[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 36 of about 36
1. Kemp EG, Harnett AN, Chatterjee S: Preoperative topical and intraoperative local mitomycin C adjuvant therapy in the management of ocular surface neoplasias. Br J Ophthalmol; 2002 Jan;86(1):31-4
Hazardous Substances Data Bank. MITOMYCIN C .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preoperative topical and intraoperative local mitomycin C adjuvant therapy in the management of ocular surface neoplasias.
  • AIMS: To demonstrate the efficacy of mitomycin C as adjuvant therapy preoperatively and intraoperatively in the management of recurrent or diffuse ocular surface neoplasias.
  • METHODS: The case notes of 11 patients receiving mitomycin C adjuvant therapy as 0.04% eye drops four times a day in two weekly courses preoperatively and/or a single intraoperative application of 0.4 mg/ml of mitomycin C were reviewed.
  • Seven patients had additional limited local excision of the residual tumour mass and one had cryotherapy.
  • RESULTS: All cases showed a favourable response to mitomycin C adjuvant therapy with regression in size or retardation of a rapid growth pattern and no serious sequelae.
  • CONCLUSION: In this series, mitomycin C adjuvant therapy of recurrent or diffuse ocular surface neoplasias was well tolerated and showed favourable clinical results.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Carcinoma / drug therapy. Eye Neoplasms / drug therapy. Melanoma / drug therapy. Mitomycin / administration & dosage
  • [MeSH-minor] Administration, Topical. Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant / methods. Female. Follow-Up Studies. Humans. Intraoperative Care / methods. Male. Middle Aged. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / surgery. Ophthalmic Solutions / administration & dosage. Preoperative Care / methods

  • MedlinePlus Health Information. consumer health - Eye Cancer.
  • MedlinePlus Health Information. consumer health - Melanoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Ophthalmol. 1999 Nov;128(5):638-40 [10577537.001]
  • [Cites] Br J Ophthalmol. 1998 May;82(5):476-9 [9713051.001]
  • [Cites] Arch Ophthalmol. 2000 Jul;118(7):885-91 [10900099.001]
  • [Cites] Trans Am Ophthalmol Soc. 1976;74:154-71 [325854.001]
  • [Cites] Am J Ophthalmol. 1979 Jan;87(1):84-6 [434057.001]
  • [Cites] Trans Am Ophthalmol Soc. 1980;78:290-300 [7257061.001]
  • [Cites] Am J Ophthalmol. 1983 Mar;95(3):359-63 [6829682.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1990 Oct;31(10):2136-44 [2211010.001]
  • [Cites] Ophthalmology. 1990 Sep;97(9):1204-10 [2122349.001]
  • [Cites] Ophthalmology. 1991 Mar;98(3):317-21 [2023752.001]
  • [Cites] Arch Ophthalmol. 1991 Aug;109(8):1141-6 [1907822.001]
  • [Cites] Trans Am Ophthalmol Soc. 1991;89:285-98; discussion 298-301 [1808811.001]
  • [Cites] Ophthalmology. 1992 Dec;99(12):1809-14 [1480395.001]
  • [Cites] Ophthalmology. 1997 May;104(5):844-8 [9160032.001]
  • [Cites] Ophthalmic Surg Lasers. 1997 Aug;28(8):662-9 [9268998.001]
  • [Cites] Ophthalmology. 1997 Dec;104(12):2085-93 [9400769.001]
  • [Cites] Am J Ophthalmol. 1997 Sep;124(3):303-11 [9439356.001]
  • [Cites] Cornea. 2000 Jan;19(1):1-6 [10631999.001]
  • (PMID = 11801499.001).
  • [ISSN] 0007-1161
  • [Journal-full-title] The British journal of ophthalmology
  • [ISO-abbreviation] Br J Ophthalmol
  • [Language] eng
  • [Publication-type] Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Ophthalmic Solutions; 50SG953SK6 / Mitomycin
  • [Other-IDs] NLM/ PMC1770962
  •  go-up   go-down


2. Yoon WH, Jung YJ, Kim TD, Li G, Park BJ, Kim JY, Lee YC, Kim JM, Park JI, Park HD, No ZS, Lim K, Hwang BD, Kim YS: Gabexate mesilate inhibits colon cancer growth, invasion, and metastasis by reducing matrix metalloproteinases and angiogenesis. Clin Cancer Res; 2004 Jul 1;10(13):4517-26
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Gabexate mesilate (GM), a synthetic protease inhibitor, has an antiproteinase activity on various types of plasma serine proteases.
  • Liver metastatic ability and tumorigenic potential in nude mice were remarkably reduced on treatment with GM.
  • Immunohistochemical analysis of GM-treated tumors in mice showed a marked increase in apoptosis and a significant reduction in tumor angiogenesis.
  • Human umbilical vein endothelial cell proliferation, tube formation, and neoangiogenesis in the rabbit cornea and Matrigel implanted in mice were significantly inhibited by GM.
  • [MeSH-major] Colonic Neoplasms / drug therapy. Gabexate / pharmacology. Neovascularization, Pathologic
  • [MeSH-minor] Animals. Capillaries / metabolism. Cell Line. Cell Line, Tumor. Cell Movement. Cell Proliferation. Cells, Cultured. Collagen / chemistry. Collagen / metabolism. Dose-Response Relationship, Drug. Drug Combinations. Endothelium, Vascular / cytology. Female. Gels. Humans. Immunohistochemistry. Laminin / chemistry. Laminin / metabolism. Liver / pathology. Liver Neoplasms / pathology. Male. Matrix Metalloproteinase 2 / biosynthesis. Matrix Metalloproteinase 9 / biosynthesis. Matrix Metalloproteinases / metabolism. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Nude. Neoplasm Invasiveness. Neoplasm Metastasis. Proteoglycans / chemistry. Proteoglycans / metabolism. Rabbits. Serine Proteinase Inhibitors / pharmacology. Temperature. Time Factors. Umbilical Veins / cytology. Urokinase-Type Plasminogen Activator / biosynthesis

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15240544.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Gels; 0 / Laminin; 0 / Proteoglycans; 0 / Serine Proteinase Inhibitors; 119978-18-6 / matrigel; 4V7M9137X9 / Gabexate; 9007-34-5 / Collagen; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


3. Rogers MS, Christensen KA, Birsner AE, Short SM, Wigelsworth DJ, Collier RJ, D'Amato RJ: Mutant anthrax toxin B moiety (protective antigen) inhibits angiogenesis and tumor growth. Cancer Res; 2007 Oct 15;67(20):9980-5
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutant anthrax toxin B moiety (protective antigen) inhibits angiogenesis and tumor growth.
  • Bacillus anthracis protective antigen (PA), the B subunit of the binary anthrax toxin, binds to the cellular receptors capillary morphogenesis gene 2 protein and tumor endothelial marker 8 with high affinity.
  • Here, we show that wild-type PA inhibits both vascular endothelial growth factor-induced and basic fibroblast growth factor-induced angiogenesis at moderate but statistically significant levels.
  • Structure-activity studies identified a PA mutant that exhibited markedly enhanced inhibition of angiogenesis and also inhibited tumor growth in vivo.
  • We conclude that high-affinity anthrax toxin receptor (ATR) ligands, such as PA and PASSSR, are angiogenesis inhibitors and that ATRs are useful targets for antiangiogenic therapy.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Antigens, Bacterial / pharmacology. Bacterial Toxins / pharmacology. Carcinoma, Lewis Lung / blood supply. Carcinoma, Lewis Lung / drug therapy
  • [MeSH-minor] Animals. Cell Growth Processes / drug effects. Cornea / blood supply. Corneal Neovascularization / chemically induced. Endothelial Cells / cytology. Endothelial Cells / drug effects. Endothelial Cells / metabolism. Fibroblast Growth Factor 2 / antagonists & inhibitors. Humans. Membrane Proteins / biosynthesis. Membrane Proteins / metabolism. Mice. Mice, Inbred C57BL. Mutation. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / metabolism. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / pathology. Neovascularization, Physiologic / drug effects. Receptors, Cell Surface / biosynthesis. Receptors, Cell Surface / metabolism. Receptors, Peptide. Vascular Endothelial Growth Factor A / antagonists & inhibitors

  • Genetic Alliance. consumer health - Anthrax.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17942931.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANTXR1 protein, human; 0 / ANTXR2 protein, human; 0 / Angiogenesis Inhibitors; 0 / Antigens, Bacterial; 0 / Bacterial Toxins; 0 / Membrane Proteins; 0 / Neoplasm Proteins; 0 / Receptors, Cell Surface; 0 / Receptors, Peptide; 0 / Vascular Endothelial Growth Factor A; 0 / anthrax toxin; 103107-01-3 / Fibroblast Growth Factor 2
  •  go-up   go-down


Advertisement
4. Guha S, Eibl G, Kisfalvi K, Fan RS, Burdick M, Reber H, Hines OJ, Strieter R, Rozengurt E: Broad-spectrum G protein-coupled receptor antagonist, [D-Arg1,D-Trp5,7,9,Leu11]SP: a dual inhibitor of growth and angiogenesis in pancreatic cancer. Cancer Res; 2005 Apr 1;65(7):2738-45
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • SPA also significantly attenuated the growth of HPAF-II tumor xenografts in nude mice beyond the treatment period.
  • Interestingly, SPA markedly increased apoptosis but moderately decreased proliferation marker, Ki-67 in the tumor xenografts implying additional mechanism(s) for the significant growth inhibitory effect observed in vivo.
  • SPA inhibited CXCR2-mediated Ca(2+) mobilization and blocked specifically IL-8/CXCL8-induced angiogenesis in rat corneal micropocket assay in vivo.
  • A salient feature of the results presented here is that SPA markedly reduced tumor-associated angiogenesis in the HPAF-II xenografts in vivo.
  • Our results show that SPA, a broad-spectrum GPCR antagonist attenuates tumor growth in pancreatic cancer via a dual mechanism involving both the antiproliferative and antiangiogenic properties.
  • We conclude that this novel dual-inhibitory property of SPA could be of significant therapeutic value in pancreatic cancer, when used in combination with other antiproliferative and/or antiangiogenic agents.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / drug therapy. Pancreatic Neoplasms / drug therapy. Receptors, G-Protein-Coupled / antagonists & inhibitors. Substance P / analogs & derivatives. Substance P / pharmacology
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Growth Processes / drug effects. Cornea / blood supply. DNA, Neoplasm / biosynthesis. Humans. Interleukin-8 / antagonists & inhibitors. Ki-67 Antigen / biosynthesis. Male. Mice. Mice, Nude. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / pathology. Neovascularization, Physiologic / drug effects. Rats. Xenograft Model Antitumor Assays

