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Background: We present a case of hypertensive choroidopathy due to malignant hypertension with exudative retinal detachment as a sole finding. We use OCT- angiography for initial diagnosis and report findings from extensive follow up. Case presentation: A 51-year-old female with no past medical history, presented to our clinic with painless loss of vision in her left eye. Fundus examination revealed only exudative retinal detachment in her left eye that was confirmed with Optical Coherence Tomography. Fluorescein angiography showed hyperfluorescent spots with leakage in late phases. OCTA manifested a focal dark area in the choriocapillaris slab corresponding to flow signal voids, signifying regions of non-perfusion. Her blood pressure was 220/120 mmHG. Complete blood work -up failed to reveal any other possible etiology. During follow-up period of 9 months blood pressure normalized, patient regained visual function and choriocapillaris perfusion was completely restored. Discussions and conclusions: Hypertensive choroidopathy with exudative retinal detachment can be the only sign of malignant hypertension and no pre-existing history of a systemic disease is required in order to become apparent. OCTA reveals areas of non-perfusion at choriocapillaris level, proving that it is an essential tool in the diagnosis and follow up of patients with hypertensive choroidopathy. Finally, we propose that early diagnosis prevents permanent damage of the RPE and leads to complete choroidal remodeling and better visual outcomes. © 2023, The Author(s).

Background: Flavonoids have physiological activity and a variety of pharmacological properties, including anticancer activity in vitro, but structure-anticancer activity relationships are unclear. Aim: The objectives of this work were to investigate the activity of dietary flavonol congeners against cell lines derived from human solid tumours and to examine whether the in vitro activity was associated with specific structural feature(s) of the molecules. Methods: Antiproliferative activity of the flavonol congeners was investigated against eight different human cancer cell lines representing different types of human solid tumour, using the sulforhodamine B (SRB) assay in accordance with the instructions published by the NCI. Cell cycle perturbations caused by the congeners were monitored by flow-cytometric analysis of DNA stained with propidium iodide. Results: Most of the flavonols examined had weak antiproliferative and cytotoxic activity. Of all the flavonol congeners tested peracetylated tiliroside found to be the most powerful, with significant antiproliferative and cytotoxic activity. Most flavonols induced similar cell cycle perturbations, whereas induction of apoptosis was significant only for cells treated with peracetylated tiliroside. Conclusions: These findings indicated that the -OH groups of aromatic ring B were not linked to the cytotoxic and antiproliferative activity of the tested flavonols whereas peracetylation of the glycosides resulted in moderate improvement. In contrast, acetylation of tiliroside esterified with coumaric acid at position 5 of the sugar moiety greatly improved the activity of this congener. Overall, the results of this study suggest a critical role of sugar moiety substituents in the anticancer activity of the flavonols. © Springer-Verlag 2011.

Purpose: The purpose of our study was to evaluate the effectiveness of preoperative and postoperative addition of topical diclofenac to chloramphenicol/dexamethasone in patients undergoing uneventful phacoemulsification cataract surgery. Methods: Patients were randomized to (1) chloramphenicol 0.5%-dexamethasone 0.1%, 1 drop 4 times a day (n=41), or (2) chloramphenicol 0.5%-dexamethasone 0.1%, 1 drop 4 times a day, plus diclofenac 0.1%, 1 drop 3 times a day (n=38). Patients in the second group also received diclofenac 0.1% for 3 days before surgery. Topical treatment was administered for 28 days after phacoemulsification. On postoperative days 1, 14, and 28, best corrected visual acuity, macular thickness, endothelial cell density, and central corneal thickness (CCT) were measured. Results: The 2 groups did not have a statistically significant difference for CCT, endothelial cell density, macular thickness, and visual acuity at the 3 time points of the follow-up period. Conclusions: The addition of diclofenac did not seem to offer any additional benefit after uneventful phacoemulsification. © Copyright 2012, Mary Ann Liebert, Inc.

