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1. Philibert JC, Snyder PW, Glickman N, Glickman LT, Knapp DW, Waters DJ: Influence of host factors on survival in dogs with malignant mammary gland tumors. J Vet Intern Med; 2003 Jan-Feb;17(1):102-6
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  • [Title] Influence of host factors on survival in dogs with malignant mammary gland tumors.
  • The purpose of our study was to determine if specific host factors, such as age at diagnosis, obesity, and hormone status, influence the prognosis of canine mammary gland carcinomas and to confirm if previously reported risk factors (ie, histologic subtype, tumor size, and World Health Organization [WHO] stage) were important in a large series of affected dogs.
  • Ninety-nine female dogs with mammary gland carcinomas, no previous therapy, an excisional biopsy, and known cause of death were studied.
  • No significant association with survival was noted for age at diagnosis (chronologic or physiologic), obesity, or hormone status (ie, spayed versus intact, regardless of time of being spayed).
  • Of the tumor factors analyzed, the histologic subtype anaplastic carcinoma (P = .02), WHO stage I (P = .01), evidence of metastasis at the time of diagnosis (P = .004), and tumor size of 3 cm or smaller (P = .005) all significantly influenced survival.
  • Dogs that were classified as having tumor-related mortality had a shorter postoperative survival compared to dogs that died of other causes (14 months versus 23 months; P = .03).
  • In conclusion, histologic subtype, WHO stage, and tumor size remain important prognostic factors in canine mammary gland tumors.
  • Further study of other prognostic factors is needed to determine which tumors are adequately addressed with local therapy only and which dogs may require adjuvant treatment with chemotherapy.

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  • (PMID = 12564734.001).
  • [ISSN] 0891-6640
  • [Journal-full-title] Journal of veterinary internal medicine
  • [ISO-abbreviation] J. Vet. Intern. Med.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gonadal Steroid Hormones
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2. Hayashi M, Nishiya H, Chiba T, Endoh D, Kon Y, Okui T: Trientine, a copper-chelating agent, induced apoptosis in murine fibrosarcoma cells in vivo and in vitro. J Vet Med Sci; 2007 Feb;69(2):137-42
Hazardous Substances Data Bank. TRIETHYLENETETRAMINE .

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  • Anti-copper treatments have been investigated to determine whether they suppress angiogenesis and tumor development since Cu is widely accepted as being required for angiogenesis.
  • We examined the effects of treatment with trientine, a copper-chelating agent, on tumor development in a murine xenograft model using fibrosarcoma-derived transplantable QRsp-11 cells and C57BL/6 mice and induction of apoptosis in tumor cells and endothelial cells in vivo and in vitro.
  • The tumor volumes increased more slowly in trientine-treated mice than in untreated mice.
  • Tumor volumes in the treated mice were significantly smaller than those in the untreated mice at 24 days postinoculation (d.p.i.) of tumor cells.
  • A cluster of pyknotic tumor cells and morphological abnormalities in capillary endothelial cells were observed in the tumors of trientine-treated mice but not in the tumors of untreated mice.
  • The proportions of apoptotic and necrotic cells in the tumors of treated mice were approximately 3.5-fold higher than those in the tumors of untreated mice at 14 d.p.i.
  • However, the proportion of apoptotic cells in endothelial cells was significantly lower than that in QRsp-11 cells after treatment with trientine.
  • These results show that apoptosis was induced in tumor cells by treatment with trientine in vivo and in vitro.