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15805273.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK55003; United States / NCI NIH HHS / CA / P50CA90388
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Interleukin-8; 0 / Ki-67 Antigen; 0 / Receptors, G-Protein-Coupled; 0 / substance P, Arg(1)-Trp(5,7,9)-Leu(11)-; 33507-63-0 / Substance P
  •  go-up   go-down


5. Jia WD, Xu GL, Sun HC, Wang L, Xu RN, Xue Q: Effect of octreotide on angiogenesis induced by hepatocellular carcinoma in vivo. Hepatobiliary Pancreat Dis Int; 2003 Aug;2(3):404-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: LCI-D20 corneal micropocket model in nude mouse was used to dynamically observe angiogenesis under a stereoscopic zoom microscope and a digital camera system and to evaluate the effect of octreotide on angiogenesis.
  • Male nude mice were subcutaneously implanted with LCI-D20 tumor tissues for tumor xenograft studies.
  • Microvessel density in CD34-stained tumor sections was analyzed by immunohistochemical SP method.
  • RESULTS: Tumor tissues from LCI-D20 implanted into the corneal micropocket induced angiogenesis.
  • When animals received systemic octreotide treatment, angiogenesis response in the cornea of mice was moderate, the appearance of vascular buds was delayed, and the new capillaries were sparse and grew slowly.
  • Compared with the control group, the neovascularization induced by HCC in the cornea of mice was markedly inhibited on day 7, 9, 12, 15, 18 and 21 after implantation in the octreotide-treated group (P<0.05).
  • Immunohistochemical studies of tumor tissues revealed decreased microvessel density in the octreotide-treated animals as compared with the controls (21.7+/-4.27 versus 31.8+/-3.87, P<0.01).
  • CONCLUSION: Somatostatin analogue octreotide is able to inhibit angiogenesis induced by HCC in vivo and may provide a new approach to the treatment of HCC.
  • [MeSH-major] Antineoplastic Agents, Hormonal / pharmacology. Carcinoma, Hepatocellular / drug therapy. Liver Neoplasms, Experimental / drug therapy. Neovascularization, Pathologic / drug therapy. Octreotide / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Cornea / blood supply. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Xenograft Model Antitumor Assays

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14599948.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; RWM8CCW8GP / Octreotide
  •  go-up   go-down


6. da Silva BB, da Silva Júnior RG, Borges US, da Silveira Filho MA, Pimentel IC, Gebrim LH, Simões Mde J, Baracat EC: Quantification of angiogenesis induced in rabbit cornea by breast carcinoma of women treated with tamoxifen. J Surg Oncol; 2005 May 1;90(2):77-80
Hazardous Substances Data Bank. TAMOXIFEN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Quantification of angiogenesis induced in rabbit cornea by breast carcinoma of women treated with tamoxifen.
  • BACKGROUND: The aim of this study was to evaluate the effect of tamoxifen on angiogenesis induced in rabbit cornea by breast carcinoma from post-menopausal women.
  • METHODS: Thirteen post-menopausal women with operable, estrogen receptor-positive breast carcinomas, treated with 20 mg of tamoxifen daily for 30 days prior to undergoing definitive surgery, participated in this study.
  • Twenty-six virgin female New Zealand white rabbits, 3-4 months old, weighing approximately 2.5 kg each, were divided into two groups of 13 animals and received corneal implants of tumor either pre- or post-tamoxifen treatment.
  • After 10 days, the animals were sacrificed, the region of the cornea between the tumor implant and the limbus was removed and quantification of angiogenesis was carried out by evaluating the entire hematoxylin-eosin stained slide, using a 10x objective lens (100x magnification).
  • RESULTS: Mean microvessel count was 106.8 +/- 5.9 pre-tamoxifen treatment and 54 +/- 5.6 post-treatment.
  • According to Student t-test, there was a significant reduction in mean microvessel density following treatment with tamoxifen (P < 0.001).
  • CONCLUSIONS: Rabbit cornea proved to be an interesting experimental model for the quantification of angiogenesis.
  • Tamoxifen, when administered for 30 days to post-menopausal women with breast cancer, significantly inhibited angiogenesis induced by tumor fragments in rabbit cornea.
  • [MeSH-major] Breast Neoplasms / drug therapy. Cornea / drug effects. Eye Neoplasms / blood supply. Neovascularization, Pathologic / etiology. Tamoxifen / pharmacology
  • [MeSH-minor] Animals. Female. Humans. Neoplasm Transplantation. Postmenopause. Rabbits

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Eye Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15844191.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 094ZI81Y45 / Tamoxifen
  •  go-up   go-down


7. Goyal S, Chauhan SK, Zhang Q, Dana R: Amelioration of murine dry eye disease by topical antagonist to chemokine receptor 2. Arch Ophthalmol; 2009 Jul;127(7):882-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Amelioration of murine dry eye disease by topical antagonist to chemokine receptor 2.
  • OBJECTIVE: To determine the effect of a topical antagonist to the chemokine receptor 2 (CCR2) in a murine model of dry eye disease.
  • METHODS: The effects of a topical CCR2 antagonist and a vehicle control treatment were studied in murine dry eyes.
  • A controlled environment chamber induced dry eye by exposing mice to high-flow desiccated air.
  • Corneal fluorescein staining and enumeration of corneal CD11b(+) and conjunctival CD3(+) T cells were performed in the different groups.
  • Real-time polymerase chain reaction was performed to quantify expression of different inflammatory cytokine transcripts in the cornea and conjunctiva.
  • RESULTS: Eyes receiving the formulation containing CCR2 antagonist showed a significant decrease in corneal fluorescein staining and decreased infiltration of corneal CD11b(+) cells and conjunctival T cells compared with the vehicle-treated and untreated dry eye groups.
  • The CCR2 antagonist also significantly decreased messenger RNA expression levels of interleukins 1alpha and 1beta in the cornea, and tumor necrosis factor alpha and interleukin 1beta in the conjunctiva.
  • CONCLUSION: Topical application of CCR2 antagonist is associated with significant improvement in dry eye disease and is reflected by a decrease in inflammation at the clinical, molecular, and cellular levels.
  • Clinical Relevance Topical application of CCR2 antagonist may hold promise as a therapeutic modality in dry eye disease.
  • [MeSH-major] Disease Models, Animal. Dry Eye Syndromes / drug therapy. Receptors, CCR2 / antagonists & inhibitors
  • [MeSH-minor] Administration, Topical. Animals. Antigens, CD11b / immunology. Antigens, CD3 / immunology. Conjunctiva / immunology. Cornea / immunology. Female. Fluorescent Antibody Technique, Indirect. Interleukin-1alpha / genetics. Interleukin-1beta / genetics. Lymphocyte Count. Mice. Mice, Inbred C57BL. Monocytes / immunology. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. T-Lymphocytes / immunology. Tumor Necrosis Factor-alpha / genetics

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19597109.001).
  • [ISSN] 1538-3601
  • [Journal-full-title] Archives of ophthalmology (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch. Ophthalmol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Antigens, CD3; 0 / Ccr2 protein, mouse; 0 / Interleukin-1alpha; 0 / Interleukin-1beta; 0 / RNA, Messenger; 0 / Receptors, CCR2; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


8. Priyadarshini O, Biswas G, Biswas S, Padhi R, Rath S: Neoadjuvant chemotherapy in recurrent sebaceous carcinoma of eyelid with orbital invasion and regional lymphadenopathy. Ophthal Plast Reconstr Surg; 2010 Sep-Oct;26(5):366-8
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neoadjuvant chemotherapy in recurrent sebaceous carcinoma of eyelid with orbital invasion and regional lymphadenopathy.
  • A 35-year-old man presented with a recurrent temporal conjunctival mass (25 × 12 mm) involving about six-clock hours of the limbus in the left eye.
  • The mass encroached onto the temporal half of cornea and showed surface keratin, large intrinsic and feeder vessels.
  • It infiltrated the deep corneal stroma.
  • Ultrasound biomicroscopy confirmed infiltration of deep corneal stroma without intraocular invasion.
  • Surgery involved excision of the conjunctival component with 4-mm margin, lamellar sclerectomy and a penetrating sclerokeratoplasty with 3 mm of healthy corneal margin.
  • A thin layer of deep corneal stroma and all conjunctival margins were uninvolved.
  • At thirty-six weeks after treatment the left eye recorded a visual acuity of finger counting at 1 meter distance and no recurrence.
  • [MeSH-major] Adenocarcinoma, Sebaceous / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Eyelid Neoplasms / drug therapy. Neoplasm Recurrence, Local / drug therapy. Orbital Neoplasms / drug therapy. Sebaceous Gland Neoplasms / drug therapy
  • [MeSH-minor] Cisplatin / administration & dosage. Fluorouracil / administration & dosage. Humans. Lymph Node Excision. Lymphatic Metastasis. Male. Middle Aged. Neoadjuvant Therapy. Neoplasm Invasiveness. Tomography, X-Ray Computed

  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20856079.001).
  • [ISSN] 1537-2677
  • [Journal-full-title] Ophthalmic plastic and reconstructive surgery
  • [ISO-abbreviation] Ophthal Plast Reconstr Surg
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
  •  go-up   go-down