The labdane diterpene sclareol has demonstrated significant cytotoxicity against human tumor cell lines and human colon cancer xenografts. Therefore, there is need to elucidate the mode of action of this compound as very little information is known for the anticancer activity of sclareol and other labdane diterpenes, in general. COMPARE analysis of GI50 values for a number of human cancer cell lines was initially implicated in an effort to assign a putative mechanism of action to the compound. Sclareol-induced cell cycle arrest and apoptosis were assessed by flow cytometry and Western blot analyses. Finally, the anticancer ability of sclareol in vivo was assessed by using human colon cancer xenograft/mouse models. Sclareol arrested in vitro the growth of p53-deficient (HCT116p53-/-) human colon cancer cells and subsequently induced apoptosis by activating both caspases-8 and -9. Intraperitoneal administration of liposome-encapsulated sclareol at the maximum tolerated dose induced a marked growth suppression of HCT116p53-/- tumors established as xenografts in immunodeficient NOD/SCID mice. In conclusion, we demonstrate herein that sclareol kills human tumor cells by inducing arrest at the G1-phase of the cell cycle followed by apoptosis that involves activation of caspases-8, -9 and -3 via a p53-independent mechanism. These findings suggest that liposome-encapsulated sclareol possesses chemotherapeutic potential for the treatment of colorectal and other types of human cancer regardless of the p53-status. © 2011 Elsevier B.V.

In this report, we demonstrate that a 50% ethanol extract of the plant-derived product, Chios mastic gum (CMG), contains compounds which inhibit proliferation and induce death of HCT116 human colon cancer cells in vitro. CMG-treatment induces cell arrest at G1, detachment of the cells from the substrate, activation of pro-caspases-8, -9 and -3, and causes several morphological changes typical of apoptosis in cell organelles. These events, furthermore, are time- and dose-dependent, but p53- and p21-independent. Apoptosis induction by CMG is not inhibited in HCT116 cell clones expressing high levels of the anti-apoptotic protein, Bcl-2, or dominant-negative FADD, thereby indicating that CMG induces cell death via a yet-to-be identified pathway, unrelated to the death receptor- and mitochondrion-dependent pathways. The findings presented here suggest that CMG (a) induces an anoikis form of cell death in HCT116 colon cancer cells that includes events associated with caspase-dependent pathways; and (b) might be developed into a chemotherapeutic agent for the treatment of human colon and other cancers. © 2006 Elsevier GmbH. All rights reserved.

Labd-14-ene-8, 13-diol (sclareol) is a labdane-type diterpene, which has demonstrated significant cytotoxic activity against human leukemic cell lines, but its effect on solid tumor-derived cells is uknown. Here, we demonstrate that addition of sclareol to cultures of human colon cancer HCT116 cells results in inhibition of DNA synthesis, arrest of cells at the G1 phase of the cell cycle, activation of caspases-8, -9, PARP degradation, and DNA fragmentation, events characteristic of induction of apoptosis. Intraperitoneal (ip) administration of sclareol alone, at the maximum tolerated dose, was unable to induce suppression of growth of HCT116 tumors established as xenografts in immunodeficient SCID mice. In contrast, ip administration of liposome-encapsulated sclareol, following a specific schedule, induced suppression of tumor growth by arresting tumor cell proliferation as assessed by detecting the presence of the cell proliferation-associated nuclear protein, Ki67, in thin tumor sections. These findings suggest that sclareol incorporated into liposomes may possess chemotherapeutic potential for the treatment of colorectal and other types of human cancer. © 2007 Springer Science+Business Media, LLC.

Purpose: The plant-derived compound curcumin has shown promising abilities as a cancer chemoprevention and chemotherapy agent in vitro and in vivo but exhibits poor bioavailability. Therefore, there is a need to investigate modified curcumin congeners for improved anticancer activity and pharmacokinetic properties. Experimental Design: The synthetic curcumin analogue dimethoxycurcumin was compared with curcumin for ability to inhibit proliferation and apoptosis of human HCT116 colon cancer cells in vitro by estimating the Gl50 and LC50 values and detecting the extent of apoptosis by flow cytometry analysis of the cell cycle. Metabolic stability and/or identification of metabolites were evaluated by recently developed mass spectrometric approaches after incubation with mouse and human liver microsomes and cancer cells in vitro. Additionally, circulating levels of dimethoxycurcumin and curcumin were determined in mice following i.p. administration. Results: Dimethoxycurcumin is significantly more potent than curcumin in inhibiting proliferation and inducing apoptosis in HCT116 cells treated for 48 h. Nearly 100% of curcumin but <30% of dimethoxycurcumin was degraded in cells treated for 48 h, and incubation with liver microsomes confirmed the limited metabolism of dimethoxycurcumin. Both compounds were rapidly degraded in vivo but dimethoxycurcumin was more stable. Conclusions: Compared with curcumin, dimethoxycurcumin is (a) more stable in cultured cells, (b) more potent in the ability to kill cancer cells by apoptosis, (c) less extensively metabolized in microsomal systems, and (d) more stable in vivo. It is likely that the differential extent of apoptosis induced by curcumin and dimethoxycurcumin in vitro is associated with the metabolite profiling and/or the extent of stability. © 2007 American Association for Cancer Research.