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  • (PMID = 17339757.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Chelating Agents; SJ76Y07H5F / Trientine
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3. Papo N, Seger D, Makovitzki A, Kalchenko V, Eshhar Z, Degani H, Shai Y: Inhibition of tumor growth and elimination of multiple metastases in human prostate and breast xenografts by systemic inoculation of a host defense-like lytic peptide. Cancer Res; 2006 May 15;66(10):5371-8
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  • [Title] Inhibition of tumor growth and elimination of multiple metastases in human prostate and breast xenografts by systemic inoculation of a host defense-like lytic peptide.
  • We report on a short host defense-like peptide that targets and arrests the growth of aggressive and hormone-resistant primary human prostate and breast tumors and prevents their experimental and spontaneous metastases, respectively, when systemically inoculated to immunodeficient mice.
  • These effects are correlated with increased necrosis of the tumor cells and a significant decrease in the overall tumor microvessel density, as well as newly formed capillary tubes and prostate-specific antigen secretion (in prostate tumors).
  • Growth inhibition of orthotopic tumors derived from stably transfected highly fluorescent human breast cancer cells and prevention of their naturally occurring metastases were visualized in real time by using noninvasive whole-body optical imaging.
  • The exclusive selectivity of the peptide towards cancer derives from its specific binding to surface phosphatidylserine and the killing of the cancer cells via cytoplasmic membrane depolarization.
  • These data indicate that membrane disruption can provide a therapeutic means of inhibiting tumor growth and preventing metastases of various cancers.
  • [MeSH-major] Adenocarcinoma / drug therapy. Breast Neoplasms / drug therapy. Leucine / analogs & derivatives. Leucine / pharmacology. Lysine / analogs & derivatives. Lysine / pharmacology. Peptides / pharmacology. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Growth Processes / drug effects. Cell Line, Tumor. Female. Humans. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Male. Membrane Potentials / drug effects. Mice. Mice, SCID. Neoplasm Metastasis. Phosphatidylserines / metabolism. Prostate-Specific Antigen / secretion. Xenograft Model Antitumor Assays

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  • (PMID = 16707464.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Peptides; 0 / Phosphatidylserines; EC 3.4.21.77 / Prostate-Specific Antigen; GMW67QNF9C / Leucine; K3Z4F929H6 / Lysine
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4. Devitt JJ, Maranon DG, Ehrhart EJ, Bachand AM, Lana SE, LaRue SM: Correlations between numerical chromosomal aberrations in the tumor and peripheral blood in canine lymphoma. Cytogenet Genome Res; 2009;124(1):12-8
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  • [Title] Correlations between numerical chromosomal aberrations in the tumor and peripheral blood in canine lymphoma.
  • Untreated, the survival times are approximately one month.
  • Chemotherapy is the current standard of care and can initiate and temporarily maintain remission, with average remission times of one year.
  • Cytogenetic abnormalities can aid in diagnosing tumors as well as in giving a more accurate prognosis for the specific mutations present.
  • Evaluating peripheral lymphocytes instead of tumor cells is less invasive for the affected dog and technically easier.
  • This study was designed to investigate a correspondence between numerical aberrations detected in the tumor and the peripheral blood in dogs with lymphoma.
  • A significant correspondence between the numerical aberrations in the tumor and the peripheral blood was found.
  • When tumor analysis is not possible, the peripheral blood offers a viable option for cytogenetic assessment.
  • Additionally, this may provide a method to evaluate the efficacy of the treatment protocol during the course of treatment.
  • [MeSH-major] Chromosome Aberrations / veterinary. Dog Diseases / genetics. Lymph Nodes / pathology. Lymphoma / genetics. Lymphoma / veterinary
  • [MeSH-minor] Animals. Chromosomes, Mammalian. Cytogenetics. Dogs. Female. Immunophenotyping. In Situ Hybridization, Fluorescence. Male. Neoplasm Staging. Sensitivity and Specificity. Trisomy. Tumor Cells, Cultured