9. Zaki AA, Farid SF: Management of intraepithelial and invasive neoplasia of the cornea and conjunctiva: a long-term follow up. Cornea; 2009 Oct;28(9):986-8
Hazardous Substances Data Bank. CYCLOSPORIN A .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of intraepithelial and invasive neoplasia of the cornea and conjunctiva: a long-term follow up.
  • PURPOSE: The aim of this work is to report the long-term results of using immunotherapy for the management of cornea and conjunctiva intraepithelial neoplasia and squamous cell carcinoma after surgical excision of the neoplasm.
  • METHODS: Ten eyes of 10 patients with cornea and conjunctiva intraepithelial neoplasia or squamous cell carcinoma had wide surgical excisions of the neoplasm after evaluation of the level of corneal involvement using ultrasound biomicroscopy.
  • All eyes received topical cyclosporine A (0.05%) and topical mitomycin C (0.01%) 4 times daily for 12 weeks after surgery.
  • Epithelial toxicity (punctate keratopathy) occurred in 3 eyes, ocular irritation and mild conjunctival hyperemia in 5 eyes, and lid toxicity in 2 cases during the treatment with mitomycin C.
  • There were no serious complications that necessitated stopping the treatment.
  • CONCLUSION: During a 2-year follow-up period, the use of topical cyclosporine A (0.05%) combined with mitomycin C (0.01%) as an adjunctive treatment after surgical excision in cornea and conjunctiva intraepithelial neoplasia and squamous cell carcinoma was found to prevent tumor recurrence, especially in extensive lesions, when surgical excision cannot ensure a tumor-free margin.
  • [MeSH-major] Carcinoma in Situ / therapy. Carcinoma, Squamous Cell / therapy. Conjunctival Neoplasms / therapy. Corneal Diseases / therapy. Eye Neoplasms / therapy
  • [MeSH-minor] Aged. Chemotherapy, Adjuvant. Combined Modality Therapy. Cyclosporine / administration & dosage. Drug Therapy, Combination. Female. Follow-Up Studies. Humans. Male. Mitomycin / administration & dosage. Neoplasm Invasiveness. Ophthalmologic Surgical Procedures. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Corneal Disorders.
  • MedlinePlus Health Information. consumer health - Eye Cancer.
  • Hazardous Substances Data Bank. MITOMYCIN C .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Cornea. 2012 Apr;31(4):465 [22314824.001]
  • [CommentIn] Cornea. 2011 Apr;30(4):486; author reply 486-7 [21107255.001]
  • (PMID = 19724215.001).
  • [ISSN] 1536-4798
  • [Journal-full-title] Cornea
  • [ISO-abbreviation] Cornea
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 50SG953SK6 / Mitomycin; 83HN0GTJ6D / Cyclosporine
  •  go-up   go-down


10. Yeh S, Fine HA, Smith JA: Corneal verticillata after dual anti-epidermal growth factor receptor and anti-vascular endothelial growth factor receptor 2 therapy (vandetanib) for anaplastic astrocytoma. Cornea; 2009 Jul;28(6):699-702
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Corneal verticillata after dual anti-epidermal growth factor receptor and anti-vascular endothelial growth factor receptor 2 therapy (vandetanib) for anaplastic astrocytoma.
  • PURPOSE: To describe a patient with a history of epithelial basement membrane dystrophy who developed symptomatic corneal verticillata after vandetanib therapy for anaplastic astrocytoma.
  • RESULTS: A 48-year-old female patient with a history of anaplastic astrocytoma status post resection, external beam radiation, and chemotherapy presented with glare symptoms, decreased contrast sensitivity, and increased lacrimation after approximately 12 months of therapy with the anti-epidermal growth factor receptor (EGFR) and anti-vascular endothelial growth factor receptor 2 protein tyrosine kinase inhibitor, vandetanib.
  • Ophthalmic examination revealed diffuse corneal verticillata and fine subepithelial opacities.
  • Therapy with carboxymethylcellulose, 5% sodium chloride ointment, and a decrease in the dose of vandetanib led to an improvement in the patient's ophthalmic symptoms despite persistence of the corneal findings.
  • The patient remained under surveillance for tumor recurrence.
  • CONCLUSIONS: Vandetanib (ZD6474), a protein tyrosine kinase inhibitor with dual anti-EGFR and anti-vascular endothelial growth factor receptor 2 action, may have contributed to the formation of corneal verticillata in our patient.
  • Inhibition of EGFR, which is involved with corneal epithelial cell migration and wound healing, may play a role in the pathogenesis underlying corneal vortex keratopathy and ocular surface conditions with significant epithelial turnover.
  • [MeSH-major] Astrocytoma / drug therapy. Brain Neoplasms / drug therapy. Corneal Diseases / chemically induced. Neoplasm Recurrence, Local / drug therapy. Piperidines / adverse effects. Quinazolines / adverse effects. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors
  • [MeSH-minor] Cellulase / therapeutic use. Corneal Opacity / chemically induced. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Therapy, Combination. Female. Humans. Middle Aged. Ointments. Retrospective Studies. Sodium Chloride / therapeutic use

  • Genetic Alliance. consumer health - Anaplastic Astrocytoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • MedlinePlus Health Information. consumer health - Corneal Disorders.
  • Hazardous Substances Data Bank. SODIUM CHLORIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19512898.001).
  • [ISSN] 1536-4798
  • [Journal-full-title] Cornea
  • [ISO-abbreviation] Cornea
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Ointments; 0 / Piperidines; 0 / Quinazolines; 451W47IQ8X / Sodium Chloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 3.2.1.4 / Cellulase; EC 3.2.1.4 / carboxymethylcellulase
  •  go-up   go-down


11. Karasawa K, Matsuda H, Tanaka A: Superficial keratectomy and topical mitomycin C as therapy for a corneal squamous cell carcinoma in a dog. J Small Anim Pract; 2008 Apr;49(4):208-10
Hazardous Substances Data Bank. MITOMYCIN C .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Superficial keratectomy and topical mitomycin C as therapy for a corneal squamous cell carcinoma in a dog.
  • A 10-year-old female West Highland white terrier was presented with refractory hyperplastic keratitis of the left cornea of one month's duration.
  • At this time, a vascularised and rough lesion 5 mm in diameter was observed on the left cornea.
  • No other abnormality was recognised on the affected eye.
  • The corneal neoplasm was surgically removed and histologically diagnosed as a squamous cell carcinoma.
  • For two months after the surgery, 0.04 percent mitomycin C (MMC) eye drops were applied as adjuvant chemotherapy.
  • Primary corneal squamous cell carcinoma with no history of keratoconjunctivitis sicca is rare in dogs.
  • In the present report, surgical removal of the neoplasm was combined with the topical administration of the anticancer drug mitomycin C and a good prognosis was obtained.
  • The result indicates that the combination treatment used in this case may be an appropriate therapeutic choice for corneal squamous cell carcinoma in dogs.
  • [MeSH-major] Carcinoma, Squamous Cell / veterinary. Corneal Diseases / veterinary. Dog Diseases / drug therapy. Dog Diseases / surgery. Eye Neoplasms / veterinary
  • [MeSH-minor] Administration, Topical. Animals. Combined Modality Therapy. Corneal Surgery, Laser / methods. Corneal Surgery, Laser / veterinary. Dogs. Female. Mitomycin / administration & dosage. Mitomycin / therapeutic use. Prognosis. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Corneal Disorders.
  • MedlinePlus Health Information. consumer health - Eye Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17725585.001).
  • [ISSN] 0022-4510
  • [Journal-full-title] The Journal of small animal practice
  • [ISO-abbreviation] J Small Anim Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 50SG953SK6 / Mitomycin
  •  go-up   go-down


12. Iovieno A, Lambiase A, Moretti C, Perrella E, Bonini S: Therapeutic effect of topical 5-fluorouracil in conjunctival squamous carcinoma is associated with changes in matrix metalloproteinases and tissue inhibitor of metalloproteinases expression. Cornea; 2009 Aug;28(7):821-4
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapeutic effect of topical 5-fluorouracil in conjunctival squamous carcinoma is associated with changes in matrix metalloproteinases and tissue inhibitor of metalloproteinases expression.
  • PURPOSE: To evaluate matrix metalloproteinases (MMP)-2, MMP-9, and tissue inhibitor of metalloproteinase (TIMP)-1 expression in a case of conjunctival intraepithelial squamous cell carcinoma (SCC) treated with topical 5-fluorouracil (5-FU) chemotherapy.
  • Conjunctival biopsies, impression cytologies, and tear samples were taken from the mass and the contralateral healthy eye.
  • An overexpression of MMP-2, MMP-9, and TIMP-1 was observed in the tumor by immunohistochemistry.
  • Clinical resolution of the neoplasm obtained using topical 5-FU was accompanied by a reduction in the expression of MMP-2, MMP-9, and TIMP-1 in tears and dysplastic conjunctival epithelium.
  • CONCLUSIONS: In our case report, we have shown that gelatinase and TIMP-1 are unregulated in conjunctival SCC and can be monitored as a marker of response to topical chemotherapy.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Conjunctival Neoplasms / drug therapy. Fluorouracil / therapeutic use. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 9 / metabolism. Tissue Inhibitor of Metalloproteinase-1 / metabolism
  • [MeSH-minor] Administration, Topical. Aged. Biomarkers, Tumor / metabolism. Carcinoma in Situ / drug therapy. Carcinoma in Situ / enzymology. Humans. Male. Neoplasm Proteins / metabolism

  • Hazardous Substances Data Bank. FLUOROURACIL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19574900.001).
  • [ISSN] 1536-4798
  • [Journal-full-title] Cornea
  • [ISO-abbreviation] Cornea
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Tissue Inhibitor of Metalloproteinase-1; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9; U3P01618RT / Fluorouracil
  •  go-up   go-down