Objectives: To identify parameters/factors that may contribute to the differential sensitivity to etoposide in two clones isolated from the human ovarian carcinoma SKOV-3 cell line, which does not express p53 and is resistant to platinum-based regimens. Methods: Differential sensitivity of the cells to etoposide was monitored by microscopy to observe morphological changes, by flow cytometry analyses to detect cell cycle perturbations, and by molecular/biochemical assays to identify events involved in induction of apoptosis. Results: Etoposide treatment (1) induced apoptosis in one clone, ES, but not in another clone, ER, (2) had no effect on the expression of the antiapoptotic proteins Bcl-2 and Bcl-X L in both cell clones, whereas the proapoptotic proteins Bak and Bax were dramatically upregulated in ES, but not ER cells, and (3) induced more extensive processing of procaspase-8, procaspase-9, and the caspase-3-targeted substrates, topoisomerase I and PARP, in ES cells. Ectopic overexpression of Bcl-2 in ES cells failed to inhibit etoposide-induced apoptosis. Conclusions: The differential susceptibility of ES and ER cells to etoposide-induced apoptosis is associated with differences in several events rather than with a specific single genetic regulator of the apoptotic machinery. We propose that the differential response of ovarian cancer patients to etoposide treatment is associated with the number of etoposide-sensitive cells in the tumor. Copyright © 2006 S. Karger AG.

Sclareol is a labdane-type diterpene that has demonstrated a significant cytotoxic activity against human leukemic cell lines. Here, we report the effect of sclareol against the human breast cancer cell lines MN1 and MDD2 derived from the parental cell line, MCF7. MN1 cells express functional p53, whereas MDD2 cells do not express p53. Flow cytometry analysis of the cell cycle indicated that sclareol was able to inhibit DNA synthesis induce arrest at the G0/1 phase of the cycle apoptosis independent of p53. Sclareol-induced apoptosis was further assessed by detection of fragmented DNA in the cells. Furthermore, sclareol enhanced the activity of known anticancer drugs, doxorubicin, etoposide and cisplatinum, against MDD2 breast cancer cell line. © 2006 Elsevier SAS. All rights reserved.

Human malignant epithelial cell lines were analyzed for expression of platelet-derived growth factor (PDGF) genes. Of the 12 cell lines tested, 9, derived from breast, lung, gastric, and ovarian carcinomas, were found to express both PDGF-1 and PDGF-2 genes. The levels of both PDGF-1 and PDGF-2 transcripts were superinduced when these cells were treated with cycloheximide, an inhibitor of protein synthesis. These cells also released an activity that in studies with BALB-c/3T3 cells, inhibited binding of 125I-labeled PDGF and stimulated incorporation of [3H]thymidine. This stimulating activity was inhibited after reduction of the conditioned media by mercaptoethanol or after preincubation with antibodies to PDGF. Moreover, this activity was not affected by heat treatment. Immunoprecipitation studies revealed that breast, lung, and gastric carcinoma cells produced PDGF-like proteins that migrated as 30- and 32-kD species under nonreducing conditions and as 15- and 16-kD species under reducing conditions. In contrast, malignant cells of ovarian origin produced 14-16-kD PDGF-like proteins that were unchanged in mobility after reduction. As PDGF receptors were not detected on these malignant epithelial cells, the production of PDGF-like proteins may affect other cells in the microenvironment by paracrine mechanisms and may contribute to excessive cell proliferation, inflammatory reactions, and connective tissue remodeling seen in certain carcinomas., Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., info:eu-repo/semantics/published