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  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19372664.001).
  • [ISSN] 1424-859X
  • [Journal-full-title] Cytogenetic and genome research
  • [ISO-abbreviation] Cytogenet. Genome Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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5. Yu KN, Minai-Tehrani A, Chang SH, Hwang SK, Hong SH, Kim JE, Shin JY, Park SJ, Kim JH, Kwon JT, Jiang HL, Kang B, Kim D, Chae CH, Lee KH, Yoon TJ, Beck GR, Cho MH: Aerosol delivery of small hairpin osteopontin blocks pulmonary metastasis of breast cancer in mice. PLoS One; 2010 Dec 22;5(12):e15623
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  • Conventional therapies such as chemotherapy and surgery are somewhat successful, however, metastasis-related breast cancer morbidity remains high.
  • Thus, a novel approach to prevent breast tumor metastasis is needed.
  • Our results showed that noninvasive targeting of pulmonary osteopontin or other specific genes responsible for cancer metastasis could be used as an effective therapeutic regimen for the treatment of metastatic epithelial tumors.

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  • (PMID = 21203518.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NIAMS NIH HHS / AR / R01 AR056090; United States / NCI NIH HHS / CA / R03 CA136059; United States / NIAMS NIH HHS / AR / AR056090; United States / NCI NIH HHS / CA / CA136059
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aerosols; 106441-73-0 / Osteopontin
  • [Other-IDs] NLM/ PMC3008732
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6. Al-Wadei HA, Schuller HM: Cyclic adenosine monophosphate-dependent cell type-specific modulation of mitogenic signaling by retinoids in normal and neoplastic lung cells. Cancer Detect Prev; 2006;30(5):403-11
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  • [Title] Cyclic adenosine monophosphate-dependent cell type-specific modulation of mitogenic signaling by retinoids in normal and neoplastic lung cells.
  • The observed stimulation of cAMP/PKA may inhibit the development of small cell lung carcinoma and other tumors derived from large airway epithelia whereas it may selectively promote the development of lung tumors derived from small airway epithelial cells, such as adenocarcinoma.

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  • (PMID = 17067750.001).
  • [ISSN] 0361-090X
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA088809; United States / NCI NIH HHS / CA / R01 CA096128; United States / NCI NIH HHS / CA / R01-CA088809; United States / NCI NIH HHS / CA / R01-CA096128
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 5300-03-8 / alitretinoin; 5688UTC01R / Tretinoin; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EH28UP18IF / Isotretinoin
  • [Other-IDs] NLM/ NIHMS14425; NLM/ PMC1761122
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7. Von Euler HP, Rivera P, Aronsson AC, Bengtsson C, Hansson LO, Eriksson SK: Monitoring therapy in canine malignant lymphoma and leukemia with serum thymidine kinase 1 activity--evaluation of a new, fully automated non-radiometric assay. Int J Oncol; 2009 Feb;34(2):505-10
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  • [Title] Monitoring therapy in canine malignant lymphoma and leukemia with serum thymidine kinase 1 activity--evaluation of a new, fully automated non-radiometric assay.
  • Serum TK levels correlate to the proliferative activity of tumor disease.
  • A non-radiometric method based on a competitive immunoassay with specific anti-3'-azido-deoxythymidine monophosphate (AZTMP) antibodies has been further developed into the fully automated Liaison TK assay (DiaSorin).
  • Sera from healthy dogs (n=30), and dogs with leukemia (LEUK) (n=35), ML (n=84), non-hematological tumors (n=50), and inflammatory disease (n=14) were tested using both methods.
  • Lymphoma and LEUK samples were available before and during chemotherapy.
  • The TK1 levels measured during chemotherapy gave very clear differences between dogs in complete remission and dogs out of remission.
  • The Liaison TK assay provides valuable clinical information in the treatment and management of canine LEUK and ML, with a potential to be further validated in human trials.
  • [MeSH-major] Dog Diseases / drug therapy. Leukemia / veterinary. Lymphoma / veterinary. Neoplasms / veterinary
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Cell Cycle. Dogs. Remission Induction. Treatment Outcome