13. Khokhar S, Soni A, SinghSethi H, Sudan R, Sony P, Pangtey MS: Combined surgery, cryotherapy, and mitomycin-C for recurrent ocular surface squamous neoplasia. Cornea; 2002 Mar;21(2):189-91
Hazardous Substances Data Bank. MITOMYCIN C .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined surgery, cryotherapy, and mitomycin-C for recurrent ocular surface squamous neoplasia.
  • PURPOSE: To report the outcome of combined excision, cryotherapy, and antimetabolite treatment of recurrent ocular surface squamous neoplasia.
  • METHODS: The patients with recurrent ocular surface squamous neoplasia were treated by excision of lesion, cryotherapy of limbus, and conjunctival margin followed by 0.02% Mitomycin C application at the time of surgery.
  • RESULTS: A total of five eyes of five patients with recurrent ocular surface squamous neoplasia were treated by combined excision, cryotherapy, and Mitomycin C.
  • Histopathologic diagnosis included invasive squamous cell carcinoma in four cases and squamous dysplasia in one case.
  • CONCLUSION: Combining excision with cryotherapy and Mitomycin C application at the time of surgery is a very effective therapy for recurrent ocular surface squamous neoplasia.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Carcinoma, Squamous Cell / therapy. Cryosurgery. Eye Neoplasms / therapy. Mitomycin / therapeutic use. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / surgery
  • [MeSH-minor] Adult. Combined Modality Therapy. Conjunctival Neoplasms / therapy. Corneal Diseases / therapy. Humans. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Eye Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11862092.001).
  • [ISSN] 0277-3740
  • [Journal-full-title] Cornea
  • [ISO-abbreviation] Cornea
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 50SG953SK6 / Mitomycin
  •  go-up   go-down


14. Yuen HK, Yeung EF, Chan NR, Chi SC, Lam DS: The use of postoperative topical mitomycin C in the treatment of recurrent conjunctival papilloma. Cornea; 2002 Nov;21(8):838-9
Hazardous Substances Data Bank. MITOMYCIN C .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The use of postoperative topical mitomycin C in the treatment of recurrent conjunctival papilloma.
  • PURPOSE: To describe the use of postoperative topical mitomycin C (MMC) in the treatment of recurrent conjunctival papilloma.
  • He was then treated with excision by cryotherapy, followed by a 2-week course of topical MMC eyedrops prescribed at postoperative day 7 (0.02 mg/mL, four times daily).
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Conjunctival Neoplasms / drug therapy. Mitomycin / therapeutic use. Neoplasm Recurrence, Local / drug therapy. Papilloma / drug therapy
  • [MeSH-minor] Adult. Conjunctiva / drug effects. Conjunctiva / pathology. Humans. Male. Ophthalmic Solutions. Postoperative Period. Treatment Outcome

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12410049.001).
  • [ISSN] 0277-3740
  • [Journal-full-title] Cornea
  • [ISO-abbreviation] Cornea
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Ophthalmic Solutions; 50SG953SK6 / Mitomycin
  •  go-up   go-down


17. Teicher BA, Alvarez E, Menon K, Esterman MA, Considine E, Shih C, Faul MM: Antiangiogenic effects of a protein kinase Cbeta-selective small molecule. Cancer Chemother Pharmacol; 2002 Jan;49(1):69-77

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The compound 317615 x 2HCl was tested in culture and in vivo in the rat corneal micropocket and in the SW2 small-cell lung carcinoma human tumor xenograft.
  • When administered orally twice daily for 10 days, the compound 317615 x 2HCl markedly decreased the neoangiogenesis induced by VEGF or bFGF in the rat corneal micropocket assay.
  • To assess antitumor efficacy, 317615 x 2HCl was administered orally twice daily to nude mice bearing SW2 xenograft tumors on days 14 through 30 after tumor implantation.
  • The decrease in intratumoral vessels was paralleled by increases in tumor growth delay.
  • Treatment of the tumor-bearing animals with paclitaxel or carboplatin followed by treatment with 317615 x 2HCl resulted in a 2.5- to 3.0-fold increase in tumor growth delay compared with the standard chemotherapeutic agents alone.
  • CONCLUSIONS: 317615 x 2HCl represents a new approach to antiangiogenic therapy in cancer-blocking multiple growth factor signaling pathways in endothelial cells with a single agent.
  • [MeSH-minor] Angiogenesis Inducing Agents / pharmacology. Animals. Aorta, Thoracic / cytology. Aorta, Thoracic / drug effects. Basic Helix-Loop-Helix Transcription Factors. Carcinoma, Small Cell / blood supply. Carcinoma, Small Cell / pathology. Cornea / blood supply. Cornea / pathology. Endothelial Growth Factors / pharmacology. Endothelium, Vascular / cytology. Endothelium, Vascular / drug effects. Female. Humans. Lung Neoplasms / blood supply. Lung Neoplasms / pathology. Lymphokines / pharmacology. Male. Mice. Mice, Nude. Neoplasm Transplantation. Neovascularization, Pathologic / prevention & control. Organic Chemicals. Protein Kinase C beta. Rats. Rats, Inbred F344. Trans-Activators / pharmacology. Tumor Cells, Cultured. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11855754.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 317615 x 2HCl; 0 / Angiogenesis Inducing Agents; 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents, Alkylating; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Endothelial Growth Factors; 0 / Enzyme Inhibitors; 0 / Isoenzymes; 0 / Lymphokines; 0 / Organic Chemicals; 0 / Trans-Activators; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 0 / endothelial PAS domain-containing protein 1; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.13 / Protein Kinase C beta
  •  go-up   go-down


18. Kumar A, D'Souza SS, Tickoo S, Salimath BP, Singh HB: Antiangiogenic and proapoptotic activities of allyl isothiocyanate inhibit ascites tumor growth in vivo. Integr Cancer Ther; 2009 Mar;8(1):75-87
Hazardous Substances Data Bank. ALLYL ISOTHIOCYANATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiangiogenic and proapoptotic activities of allyl isothiocyanate inhibit ascites tumor growth in vivo.
  • The authors investigate the antiangiogenic and proapoptotic effects of mustard essential oil containing allyl isothiocyanate (AITC) and explore its mechanism of action on Ehrlich ascites tumor (EAT) cells.
  • It significantly reduced ascites secretion and tumor cell proliferation by about 80% and inhibited vascular endothelial growth factor expression in tumor-bearing mice in vivo.
  • It also reduced vessel sprouting and exhibited potent antiangiogenic activity in the chorioallantoic membrane and cornea of the rat.
  • The results clearly suggest that AITC inhibits tumor growth by both antiangiogenic and proapoptotic mechanisms.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Carcinoma, Ehrlich Tumor / drug therapy. Isothiocyanates / pharmacology. Neovascularization, Pathologic / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line. Cell Line, Tumor. Cell Proliferation / drug effects. G1 Phase / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Mustard Plant / chemistry. Neoplasm Transplantation. Plant Oils / chemistry. Rabbits. Rats. Vascular Endothelial Growth Factor A / drug effects. Vascular Endothelial Growth Factor A / genetics

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19223371.001).
  • [ISSN] 1534-7354
  • [Journal-full-title] Integrative cancer therapies
  • [ISO-abbreviation] Integr Cancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Isothiocyanates; 0 / Plant Oils; 0 / Vascular Endothelial Growth Factor A; BN34FX42G3 / allyl isothiocyanate
  •  go-up   go-down


19. Robinson JW, Brownstein S, Jordan DR, Hodge WG: Conjunctival mucoepidermoid carcinoma in a patient with ocular cicatricial pemphigoid and a review of the literature. Surv Ophthalmol; 2006 Sep-Oct;51(5):513-9
Hazardous Substances Data Bank. Ofloxacin .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The woman was undergoing mitomycin C injections for ocular cicatricial pemphigoid, diagnosed in the same eye 2 years prior to identification of the neoplasm.
  • The tumor invaded the cornea, sclera, lacrimal gland, regional small nerves, and lymphatics, but did not show intraocular involvement.
  • [MeSH-minor] Basement Membrane / pathology. Biopsy. Drug Therapy, Combination. Female. Fluorometholone / therapeutic use. Humans. Middle Aged. Mitomycin / therapeutic use. Neoplasm Invasiveness. Ofloxacin / therapeutic use


20. Molteni A, Ward WF, Ts'ao CH, Taylor J, Small W Jr, Brizio-Molteni L, Veno PA: Cytostatic properties of some angiotensin I converting enzyme inhibitors and of angiotensin II type I receptor antagonists. Curr Pharm Des; 2003;9(9):751-61
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytostatic properties of some angiotensin I converting enzyme inhibitors and of angiotensin II type I receptor antagonists.
  • Angiotensin converting enzyme (ACE) inhibitors and angiotensin II (AII) type 1 receptor antagonists have strong cytostatic properties on in vitro cultures of many normal and neoplastic cells.
  • ACE inhibitors and AII type 1 receptor antagonists are also effective in reducing excessive vascular neoformation in a model of injury to the cornea of rats and rabbits, and in controlling the excessive angiogenesis observed in the Solt-Farber model of experimentally induced hepatoma, in methylcholantrene or radiation-induced fibrosarcomas, in radiation-induced squamous cell carcinomas and in the MA-16 viral-induced mammary carcinoma of the mouse.
  • Captopril was, in addition, effective in controlling tumor growth in a case of Kaposi's sarcoma in humans.
  • The mitogenic effect of AII is well established and a reduction of AII synthesis may well explain cell and neoplasm delayed growth.
  • Moreover, AII regulates and enhances the activity of several growth factors including transforming growth factor B (TGFB) and smooth muscle actin (SMA); and many of these factors are reduced in tissues of animals treated with ACE inhibitors and AII type 1 receptor antagonists.
  • The ACE inhibitors containing a sulphydril (SH) or thiol radical in their moiety (Captopril and CL242817) seemed to be more effective in controlling fibrosis and the growth of some neoplastic cells than those ACE inhibitors without this thiol radical in their structure, even if the second group of these drugs show in vitro a stronger inhibitory effect on converting enzyme activity.
  • However, although these additional properties are pharmacologically relevant, the blockade of AII synthesis plays an essential role in the cytostatic activity of these two categories of drugs.
  • These observations underline that in addition to the beneficial effect of these drugs on the cardiovascular system, new potential applications are opening for their wider deployment.
  • [MeSH-minor] Animals. Humans. Neoplasms / drug therapy. Neoplasms / metabolism. Receptors, Angiotensin / physiology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12570792.001).
  • [ISSN] 1381-6128
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 24652; United States / NCI NIH HHS / CA / CA 52750; United States / NCI NIH HHS / CA / CA 64239; United States / NIDDK NIH HHS / DK / DK 15612; United States / NHLBI NIH HHS / HL / HL 25106
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiotensin Receptor Antagonists; 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Antineoplastic Agents; 0 / Receptors, Angiotensin
  • [Number-of-references] 70
  •  go-up   go-down