The colony-stimulating factor-1 (CSF-1) regulates survival, growth, and differentiation of monocytes by binding to a single class of high-affinity receptors. The CSF-1 receptor is identical to the product of the c-fms protooncogene. The present studies monitored the effects of TPA and CSF-1 on c-fms gene expression in human monocytes. The results demonstrate that TPA downmodulates the constitutive expression of c-fms mRNA to low but detectable levels. Treatment of human monocytes with TPA was similarly associated with decreases in levels of the 138- and 125-Kd c-fms-encoded proteins. However, the kinetics of c-fms protein downmodulation indicated independent effects of TPA on c-fms expression at the RNA and protein levels. Furthermore, c-fms protein levels subsequently recovered despite persistently low levels of c-fms mRNA. Although previous studies demonstrated that c-fms protein is down-regulated in the presence of CSF-1, the present results indicate that CSF-1 also downregulates levels of c-fms mRNA. Moreover, the results indicate that CSF-1 increases protein kinase C activity in the membrane fraction. Together, these findings suggest that c-fms gene expression is differentially regulated at both the RNA and protein levels after activation of protein kinase C in human monocytes treated with TPA and CSF-1., In Vitro, Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., info:eu-repo/semantics/published

Human T cells immortalized by human T lymphotropic virus (HTLV)-I and HTLV-II express the genes encoding both chains of platelet-derived growth factor (PDGF). These cells produce biologically active PDGF-like molecules of 31 and 32 kD, identified in the conditioned media of the virus-infected cells by direct immunoprecipitation, under non-reducing conditions, with antisera to PDGF. Upon reduction, the PDGF-like molecules are converted to mitogenically inactive single chains of 14 and 15 kD. The HTLV-transformed cells produce PDGF-like molecules regardless of their ability to produce viral particles. No PDGF-related mRNAs, PDGF-like proteins, nor PDGF-like mitogenic activity were detected in normal human T cells stimulated by phytohemagglutinin or in a T cell line which is not infected by HTLV. It is possible that one of the pathways of immortalization of T cells by HTLV-I or II might be by activation of PDGF-related genes., Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., info:eu-repo/semantics/published

In human umbilical vein and bovine aortic endothelial cells in culture c-sis gene expression and secretion of platelet-derived growth factor (PDGF) has been previously demonstrated. We now report the presence of PDGF-1 and PDGF-2/sis mRNA transcripts in primary cultures of human iliac artery endothelial cells (HIA-EC). Concomitantly, these cells synthesize and secrete PDGF-like proteins identified by direct immunoprecipitation with specific PDGF antiserum. The PDGF proteins secreted by HIA-EC have molecular weights of 31 and 35 kd under nonreducing conditions. Upon reduction these proteins are converted to the monomeric 15- and 16-kd forms. Conditioned media derived from HIA-EC stimulated the incorporation of 3H-thymidine by 3T3 cells and competed with 125I-PDGF for its binding to 3T3 cell membrane receptors. The biologic activity was stable to heating at 100 degrees C for 10 min and sensitive to reducing agents, properties similar to those of authentic PDGF. Production of PDGF-like mitogen by the human arterial endothelial cells may play an important role in the paracrine modulation of arterial wall regeneration following vascular injury., Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., FLWNA, info:eu-repo/semantics/published

Phorbol esters induce the differentiation of human myeloid leukemia cells HL-60 and U-937 along the monocytic-macrophage lineage. This process has been associated with the induction of several cellular protooncogenes, including the c-fos and c-fms genes. We now report that phorbol ester-induced differentiation of the HL-60 and U-937 cells results in the induction of the expression of the c-sis platelet-derived growth factor 2 (PDGF-2) protooncogene. sis mRNA transcripts were not detectable in the uninduced cells but were detectable within 12 hr of phorbol ester induction. Concomitantly, the induced cells were shown to synthesize and secrete biologically active PDGF-like proteins, identified in the conditioned medium of the phorbol ester-treated cells by direct immunoprecipitation with PDGF antiserum. Addition of cycloheximide to phorbol ester-treated HL-60 cells superinduced sis mRNA transcripts. c-sis gene transcripts were also detected in freshly isolated human monocytes but not in human granulocytes or in HL-60 cells induced to differentiate along the granulocytic lineage. Activation of the c-sis/PDGF-2 gene in human hematopoietic cells during monocytic differentiation may serve in the mediation of physiologic functions of the differentiated cells by means of the secretion of potent PDGF-like mitogen., Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., info:eu-repo/semantics/published