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  • (PMID = 19148486.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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8. Bauer JA, Frye G, Bahr A, Gieg J, Brofman P: Anti-tumor effects of nitrosylcobalamin against spontaneous tumors in dogs. Invest New Drugs; 2010 Oct;28(5):694-702
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  • [Title] Anti-tumor effects of nitrosylcobalamin against spontaneous tumors in dogs.
  • PURPOSE: Given the limited options available to treat canine cancers, the use of companion animals for evaluating new drugs may identify better therapies for veterinary and human oncology.
  • The anti-tumor effects of nitrosylcobalamin (NO-Cbl), an apoptosis-inducing, vitamin B12-based carrier of nitric oxide (NO), was evaluated in four dogs with spontaneous cancer.
  • (1) A 13 year-old female spayed Giant Schnauzer with inoperable thyroid carcinoma and hypercalcemia. (2) A 6 year-old male neutered Golden Retriever with a malignant peripheral nerve sheath tumor (MPNST). (3) A ten yr-old neutered male Bichon Frise with apocrine gland anal sac adenocarcinoma (AGACA). (4) A 7 year-old female spayed Labrador mix with spinal meningioma following partial surgical resection.
  • Tumor regression was measured by physical exam and verified using ultrasound (case 1) and MRI (case 2-4).
  • (1) The Giant Schnauzer demonstrated a 77% reduction in tumor volume after ten weeks of daily NO-Cbl treatment. (2) The Golden Retriever demonstrated a 53% reduction in tumor volume after 15 months of daily NO-Cbl therapy. (3) The Bichon Frise demonstrated a 43% regression of the primary tumor and a 90% regression of an iliac lymph node measured by MRI after 15 months of treatment.
  • After 61 months, the dog currently has stable disease, normal liver enzymes, CBC analysis, and no evidence of toxicity. (4) The Labrador demonstrated complete regression of the residual tumor after 6 months of treatment.
  • The use of NO-Cbl capitalizes on the tumor-specific properties of the vitamin B12 receptor and represents a promising anti-cancer therapy.
  • [MeSH-major] Dog Diseases / drug therapy. Neoplasms / veterinary. Nitroso Compounds / therapeutic use. Vitamin B 12 / analogs & derivatives
  • [MeSH-minor] Animals. Antineoplastic Agents / metabolism. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / therapeutic use. Dogs. Dose-Response Relationship, Drug. Female. Magnetic Resonance Imaging. Male. Tumor Burden. Ultrasonography

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  • [ErratumIn] Invest New Drugs. 2011 Oct;29(5):1122
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  • (PMID = 19557306.001).
  • [ISSN] 1573-0646
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA095020
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Nitroso Compounds; 0 / nitrosylcobalamin; P6YC3EG204 / Vitamin B 12
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9. Kobie K, Kawabata M, Hioki K, Tanaka A, Matsuda H, Mori T, Maruo K: The tyrosine kinase inhibitor imatinib [STI571] induces regression of xenografted canine mast cell tumors in SCID mice. Res Vet Sci; 2007 Apr;82(2):239-41
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  • [Title] The tyrosine kinase inhibitor imatinib [STI571] induces regression of xenografted canine mast cell tumors in SCID mice.
  • Canine mast cell tumors (MCTs) are the most common cutaneous tumors in the dog.
  • They have a wide range of behaviour, which can make these tumors challenging to treat.
  • The antitumor responses in SCID mice with CMC-1 xenografts following treatment with imatinib were observed.
  • Significant tumor regression occurred with 100mg/kg on days 7, 10, 14 and 21, and 200mg/kg on all days.
  • Our results indicate that imatinib is effective against canine mast cell tumor in mouse xenograft models.
  • Canine MCTs might be a potential target for imatinib therapy.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Dog Diseases / drug therapy. Mast-Cell Sarcoma / drug therapy. Mast-Cell Sarcoma / veterinary. Piperazines / pharmacology. Pyrimidines / pharmacology. Skin Neoplasms / drug therapy. Skin Neoplasms / veterinary
  • [MeSH-minor] Animals. Benzamides. Dogs. Imatinib Mesylate. Mice. Mice, SCID. Specific Pathogen-Free Organisms. Statistics, Nonparametric. Xenograft Model Antitumor Assays