21. Ambati BK, Joussen AM, Ambati J, Moromizato Y, Guha C, Javaherian K, Gillies S, O'Reilly MS, Adamis AP: Angiostatin inhibits and regresses corneal neovascularization. Arch Ophthalmol; 2002 Aug;120(8):1063-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Angiostatin inhibits and regresses corneal neovascularization.
  • OBJECTIVE: To determine the ability of angiostatin and the angiostatin-producing low-metastatic (LM) clone of Lewis lung carcinoma (LLC) to inhibit and regress corneal neovascularization, as compared with the non-angiostatin-producing high-metastatic (HM) clone.
  • METHODS: Three groups of C57BL6/J mice underwent chemical and mechanical denudation of corneal and limbal epithelium.
  • One group remained tumor free while the other 2 were implanted with LLC cells (either the HM or LM clones) subcutaneously the day before, 2 weeks after, or 4 weeks after denudation.
  • Corneas were harvested 2 weeks after tumor implantation (at 2, 4, and 6 weeks after denudation for tumor-free mice).
  • In a second experiment, recombinant angiostatin was delivered continuously for 2 weeks via an osmotic pump in mice with established corneal neovascularization.
  • RESULTS: The mean percentages of neovascularized corneal area in mice 2 weeks after LM-LLC implantation were 4.6%, 3.7%, and 37.0%, at 2, 4, and 6 weeks after scraping, respectively.
  • For tumor-free mice, the corresponding values were 62.0% (P =.003), 68.9% (P =.03), and 59.3% (P =.06).
  • Mice implanted with angiostatin pumps had a 37.7% neovascularized corneal area 2 weeks after implantation and 4 weeks after scraping while mice implanted with sham pumps had 60.5% (P =.007).
  • CONCLUSION: Angiostatin inhibits and regresses corneal neovascularization induced by mechanical and alkali corneal injury.
  • CLINICAL RELEVANCE: This appears to be the first evidence of biologically induced regression of corneal neovascularization, and the first direct demonstration of angiostatin-induced regression of neovascularization in any tissue.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Corneal Neovascularization / drug therapy. Peptide Fragments / therapeutic use. Plasminogen / therapeutic use
  • [MeSH-minor] Angiostatins. Animals. Antigens, CD31 / metabolism. Carcinoma, Lewis Lung / metabolism. Cornea / blood supply. Cornea / drug effects. Cornea / pathology. Fluorophotometry. Infusion Pumps, Implantable. Lung Neoplasms / metabolism. Male. Mice. Mice, Inbred C57BL. Neoplasm Transplantation. Recombinant Proteins

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12149060.001).
  • [ISSN] 0003-9950
  • [Journal-full-title] Archives of ophthalmology (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch. Ophthalmol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31; 0 / Peptide Fragments; 0 / Recombinant Proteins; 86090-08-6 / Angiostatins; 9001-91-6 / Plasminogen
  •  go-up   go-down


22. Liao F, Li Y, O'Connor W, Zanetta L, Bassi R, Santiago A, Overholser J, Hooper A, Mignatti P, Dejana E, Hicklin DJ, Bohlen P: Monoclonal antibody to vascular endothelial-cadherin is a potent inhibitor of angiogenesis, tumor growth, and metastasis. Cancer Res; 2000 Dec 15;60(24):6805-10
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monoclonal antibody to vascular endothelial-cadherin is a potent inhibitor of angiogenesis, tumor growth, and metastasis.
  • Here we show that a monoclonal antibody (BV13) directed to the extracellular region of VE-cad inhibits formation of adherens junctions and capillary-like structures by endothelial cells and blocks angiogenesis in the mouse cornea and in Matrigel plugs in vivo.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Cadherins / immunology. Cell Division / drug effects. Neoplasm Metastasis. Neovascularization, Pathologic. Neovascularization, Physiologic / drug effects
  • [MeSH-minor] Animals. Antigens, CD. Antigens, CD31 / metabolism. Carcinoma, Lewis Lung / drug therapy. Cell Adhesion. Collagen / metabolism. Cornea / drug effects. Dose-Response Relationship, Drug. Drug Combinations. Endothelium / metabolism. Humans. Immunoglobulin G / metabolism. Immunohistochemistry. In Situ Nick-End Labeling. Laminin / metabolism. Lung Neoplasms / drug therapy. Mice. Mice, Nude. Neoplasm Transplantation. Proliferating Cell Nuclear Antigen / metabolism. Proteoglycans / metabolism. Time Factors. Tumor Cells, Cultured

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11156369.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Antigens, CD31; 0 / Cadherins; 0 / Drug Combinations; 0 / Immunoglobulin G; 0 / Laminin; 0 / Proliferating Cell Nuclear Antigen; 0 / Proteoglycans; 0 / cadherin 5; 119978-18-6 / matrigel; 9007-34-5 / Collagen
  •  go-up   go-down


23. Pradilla G, Legnani FG, Petrangolini G, Francescato P, Chillemi F, Tyler BM, Gaini SM, Brem H, Olivi A, DiMeco F: Local delivery of a synthetic endostatin fragment for the treatment of experimental gliomas. Neurosurgery; 2005 Nov;57(5):1032-40; discussion 1032-40
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Local delivery of a synthetic endostatin fragment for the treatment of experimental gliomas.
  • In this study, a synthetic endostatin fragment (EF) was analyzed to determine its anti-angiogenic properties when locally delivered by controlled-release polymers and to establish its effect as a treatment for experimental gliomas.
  • Anti-angiogenic properties of the EF/polymer formulations were evaluated in the rat-cornea micropocket assay.
  • Mean corneal angiogenesis index 20 days after tumor implantation was 4.5 +/- 0.7 for corneas implanted with 40% EF/pCPP:SA compared with controls (8.5 +/- 1.3, P = 0.02).

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6698-703 [10823901.001]
  • [Cites] Angiogenesis. 2004;7(2):105-13 [15516831.001]
  • [Cites] FEBS Lett. 2000 Dec 15;486(3):247-51 [11119712.001]
  • [Cites] Nat Biotechnol. 2001 Jan;19(1):35-9 [11135549.001]
  • [Cites] J Neurooncol. 2000 Oct-Nov;50(1-2):109-20 [11245271.001]
  • [Cites] FASEB J. 2001 Apr;15(6):1044-53 [11292666.001]
  • [Cites] Mol Cell. 2001 Apr;7(4):811-22 [11336704.001]
  • [Cites] Cancer Res. 2001 Sep 15;61(18):6830-7 [11559558.001]
  • [Cites] Adv Anat Pathol. 2002 Jan;9(1):24-36 [11756757.001]
  • [Cites] Neuro Oncol. 2002 Jan;4(1):1-8 [11772427.001]
  • [Cites] Int J Cancer. 2002 Feb 20;97(6):839-45 [11857365.001]
  • [Cites] Nat Med. 2002 May;8(5):427 [11984567.001]
  • [Cites] J Biol Chem. 2002 May 10;277(19):16464-9 [11815623.001]
  • [Cites] Neoplasia. 2002 Nov-Dec;4(6):474-9 [12407440.001]
  • [Cites] FASEB J. 2002 Nov;16(13):1802-4 [12354694.001]
  • [Cites] Crit Rev Eukaryot Gene Expr. 2002;12(3):175-91 [12449342.001]
  • [Cites] Semin Oncol. 2002 Dec;29(6 Suppl 16):15-8 [12516034.001]
  • [Cites] Exp Cell Res. 2003 Feb 15;283(2):230-6 [12581742.001]
  • [Cites] FEBS Lett. 2003 Feb 11;536(1-3):19-24 [12586331.001]
  • [Cites] Neuro Oncol. 2003 Apr;5(2):79-88 [12672279.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4766-71 [12682293.001]
  • [Cites] Methods Find Exp Clin Pharmacol. 2003 Apr;25(3):215-24 [12743627.001]
  • [Cites] Int J Oncol. 2003 Jul;23(1):73-9 [12792778.001]
  • [Cites] J Clin Oncol. 2003 Jun 15;21(12):2299-304 [12805330.001]
  • [Cites] Hum Gene Ther. 2003 Jul 1;14(10):997-1008 [12869217.001]
  • [Cites] Neurosurgery. 2003 Sep;53(3):639-60; discussion 660-1 [12943581.001]
  • [Cites] J Med Chem. 2003 Sep 11;46(19):4165-72 [12954068.001]
  • [Cites] Clin Cancer Res. 2003 Oct 1;9(12):4619-26 [14555538.001]
  • [Cites] J Neurooncol. 2003 Sep;64(3):203-9 [14558595.001]
  • [Cites] Clin Cancer Res. 2003 Nov 1;9(14):5358-69 [14614021.001]
  • [Cites] J Vet Sci. 2001 Aug;2(2):125-30 [14614283.001]
  • [Cites] Cancer Cell. 2003 Nov;4(5):337-41 [14667500.001]
  • [Cites] Curr Pharm Des. 2004;10(1):27-37 [14754403.001]
  • [Cites] Clin Cancer Res. 2004 Feb 15;10(4):1255-62 [14977823.001]
  • [Cites] Mol Cell. 2004 Mar 12;13(5):649-63 [15023336.001]
  • [Cites] J Neurooncol. 2004 Mar-Apr;67(1-2):191-200 [15072467.001]
  • [Cites] Cancer. 2004 Apr 15;100(8):1558-77 [15073842.001]
  • [Cites] Nat Rev Drug Discov. 2004 Jun;3(6):499-508 [15173839.001]
  • [Cites] J Biomed Mater Res. 1989 Feb;23(2):253-66 [2708412.001]
  • [Cites] Cancer Res. 1991 Jan 15;51(2):672-5 [1702361.001]
  • [Cites] Methods Enzymol. 1991;198:440-50 [1857235.001]
  • [Cites] J Immunol Methods. 1993 Jan 4;157(1-2):203-7 [8423364.001]
  • [Cites] Cancer Res. 1993 Dec 1;53(23):5822-7 [7694795.001]
  • [Cites] J Neurosurg. 1995 Apr;82(4):635-40 [7897527.001]
  • [Cites] Lancet. 1995 Apr 22;345(8956):1008-12 [7723496.001]
  • [Cites] Cell. 1997 Jan 24;88(2):277-85 [9008168.001]
  • [Cites] Cancer Res. 1998 Feb 15;58(4):672-84 [9485020.001]
  • [Cites] Cancer Res. 1998 Jul 1;58(13):2784-92 [9661892.001]
  • [Cites] Nature. 1998 Jul 16;394(6690):287-91 [9685160.001]
  • [Cites] Cancer Res. 1999 Oct 1;59(19):4770-5 [10519381.001]
  • [Cites] Cancer Res. 2000 Oct 1;60(19):5410-3 [11034081.001]
  • (PMID = 16284573.001).
  • [ISSN] 1524-4040
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U19 CA052857; United States / NCI NIH HHS / CA / CA52857
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Endostatins
  • [Other-IDs] NLM/ NIHMS11341; NLM/ PMC1635009
  •  go-up   go-down


