this model, studies of the biology of human BCC may be possible.
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PMID:Transplantation of human basal cell carcinomas to athymic mice. 389 Oct 70

The effect of a single blood transfusion on the formation and outgrowth of experimental lung metastases was assessed in two tumor models in rats. The transfusions were given either 1 week before (day -7) or 1 week after (day +7) tumor cell inoculation. The first approach was performed to investigate the effect of transfusions on the formation of lung colonies, the second approach to study the effect on the outgrowth of established metastases. The first tumor model used was a transplantable, nonimmunogenic sarcoma (LS175) in BN rats. Animals were injected i.v. with 10(5) tumor cells and the number of metastases developing in the lungs was counted after 18 days. Experimental animals received 1 ml of allogeneic WAG blood, controls were given 1 ml of syngeneic BN blood. A single allogeneic transfusion given on day -7 had no effect on the formation of LS175 lung colonies but, when given day +7, stimulated the outgrowth of established metastases. The second tumor model was a highly immunogenic transplantable basal cell carcinoma (BC1618) in inbred WAG rats. Rats were injected i.v. with 10(6) tumor cells and the numbers of lung colonies were counted after 21 days. Experimental animals were transfused with 1 ml of BN blood, controls received 1 ml of WAG blood. An allogeneic transfusion on day -7 led to a significant inhibition of lung metastases, whereas a transfusion on day +7 had no effect. The results clearly indicate that allogeneic blood transfusions can modulate tumor growth and metastasis. Although immunological factors seem to play a crucial role in this transfusion phenomenon, there was no clear-cut correlation between the observed effects (accelerated tumor growth vs inhibition of metastasis) and the type of immunomodulation evoked.
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PMID:Modulation of tumor growth by allogeneic blood transfusion. 394 50

Stromelysin-3 is produced in the stroma of various malignant tumors, and in breast carcinoma there seems to be a positive correlation between aggressive disease and intensity of stromelysin-3 expression, suggesting that stromelysin-3 participates in the tumor spread. In basal cell carcinoma, previous findings on stromelysin-3 have been inconclusive in this respect. Our study was undertaken to determine the pattern of stromelysin-3 production in relation to different histologic subtypes and stromal reactions in basal cell carcinoma. By in situ hybridization, stromelysin-3 mRNA was detected in stromal fibroblastic cells in 51/56 samples. Furthermore, there was a significant correlation between strong signal for stromelysin-3 mRNA and infiltrative tumor growth. In all tumors, there was ongoing collagen synthesis as shown by a signal for procollagen I mRNA; this signal co-localized with stromelysin-3 around tumor nests. Our findings suggest a link between stromelysin-3 and fibrotic stromal response, which prompted us to evaluate the expression of stromelysin-3 in other fibrotic skin tumors. Interestingly, stromelysin-3, co-localizing with procollagen I mRNA, was consistently expressed in lesional cells in dermatofibromas (19/19), but not in dermatofibrosarcomas (0/7). Thus, our results indicate that in addition to being a marker for malignant disease, stromelysin-3 is produced by fibroblastic cells associated with benign fibrosis. A subset of cells producing stromelysin-3 appears to be myofibroblasts as demonstrated by immunoreactivity for alpha smooth muscle actin in both basal cell carcinoma and dermatofibroma.
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PMID:Stromelysin-3 mRNA associated with myofibroblasts is overexpressed in aggressive basal cell carcinoma and in dermatofibroma but not in dermatofibrosarcoma. 875 54

Topical diclofenac in 2.5% hyaluronan inhibits basal cell carcinoma, actinic keratosis, and murine colon-26 growth in vivo. colon-26 tumor growth was preceded by angiogenesis and reduced apoptotic and mitotic indices. Diclofenac reduced proliferation and viability in vitro, and stimulated apoptosis. Hyaluronan inhibited proliferation and viability at 1 mg/ml but was inactive below this level. Topical application of diclofenac inhibited tumor prostaglandin synthesis and retarded angiogenesis and tumor growth (ratio of treatment:control, 0.174). The mitotic index remained unaltered in vivo, whereas the apoptotic index and necrosis were increased. Topical vehicle exhibited slight antitumor and antiangiogenesis activity. The substantial quantities of diclofenac delivered locally in hyaluronan may exhibit antitumor activity in similar fashion to those seen in vitro and explain its clinical efficacy.
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PMID:The inhibition of colon-26 adenocarcinoma development and angiogenesis by topical diclofenac in 2.5% hyaluronan. 913 96

Basal cell carcinomas (BCCs) are frequently associated with a peritumoral mononuclear infiltrate. Until now, the function of this inflammatory infiltrate and its possible role in the control of tumor growth is unclear. Mechanisms controlling endothelial and target cell adhesiveness for leukocytes are important features in the development of a specific local immune response. The expression and distribution of the adhesion molecules ICAM-1, VCAM-1 and E-selectin by microvascular endothelial cells and tumor cells, together with their leukocyte receptors LFA-1, VLA-4 and CLA respectively, were studied in 33 BCCs of different histological subtypes. In normal skin, ICAM-1 is expressed by resting endothelial cells, whereas VCAM-1 and E-selectin expression correlates with endothelial activation. The epidermis in normal conditions displays no ICAM-1, VCAM-1, or E-selectin expression. In BCC, endothelial ICAM-1 expression was only slightly increased compared to normal skin, whereas expression of endothelial VCAM-1 and E-selectin was low or absent in all BCCs examined. Peritumoral infiltrates contained mostly LFA-1-expressing lymphocytes, with minimal VLA-4 and CLA positivity. In none of the cases studied was adhesion molecule expression by BCC tumor cells identified. The lack of significant expression of adhesion molecules on peritumoral vascular endothelial cells and BCC tumor cells does not support the idea of specific, cell-mediated immunity being an important mechanism in limiting BCC tumor spread.
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PMID:Adhesion molecule expression in basal cell carcinoma. 964 78


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