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  • (PMID = 16919303.001).
  • [ISSN] 0034-5288
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
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10. Lee JJ, Chen PB, Yang SH, Cheng CH, Chueh LL, Pang VF, Hsiao M, Lin CT: Effect of the VP3 gene of chicken anemia virus on canine mammary tumor cells. Am J Vet Res; 2007 Apr;68(4):411-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of the VP3 gene of chicken anemia virus on canine mammary tumor cells.
  • OBJECTIVE: To investigate the antitumor effect of the chicken anemia virus (CAV) VP3 gene in canine mammary tumor (CMT) cells.
  • On the basis of such tumor cell-specific killing, the VP3 gene may be a promising agent for the treatment of malignant mammary gland tumors in dogs.
  • [MeSH-major] Apoptosis / drug effects. Capsid Proteins / therapeutic use. Chicken anemia virus / genetics. Dog Diseases / therapy. Gene Expression Regulation, Neoplastic / drug effects. Genetic Therapy / methods. Mammary Neoplasms, Animal / therapy
  • [MeSH-minor] Animals. Blotting, Western / veterinary. Cell Line, Tumor. Dogs. Genetic Vectors. In Situ Nick-End Labeling / veterinary. Lentivirus. Microscopy, Fluorescence / veterinary

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  • (PMID = 17397298.001).
  • [ISSN] 0002-9645
  • [Journal-full-title] American journal of veterinary research
  • [ISO-abbreviation] Am. J. Vet. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Capsid Proteins; 0 / VP3 protein, Chicken anemia virus
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11. Ferreira AJ, Jaggy A, Varejão AP, Ferreira ML, Correia JM, Mulas JM, Almeida O, Oliveira P, Prada J: Brain and ocular metastases from a transmissible venereal tumour in a dog. J Small Anim Pract; 2000 Apr;41(4):165-8
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  • [Title] Brain and ocular metastases from a transmissible venereal tumour in a dog.
  • A presumptive diagnosis of transmissible venereal tumour (TVT) and iridocyclitis was made based on the results of fine needle aspiration.
  • Chemotherapy with vincristine and prednisolone was initiated and after four months the dog made a complete recovery.
  • In addition, the dog exhibited generalised 'grand mal' type seizures.
  • On histopathology, metastases of TVT in the left eye and left cerebral hemisphere were found, showing no specific staining for CD3, immunoglobulin (Ig) G, IgM and lambda light chains.
  • It was therefore concluded that the tumour growth was progressive, and that there was an absence of local humoral immune response against TVT in this case.
  • [MeSH-major] Brain Neoplasms / veterinary. Dog Diseases / pathology. Eye Neoplasms / veterinary. Venereal Tumors, Veterinary / pathology
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Dogs. Male. Seizures / veterinary