Prostate carcinoma cell lines DU-145 and PC-3 express both platelet derived growth factor (PDGF)-1 and PDGF-2/sis genes. Concomitantly, these cells synthesize and secrete PDGF-like proteins, as judged by indirect immunofluorescence and by direct immunoprecipitation with specific PDGF antiserum. Conditioned media derived from DU-145 and PC-3 cells stimulated the incorporation of [3H]thymidine by 3T3 cells and competed with 125I-labeled PDGF for its binding to cell surface receptors of 3T3 cells. The biological activity was stable to heating at 100 degrees C for 10 min, sensitive to reducing agents, and neutralized by the IgG fraction of PDGF antiserum, properties similar to those of authentic PDGF. Both DU-145 and PC-3 cell lines appear to lack receptors for PDGF as indicated by their inability to mitogenically respond to PDGF and receptor binding of 125I-labeled PDGF. Production of PDGF-like proteins by human prostate carcinoma cells may play an important role in a paracrine mode in the organization of the extracellular matrix of the malignant tissue., Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., info:eu-repo/semantics/published

The colony-stimulating factor-1 (CSF-1) regulates survival, growth, and differentiation of monocytes by binding to a single class of high-affinity receptors. The CSF-1 receptor is identical to the product of the c-fms protooncogene. The present studies monitored the effects of TPA and CSF-1 on c-fms gene expression in human monocytes. The results demonstrate that TPA downmodulates the constitutive expression of c-fms mRNA to low but detectable levels. Treatment of human monocytes with TPA was similarly associated with decreases in levels of the 138- and 125-Kd c-fms-encoded proteins. However, the kinetics of c-fms protein downmodulation indicated independent effects of TPA on c-fms expression at the RNA and protein levels. Furthermore, c-fms protein levels subsequently recovered despite persistently low levels of c-fms mRNA. Although previous studies demonstrated that c-fms protein is down-regulated in the presence of CSF-1, the present results indicate that CSF-1 also downregulates levels of c-fms mRNA. Moreover, the results indicate that CSF-1 increases protein kinase C activity in the membrane fraction. Together, these findings suggest that c-fms gene expression is differentially regulated at both the RNA and protein levels after activation of protein kinase C in human monocytes treated with TPA and CSF-1., In Vitro, Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., info:eu-repo/semantics/published

Human malignant epithelial cell lines were analyzed for expression of platelet-derived growth factor (PDGF) genes. Of the 12 cell lines tested, 9, derived from breast, lung, gastric, and ovarian carcinomas, were found to express both PDGF-1 and PDGF-2 genes. The levels of both PDGF-1 and PDGF-2 transcripts were superinduced when these cells were treated with cycloheximide, an inhibitor of protein synthesis. These cells also released an activity that in studies with BALB-c/3T3 cells, inhibited binding of 125I-labeled PDGF and stimulated incorporation of [3H]thymidine. This stimulating activity was inhibited after reduction of the conditioned media by mercaptoethanol or after preincubation with antibodies to PDGF. Moreover, this activity was not affected by heat treatment. Immunoprecipitation studies revealed that breast, lung, and gastric carcinoma cells produced PDGF-like proteins that migrated as 30- and 32-kD species under nonreducing conditions and as 15- and 16-kD species under reducing conditions. In contrast, malignant cells of ovarian origin produced 14-16-kD PDGF-like proteins that were unchanged in mobility after reduction. As PDGF receptors were not detected on these malignant epithelial cells, the production of PDGF-like proteins may affect other cells in the microenvironment by paracrine mechanisms and may contribute to excessive cell proliferation, inflammatory reactions, and connective tissue remodeling seen in certain carcinomas., Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., info:eu-repo/semantics/published