24. Chen C, Louis D, Dodd T, Muecke J: Mitomycin C as an adjunct in the treatment of localised ocular surface squamous neoplasia. Br J Ophthalmol; 2004 Jan;88(1):17-8
Hazardous Substances Data Bank. MITOMYCIN C .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mitomycin C as an adjunct in the treatment of localised ocular surface squamous neoplasia.
  • AIM: To report the outcome of topical mitomycin C (MMC) used as adjunctive treatment following primary excision of ocular surface squamous neoplasia (OSSN).
  • RESULT: 27 cases of OSSN received a treatment regimen of surgical excision, followed by topical MMC.
  • CONCLUSION: MMC treatment following surgical excision decreases the recurrence rate of primary ocular surface neoplasia and should be considered as adjunctive therapy in primary treatment.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Carcinoma in Situ / drug therapy. Carcinoma, Squamous Cell / drug therapy. Eye Neoplasms / drug therapy. Mitomycin / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Recurrence, Local / prevention & control. Prospective Studies

  • MedlinePlus Health Information. consumer health - Eye Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ophthalmology. 1997 Dec;104(12):2085-93 [9400769.001]
  • [Cites] Surv Ophthalmol. 1995 May-Jun;39(6):429-50 [7660300.001]
  • [Cites] Am J Ophthalmol. 1997 Sep;124(3):381-3 [9439364.001]
  • [Cites] Am J Ophthalmol. 1997 Sep;124(3):397-9 [9439368.001]
  • [Cites] Ophthalmology. 1999 Jan;106(1):91-7 [9917787.001]
  • [Cites] Curr Opin Ophthalmol. 1998 Aug;9(4):35-9 [10387466.001]
  • [Cites] Ophthalmic Surg Lasers Imaging. 2005 May-Jun;36(3):249-51 [15957484.001]
  • [Cites] Cornea. 2000 May;19(3):278-83 [10832683.001]
  • [Cites] Br J Ophthalmol. 2001 Sep;85(9):1115-9 [11520767.001]
  • [Cites] Br J Ophthalmol. 2002 Jan;86(1):31-4 [11801499.001]
  • [Cites] Cornea. 2002 Mar;21(2):189-91 [11862092.001]
  • [Cites] Clin Experiment Ophthalmol. 2002 Apr;30(2):94-8 [11886411.001]
  • [Cites] Am J Ophthalmol. 1994 Feb 15;117(2):164-8 [8116744.001]
  • [Cites] Arch Ophthalmol. 1992 Apr;110(4):525-7 [1562262.001]
  • [Cites] Am J Ophthalmol. 2002 May;133(5):601-6 [11992855.001]
  • [Cites] Am J Ophthalmol. 1997 Sep;124(3):303-11 [9439356.001]
  • (PMID = 14693762.001).
  • [ISSN] 0007-1161
  • [Journal-full-title] The British journal of ophthalmology
  • [ISO-abbreviation] Br J Ophthalmol
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 50SG953SK6 / Mitomycin
  • [Other-IDs] NLM/ PMC1771954
  •  go-up   go-down


25. Kim EC, Min JK, Kim TY, Lee SJ, Yang HO, Han S, Kim YM, Kwon YG: [6]-Gingerol, a pungent ingredient of ginger, inhibits angiogenesis in vitro and in vivo. Biochem Biophys Res Commun; 2005 Sep 23;335(2):300-8

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [6]-Gingerol, a pungent ingredient of ginger (Zingiber officinale Roscoe, Zingiberaceae), has anti-bacterial, anti-inflammatory, and anti-tumor-promoting activities.
  • It also blocked capillary-like tube formation by endothelial cells in response to VEGF, and strongly inhibited sprouting of endothelial cells in the rat aorta and formation of new blood vessel in the mouse cornea in response to VEGF.
  • Moreover, i.p. administration, without reaching tumor cytotoxic blood levels, to mice receiving i.v. injection of B16F10 melanoma cells, reduced the number of lung metastasis, with preservation of apparently healthy behavior.
  • Taken together, these results demonstrate that [6]-gingerol inhibits angiogenesis and may be useful in the treatment of tumors and other angiogenesis-dependent diseases.
  • [MeSH-major] Fatty Alcohols / pharmacology. Ginger / chemistry. Neoplasms, Experimental / drug therapy. Neovascularization, Pathologic
  • [MeSH-minor] Animals. Aorta / metabolism. Aorta / pathology. Blotting, Western. Catechols. Cell Cycle. Cell Line, Tumor. Cell Movement. Cell Proliferation. Cells, Cultured. Collagen / chemistry. Cornea / metabolism. Cyclin D1 / metabolism. DNA / chemistry. Dose-Response Relationship, Drug. Drug Combinations. Electrophoresis, Polyacrylamide Gel. Endothelium, Vascular / cytology. Fibroblast Growth Factor 2 / metabolism. G1 Phase. Humans. In Vitro Techniques. Laminin / chemistry. Lung Neoplasms / secondary. Male. Mice. Mice, Inbred C57BL. Models, Chemical. Mutagens. NIH 3T3 Cells. Neoplasm Metastasis. Neoplasm Transplantation. Plant Extracts. Proteoglycans / chemistry. Rats. Rats, Sprague-Dawley. Umbilical Veins / cytology. Vascular Endothelial Growth Factor A / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16081047.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Catechols; 0 / Drug Combinations; 0 / Fatty Alcohols; 0 / Laminin; 0 / Mutagens; 0 / Plant Extracts; 0 / Proteoglycans; 0 / Vascular Endothelial Growth Factor A; 103107-01-3 / Fibroblast Growth Factor 2; 119978-18-6 / matrigel; 136601-57-5 / Cyclin D1; 9007-34-5 / Collagen; 9007-49-2 / DNA; 925QK2Z900 / gingerol
  •  go-up   go-down


26. Hatzi E, Murphy C, Zoephel A, Rasmussen H, Morbidelli L, Ahorn H, Kunisada K, Tontsch U, Klenk M, Yamauchi-Takihara K, Ziche M, Rofstad EK, Schweigerer L, Fotsis T: N-myc oncogene overexpression down-regulates IL-6; evidence that IL-6 inhibits angiogenesis and suppresses neuroblastoma tumor growth. Oncogene; 2002 May 16;21(22):3552-61
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] N-myc oncogene overexpression down-regulates IL-6; evidence that IL-6 inhibits angiogenesis and suppresses neuroblastoma tumor growth.
  • Tumor angiogenesis appears to be governed by alterations of tumor suppressor or oncogenes operant in a broad range of tumors.
  • Here, we report that N-Myc overexpression results in down-regulation of interleukin-6 (IL-6) and that IL-6 is an inhibitor of endothelial cell proliferation and VEGF-induced rabbit corneal angiogenesis.
  • [MeSH-minor] Animals. Antineoplastic Agents / metabolism. Antineoplastic Agents / pharmacology. Cattle. Cell Division / drug effects. Cells, Cultured. Central Nervous System Neoplasms / blood supply. Central Nervous System Neoplasms / metabolism. Central Nervous System Neoplasms / pathology. Central Nervous System Neoplasms / therapy. Cornea / blood supply. Cornea / drug effects. DNA-Binding Proteins / metabolism. Down-Regulation. Endothelium, Vascular / cytology. Endothelium, Vascular / drug effects. Female. Gene Expression Regulation, Neoplastic. Mice. Mice, Inbred BALB C. Mice, Nude. RNA, Neoplasm / biosynthesis. Rabbits. STAT3 Transcription Factor. Trans-Activators / metabolism. Transfection. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12032857.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Interleukin-6; 0 / Oncogene Protein p55(v-myc); 0 / RNA, Neoplasm; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, mouse; 0 / Trans-Activators
  •  go-up   go-down


27. Shields JA, Demirci H, Marr BP, Eagle RC Jr, Stefanyszyn M, Shields CL: Conjunctival epithelial involvement by eyelid sebaceous carcinoma. The 2003 J. Howard Stokes lecture. Ophthal Plast Reconstr Surg; 2005 Mar;21(2):92-6
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: The medical records were reviewed retrospectively on patients with histopathologically confirmed sebaceous carcinoma of the eyelids managed at the Oncology Service at Wills Eye Hospital.
  • The incidence of metastasis and tumor-related mortality was determined.
  • Of the 28 cases, the neoplasm affected the following sites: superior tarsal and fornical conjunctiva in 28 (100%), inferior tarsal conjunctiva in 19 (68%), inferior fornical conjunctiva in 18 (64%), superior bulbar conjunctiva in 19 (68%), and inferior bulbar conjunctiva in 16 (57%).
  • The caruncle was involved in 15 (54%) and the cornea in 11 (39%).
  • Map biopsies, combined with cryotherapy, topical chemotherapy, local surgical resection, and orbital exenteration, were used to achieve local control.
  • CONCLUSIONS: Eyelid sebaceous carcinoma was found to exhibit epithelial involvement of the conjunctiva in 47% of cases, predominantly in the superior tarsal and fornical conjunctiva and less often in the inferior tarsal conjunctiva, caruncle, and cornea.
  • Treatment of this condition is challenging, and map biopsy, cryotherapy, topical chemotherapy, and newer surgical methods are being used more often by our group.
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Combined Modality Therapy. Cryotherapy. Humans. Incidence. Ophthalmologic Surgical Procedures. Retrospective Studies

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15778660.001).
  • [ISSN] 0740-9303
  • [Journal-full-title] Ophthalmic plastic and reconstructive surgery
  • [ISO-abbreviation] Ophthal Plast Reconstr Surg
  • [Language] eng
  • [Publication-type] Lectures; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


28. Oliner J, Min H, Leal J, Yu D, Rao S, You E, Tang X, Kim H, Meyer S, Han SJ, Hawkins N, Rosenfeld R, Davy E, Graham K, Jacobsen F, Stevenson S, Ho J, Chen Q, Hartmann T, Michaels M, Kelley M, Li L, Sitney K, Martin F, Sun JR, Zhang N, Lu J, Estrada J, Kumar R, Coxon A, Kaufman S, Pretorius J, Scully S, Cattley R, Payton M, Coats S, Nguyen L, Desilva B, Ndifor A, Hayward I, Radinsky R, Boone T, Kendall R: Suppression of angiogenesis and tumor growth by selective inhibition of angiopoietin-2. Cancer Cell; 2004 Nov;6(5):507-16
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppression of angiogenesis and tumor growth by selective inhibition of angiopoietin-2.
  • Angiopoietin-2 (Ang2) exhibits broad expression in the remodeling vasculature of human tumors but very limited expression in normal tissues, making it an attractive candidate target for antiangiogenic cancer therapy.
  • Systemic treatment of tumor-bearing mice with these Ang2-blocking agents resulted in tumor stasis, followed by elimination of all measurable tumor in a subset of animals.
  • These effects were accompanied by reduced endothelial cell proliferation, consistent with an antiangiogenic therapeutic mechanism.
  • Anti-Ang2 therapy also prevented VEGF-stimulated neovascularization in a rat corneal model of angiogenesis.
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Cornea / blood supply. Endothelial Cells / drug effects. Female. Mice. Mice, Nude. Neoplasm Transplantation. Neutralization Tests. Receptors, Fc. Recombinant Fusion Proteins / pharmacology. Tumor Cells, Cultured


29. Bouïs D, Hospers GA, Meijer C, Dam W, Peek R, Mulder NH: Effects of the CDT6/ANGX gene on tumour growth in immune competent mice. In Vivo; 2003 Mar-Apr;17(2):157-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of the CDT6/ANGX gene on tumour growth in immune competent mice.
  • BACKGROUND: Cornea-derived transcript 6 (CDT6, also known as AngX) has been described to inhibit tumour growth in a human melanoma growing in nude mice.
  • In another report, however, enhancement of tumour growth in comparable circumstances occurred.
  • RESULTS: We found no significant inhibition or stimulation of either lag-time or doubling-time of the tumours.
  • CONCLUSION: In contrast to an immune deficient mouse model, no anti-tumour effect could be detected with the CDT6 gene product in an immune competent mouse model.
  • [MeSH-major] Angiogenesis Inducing Agents / therapeutic use. Angiogenic Proteins / genetics. Genetic Therapy / methods. Immunocompetence. Melanoma, Experimental / therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Division / drug effects. Cell Line, Tumor. Endothelium, Vascular / drug effects. Endothelium, Vascular / pathology. Female. Humans. Mice. Mice, Inbred C57BL. Mice, Nude. RNA, Messenger / metabolism. RNA, Neoplasm / analysis. Reverse Transcriptase Polymerase Chain Reaction. Transfection

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12792978.001).
  • [ISSN] 0258-851X
  • [Journal-full-title] In vivo (Athens, Greece)
  • [ISO-abbreviation] In Vivo
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiogenesis Inducing Agents; 0 / Angiogenic Proteins; 0 / Antineoplastic Agents; 0 / RNA, Messenger; 0 / RNA, Neoplasm
  •  go-up   go-down


30. Chang SW, Huang ZL: Oral cimetidine adjuvant therapy for recalcitrant, diffuse conjunctival papillomatosis. Cornea; 2006 Jul;25(6):687-90
Hazardous Substances Data Bank. CIMETIDINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oral cimetidine adjuvant therapy for recalcitrant, diffuse conjunctival papillomatosis.
  • He underwent 3 separate surgeries; however, they did not prevent tumor recurrence.
  • To avoid postoperative symblepharon, ankyloblepharon, dry eye, and possible corneal neovascularization after extensive lesion excision, oral CIM at a dosage of 200 mg 4 times daily was administered for 4 months before surgery.
  • A debulking excision of the residual tumor with an intraoperative application of mitomycin C was performed as a secondary therapy after the main mass decreased in size.
  • The papillomatosis cleared without recurrence or symblepharon, ankyloblepharon, conjunctival scarring, or corneal neovascularization after 4 years of follow-up examinations.
  • If there is tumor shrinkage, surgical debulking with applications of mitomycin C may be sufficient to eliminate any residual tumor tissue without inducing conjunctival scarring or corneal neovascularization.
  • [MeSH-major] Cimetidine / therapeutic use. Conjunctival Neoplasms / therapy. Histamine H2 Antagonists / therapeutic use. Ophthalmologic Surgical Procedures. Papilloma / therapy. Papillomavirus Infections / therapy
  • [MeSH-minor] Administration, Oral. Alkylating Agents / administration & dosage. Child. Combined Modality Therapy. DNA, Viral / analysis. Human papillomavirus 6 / genetics. Human papillomavirus 6 / isolation & purification. Humans. Male. Mitomycin / administration & dosage. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / surgery. Neoplasm Recurrence, Local / therapy. Neoplasm Recurrence, Local / virology. Polymerase Chain Reaction

  • Hazardous Substances Data Bank. MITOMYCIN C .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17077661.001).
  • [ISSN] 0277-3740
  • [Journal-full-title] Cornea
  • [ISO-abbreviation] Cornea
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / DNA, Viral; 0 / Histamine H2 Antagonists; 50SG953SK6 / Mitomycin; 80061L1WGD / Cimetidine
  •  go-up   go-down


31. Bae DG, Gho YS, Yoon WH, Chae CB: Arginine-rich anti-vascular endothelial growth factor peptides inhibit tumor growth and metastasis by blocking angiogenesis. J Biol Chem; 2000 May 5;275(18):13588-96
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Arginine-rich anti-vascular endothelial growth factor peptides inhibit tumor growth and metastasis by blocking angiogenesis.
  • Tumor angiogenesis is a critical step for the growth and metastasis of solid tumors.
  • Vascular endothelial growth factor (VEGF) is a specific and potent angiogenic factor and contributes to the development of solid tumors by promoting tumor angiogenesis.
  • Therefore, it is a prime therapeutic target for the development of antagonists for treatment of cancer.
  • The identified peptides block the angiogenesis induced by VEGF(165) in vivo in the chick chorioallantoic membrane and the rabbit cornea.
  • Based on our results, the arginine-rich hexapeptides may be effective for the treatment of various human tumors and other angiogenesis-dependent diseases that are related to the action of VEGF and could also serve as leads for development of more effective drugs.
  • [MeSH-major] Endothelial Growth Factors / antagonists & inhibitors. Lymphokines / antagonists & inhibitors. Neoplasms, Experimental / drug therapy. Neovascularization, Pathologic / drug therapy. Peptides / pharmacology
  • [MeSH-minor] Amino Acid Sequence. Animals. Arginine. Humans. Mice. Molecular Sequence Data. Neoplasm Metastasis / drug therapy. Peptide Library. Rabbits. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. (L)-ARGININE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10788475.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Peptide Library; 0 / Peptides; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 94ZLA3W45F / Arginine
  •  go-up   go-down


32. Caujolle JP, Maschi C, Chauvel P, Herault J, Gastaud P: [Surgery and additional protontherapy for treatment of invasive and recurrent squamous cell carcinomas: technique and preliminary results]. J Fr Ophtalmol; 2009 Dec;32(10):707-14