Phorbol esters induce the differentiation of human myeloid leukemia cells HL-60 and U-937 along the monocytic-macrophage lineage. This process has been associated with the induction of several cellular protooncogenes, including the c-fos and c-fms genes. We now report that phorbol ester-induced differentiation of the HL-60 and U-937 cells results in the induction of the expression of the c-sis platelet-derived growth factor 2 (PDGF-2) protooncogene. sis mRNA transcripts were not detectable in the uninduced cells but were detectable within 12 hr of phorbol ester induction. Concomitantly, the induced cells were shown to synthesize and secrete biologically active PDGF-like proteins, identified in the conditioned medium of the phorbol ester-treated cells by direct immunoprecipitation with PDGF antiserum. Addition of cycloheximide to phorbol ester-treated HL-60 cells superinduced sis mRNA transcripts. c-sis gene transcripts were also detected in freshly isolated human monocytes but not in human granulocytes or in HL-60 cells induced to differentiate along the granulocytic lineage. Activation of the c-sis/PDGF-2 gene in human hematopoietic cells during monocytic differentiation may serve in the mediation of physiologic functions of the differentiated cells by means of the secretion of potent PDGF-like mitogen., Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., info:eu-repo/semantics/published

In human umbilical vein and bovine aortic endothelial cells in culture c-sis gene expression and secretion of platelet-derived growth factor (PDGF) has been previously demonstrated. We now report the presence of PDGF-1 and PDGF-2/sis mRNA transcripts in primary cultures of human iliac artery endothelial cells (HIA-EC). Concomitantly, these cells synthesize and secrete PDGF-like proteins identified by direct immunoprecipitation with specific PDGF antiserum. The PDGF proteins secreted by HIA-EC have molecular weights of 31 and 35 kd under nonreducing conditions. Upon reduction these proteins are converted to the monomeric 15- and 16-kd forms. Conditioned media derived from HIA-EC stimulated the incorporation of 3H-thymidine by 3T3 cells and competed with 125I-PDGF for its binding to 3T3 cell membrane receptors. The biologic activity was stable to heating at 100 degrees C for 10 min and sensitive to reducing agents, properties similar to those of authentic PDGF. Production of PDGF-like mitogen by the human arterial endothelial cells may play an important role in the paracrine modulation of arterial wall regeneration following vascular injury., Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., FLWNA, info:eu-repo/semantics/published

Human T cells immortalized by human T lymphotropic virus (HTLV)-I and HTLV-II express the genes encoding both chains of platelet-derived growth factor (PDGF). These cells produce biologically active PDGF-like molecules of 31 and 32 kD, identified in the conditioned media of the virus-infected cells by direct immunoprecipitation, under non-reducing conditions, with antisera to PDGF. Upon reduction, the PDGF-like molecules are converted to mitogenically inactive single chains of 14 and 15 kD. The HTLV-transformed cells produce PDGF-like molecules regardless of their ability to produce viral particles. No PDGF-related mRNAs, PDGF-like proteins, nor PDGF-like mitogenic activity were detected in normal human T cells stimulated by phytohemagglutinin or in a T cell line which is not infected by HTLV. It is possible that one of the pathways of immortalization of T cells by HTLV-I or II might be by activation of PDGF-related genes., Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., info:eu-repo/semantics/published

Prostate carcinoma cell lines DU-145 and PC-3 express both platelet derived growth factor (PDGF)-1 and PDGF-2/sis genes. Concomitantly, these cells synthesize and secrete PDGF-like proteins, as judged by indirect immunofluorescence and by direct immunoprecipitation with specific PDGF antiserum. Conditioned media derived from DU-145 and PC-3 cells stimulated the incorporation of [3H]thymidine by 3T3 cells and competed with 125I-labeled PDGF for its binding to cell surface receptors of 3T3 cells. The biological activity was stable to heating at 100 degrees C for 10 min, sensitive to reducing agents, and neutralized by the IgG fraction of PDGF antiserum, properties similar to those of authentic PDGF. Both DU-145 and PC-3 cell lines appear to lack receptors for PDGF as indicated by their inability to mitogenically respond to PDGF and receptor binding of 125I-labeled PDGF. Production of PDGF-like proteins by human prostate carcinoma cells may play an important role in a paracrine mode in the organization of the extracellular matrix of the malignant tissue., Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., info:eu-repo/semantics/published