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Surgery and additional protontherapy for treatment of invasive and recurrent squamous cell carcinomas: technique and preliminary results].
  • [Transliterated title] Association chirurgie-protonthérapie dans le traitement des carcinomes invasifs et récidivants de la conjonctive: technique et résultats préliminaires.
  • The improvement of tumoral control requires additional treatments such as cryotherapy, topical chemotherapy, and radiotherapy.
  • We present the technique and preliminary results of associating treatment with surgery and proton beam therapy for recurrent and invasive squamous cell carcinomas.
  • The treatment combined new surgical resection with protontherapy.
  • Specific improvements in proton beam therapy have been made at the Nice Cyclotron to adapt the treatment to conjunctival tumors.
  • In 13 cases (86.8%), the bulbar and limbic conjunctiva was involved, in five of these cases the cornea was invaded, and the anterior chamber was involved in one case.
  • In one case, the tumor was located on bulbar conjunctiva near the caruncle (6.6%) and in one case in the fornix (6.6%).
  • We obtained local tumor control for 13 patients (86.8%) and recurrences for two patients (13.2%).
  • Moreover, proton beam therapy was performed more than 6 months after the initial treatment.
  • Exenteration and enucleation had to be performed to treat these recurrences 6 and 24 months after proton beam therapy.
  • No patients developed recurrences with additional proton beam therapy performed within 6 months after initial surgical resection.
  • CONCLUSION: Traditional adjuvant treatments often failed to control recurring and invasive squamous cell carcinomas.
  • The preliminary results of the present study suggest that proton beam therapy may be considered as a good alternative to traditional treatments with acceptable side effects.
  • [MeSH-major] Carcinoma, Squamous Cell / radiotherapy. Carcinoma, Squamous Cell / surgery. Conjunctival Neoplasms / radiotherapy. Conjunctival Neoplasms / surgery. Neoplasm Recurrence, Local / radiotherapy. Neoplasm Recurrence, Local / surgery. Protons / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19942315.001).
  • [ISSN] 1773-0597
  • [Journal-full-title] Journal français d'ophtalmologie
  • [ISO-abbreviation] J Fr Ophtalmol
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Protons
  •  go-up   go-down


33. Shields CL, Naseripour M, Shields JA: Topical mitomycin C for extensive, recurrent conjunctival-corneal squamous cell carcinoma. Am J Ophthalmol; 2002 May;133(5):601-6
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Topical mitomycin C for extensive, recurrent conjunctival-corneal squamous cell carcinoma.
  • PURPOSE: To evaluate the efficacy of topical mitomycin C for extensive recurrent conjunctival and corneal squamous cell carcinoma (SCC).
  • Ten patients (ten eyes) with extensive recurrent conjunctival and corneal SCC were studied.
  • The patients received topical mitomycin C 0.04% one drop four times daily in the eye with SCC.
  • Treatment cycles were defined as 1 week using medication followed by 1 week without medication.
  • Such treatment cycles were repeated until resolution of the conjunctival malignancy was clinically evident.
  • The main outcome measures were tumor response and medication-related complications.
  • Before referral, the patients had undergone a median of two previous conjunctival tumor resections revealing the diagnosis of in situ SCC in three cases and locally invasive SCC in six cases.
  • At presentation, the tumor involved the limbus and cornea in all ten eyes, forniceal conjunctiva in three eyes, and tarsal conjunctiva in one eye.
  • The extensive tumor affected a median of 10 clock hours of limbal conjunctiva and 10 clock hours of cornea, with corneal epithelial invasion for a median of 50% (range 20%-100%) of its surface.
  • Mitomycin C 0.04% four times daily was applied for a median of three cycles (range 1-4 cycles).
  • Complete tumor regression was documented in all ten cases (100%).
  • CONCLUSIONS: Based on this small series, topical mitomycin C 0.04% appears to be a safe and effective therapy for conjunctival or corneal SCC, even when there is extensive recurrent tumor.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Conjunctival Neoplasms / drug therapy. Corneal Diseases / drug therapy. Eye Neoplasms / drug therapy. Mitomycin / therapeutic use. Neoplasm Recurrence, Local / drug therapy
  • [MeSH-minor] Administration, Topical. Adult. Aged. Drug Evaluation. Female. Humans. Male. Middle Aged. Prospective Studies. Safety. Treatment Outcome

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • MedlinePlus Health Information. consumer health - Corneal Disorders.
  • MedlinePlus Health Information. consumer health - Eye Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. MITOMYCIN C .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Am J Ophthalmol. 2003 Jan;135(1):122-3; author reply 123-4 [12504721.001]
  • (PMID = 11992855.001).
  • [ISSN] 0002-9394
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 50SG953SK6 / Mitomycin
  •  go-up   go-down


34. Zheng M, Schwarz MA, Lee S, Kumaraguru U, Rouse BT: Control of stromal keratitis by inhibition of neovascularization. Am J Pathol; 2001 Sep;159(3):1021-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This report investigates the role of neovascularization in the pathogenesis of stromal keratitis by measuring the outcome of treatment with the potent anti-angiogenesis cytokine endothelial monocyte-activating polypeptide II (EMAP II).
  • EMAP II treatment had no demonstrable pro-inflammatory or toxic effects and failed to express antiviral activity.
  • Our data document for the first time the essential role of angiogenesis in the pathogenesis of stromal keratitis and also indicate that the therapy of herpetic stromal keratitis could benefit by procedures that diminish angiogenesis.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mech Dev. 2000 Jul;95(1-2):123-32 [10906456.001]
  • [Cites] Dev Dyn. 2000 Jul;218(3):490-8 [10878614.001]
  • [Cites] Cancer Res. 2000 Aug 1;60(15):4066-9 [10945611.001]
  • [Cites] Nature. 2000 Sep 14;407(6801):242-8 [11001067.001]
  • [Cites] Nat Med. 2000 Dec;6(12):1335-40 [11100117.001]
  • [Cites] J Clin Invest. 1973 Nov;52(11):2745-56 [4355998.001]
  • [Cites] J Invest Dermatol. 1982 Mar;78(3):206-9 [6276474.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1984 Aug;25(8):938-44 [6611324.001]
  • [Cites] J Virol. 1989 Feb;63(2):769-75 [2536102.001]
  • [Cites] J Biol Chem. 1992 Oct 5;267(28):20239-47 [1400342.001]
  • [Cites] Cell. 1993 Mar 26;72(6):835-46 [7681362.001]
  • [Cites] J Biol Chem. 1994 Oct 7;269(40):25106-19 [7929199.001]
  • [Cites] J Virol. 1996 Feb;70(2):898-904 [8551629.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1996 Jul;37(8):1625-32 [8675406.001]
  • [Cites] J Immunol. 1997 Feb 1;158(3):1383-91 [9013983.001]
  • [Cites] Immunol Today. 1997 Sep;18(9):443-9 [9293161.001]
  • [Cites] Nature. 1998 Jan 1;391(6662):24-5 [9422503.001]
  • [Cites] Nature. 1998 Jan 1;391(6662):86-9 [9422510.001]
  • [Cites] Immunol Res. 1997;16(4):375-86 [9439761.001]
  • [Cites] Science. 1998 Feb 27;279(5355):1344-7 [9478893.001]
  • [Cites] Cornea. 1998 Jul;17(4):403-9 [9676913.001]
  • [Cites] Nature. 1998 Jul 30;394(6692):485-90 [9697772.001]
  • [Cites] J Immunol. 1998 Oct 15;161(8):4289-300 [9780205.001]
  • [Cites] J Interferon Cytokine Res. 1998 Sep;18(9):681-90 [9781806.001]
  • [Cites] Cancer Res. 1999 Jan 1;59(1):205-12 [9892208.001]
  • [Cites] EMBO J. 1999 Jan 15;18(2):363-74 [9889193.001]
  • [Cites] Am J Physiol. 1999 Feb;276(2 Pt 1):L365-75 [9950900.001]
  • [Cites] J Exp Med. 1999 Aug 2;190(3):341-54 [10430623.001]
  • [Cites] J Virol. 2000 Apr;74(8):3517-24 [10729125.001]
  • [Cites] Microvasc Res. 2000 Jul;60(1):70-80 [10873516.001]
  • [Cites] Cytokine. 2000 Jul;12(7):992-1000 [10880244.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Aug;41(9):2607-12 [10937573.001]
  • (PMID = 11549594.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL60061; United States / NEI NIH HHS / EY / EY05093; United States / NHLBI NIH HHS / HL / R01 HL060061; United States / NHLBI NIH HHS / HL / R29 HL060061; United States / NEI NIH HHS / EY / R01 EY005093
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cytokines; 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Neoplasm Proteins; 0 / RNA-Binding Proteins; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 0 / small inducible cytokine subfamily E, member 1
  • [Other-IDs] NLM/ PMC1850467
  •  go-up   go-down


35. Teng CC, Chin KJ, Finger PT: Subconjunctival ranibizumab for squamous cell carcinoma of the conjunctiva with corneal extension. Br J Ophthalmol; 2009 Jun;93(6):837-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subconjunctival ranibizumab for squamous cell carcinoma of the conjunctiva with corneal extension.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Conjunctival Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal, Humanized. Cornea / pathology. Humans. Middle Aged. Neoplasm Invasiveness. Ranibizumab

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19471005.001).
  • [ISSN] 1468-2079
  • [Journal-full-title] The British journal of ophthalmology
  • [ISO-abbreviation] Br J Ophthalmol
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; ZL1R02VT79 / Ranibizumab
  •  go-up   go-down


36. Panda A, Sudan R: Comment on intraoperative use of mitomycin C in excision of ocular surface neoplasia with or without limbal autograft transplantation. Cornea; 2002 Nov;21(8):840-1; author reply 841-2
Hazardous Substances Data Bank. MITOMYCIN C .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comment on intraoperative use of mitomycin C in excision of ocular surface neoplasia with or without limbal autograft transplantation.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Conjunctival Neoplasms / surgery. Mitomycin / administration & dosage
  • [MeSH-minor] Carcinoma in Situ / drug therapy. Carcinoma in Situ / surgery. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / surgery. Corneal Transplantation. Humans. Intraoperative Care. Neoplasm Recurrence, Local / prevention & control

  • Genetic Alliance. consumer health - Transplantation.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Cornea. 2002 Jan;21(1):12-6 [11805500.001]
  • [ErratumIn] Cornea. 2003 Mar;22(2):189.
  • (PMID = 12410051.001).
  • [ISSN] 0277-3740
  • [Journal-full-title] Cornea
  • [ISO-abbreviation] Cornea
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 50SG953SK6 / Mitomycin
  •  go-up   go-down






Advertisement