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  • (PMID = 10812546.001).
  • [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
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12. Yamate J, Kotera T, Kuwamura M, Kotani T: Potential osteogenic differentiation of cisplatin-resistant rat malignant fibrous histiocytoma-derived cell lines. Exp Toxicol Pathol; 2007 Apr;58(5):299-309
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  • Histological modulations in tumor cells treated with anti-cancer drugs have been reported.
  • Immunohistochemically, MT-10 reacted to vimentin, alpha-smooth muscle actin (a marker of myofibroblasts), ED1/ED2 (rat macrophage/histiocyte-specific antibodies), and A3 (rat MFH-specific antibody) in varying degrees, indicating that MFH cells have features of both fibroblasts and histiocytes.
  • MT-10 developed tumors of a storiform pattern, while MT-10R and MT-PR tumors comprise round or polygonal cells arranged in a compact sheet.
  • Additionally, MT-PR tumors included ossifying areas.
  • MT-10R and MT-PR, and their tumors showed a reaction to alkaline phosphatase (ALP), a marker of osteoblasts.
  • RT-PCR revealed that mRNAs of bone morphogenetic protein (BMP)-2, BMP-6 and osteopontin were significantly increased in MT-10R and MT-PR tumors.
  • Neoplastic cells in these tumors were immunoreactive to BMP-2 and BMP-6, while MT-10 tumors were not.
  • Cisplatin-resistant MFH cells had potential to differentiate into osteogenic tissues by producing osteogenic factors, suggesting that MFH histology may be altered under anti-cancer drug treatments.
  • Recently, cancer differentiation-based therapy, that could be induced by anti-cancer drugs, has been implied.
  • MT-10R and MT-PR become useful experimental systems for studies on cellular differentiation provoked by anti-cancer drugs.
  • [MeSH-major] Bone Morphogenetic Proteins / biosynthesis. Cell Differentiation / drug effects. Cisplatin / pharmacology. Drug Resistance, Neoplasm / drug effects. Histiocytoma, Malignant Fibrous / pathology. Osteoblasts / pathology
  • [MeSH-minor] Animals. Bone Morphogenetic Protein 1. Bone Morphogenetic Protein 6. Clone Cells. Enzyme-Linked Immunosorbent Assay. Immunohistochemistry. Metalloendopeptidases / biosynthesis. Neoplasm Transplantation. Osteopontin / biosynthesis. RNA, Messenger / biosynthesis. Rats. Rats, Inbred F344. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 17267196.001).
  • [ISSN] 0940-2993
  • [Journal-full-title] Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie
  • [ISO-abbreviation] Exp. Toxicol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Bmp6 protein, rat; 0 / Bone Morphogenetic Protein 6; 0 / Bone Morphogenetic Proteins; 0 / RNA, Messenger; 106441-73-0 / Osteopontin; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.19 / Bmp1 protein, rat; EC 3.4.24.19 / Bone Morphogenetic Protein 1; Q20Q21Q62J / Cisplatin
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13. Hess PR, Boczkowski D, Nair SK, Snyder D, Gilboa E: Vaccination with mRNAs encoding tumor-associated antigens and granulocyte-macrophage colony-stimulating factor efficiently primes CTL responses, but is insufficient to overcome tolerance to a model tumor/self antigen. Cancer Immunol Immunother; 2006 Jun;55(6):672-83
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vaccination with mRNAs encoding tumor-associated antigens and granulocyte-macrophage colony-stimulating factor efficiently primes CTL responses, but is insufficient to overcome tolerance to a model tumor/self antigen.
  • Immunization of mice with dendritic cells transfected ex vivo with tumor-associated antigen (TAA)-encoding mRNA primes cytotoxic T lymphocytes (CTL) that mediate tumor rejection.
  • Intradermal and intravenous injection of ovalbumin (OVA) mRNA generated specific CTL activity and inhibited the growth of OVA-expressing tumors.
  • Vaccination studies with DNA have demonstrated that co-administration of antigen (Ag)- and cytokine-encoding plasmids potentiate the T cell response; in analogous fashion, the inclusion of granulocyte-macrophage colony-stimulating factor (GM-CSF) mRNA enhanced OVA-specific cytotoxicity.
  • The ability of this GM-CSF-augmented mRNA vaccine to treat an established spontaneous tumor was evaluated in the Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) mouse, using the SV40 large T Ag (TAg) as a model tumor/self Ag.
  • Repeated vaccination elicited vigorous TAg-specific CTL activity in nontransgenic mice, but tumor-bearing TRAMP mice remained tolerant.
  • Adoptive transfer of naïve splenocytes into TRAMP mice prior to the first vaccination restored TAg reactivity, and slowed tumor progression.
  • Nonetheless, limitations of such vaccines in overcoming tolerance to tumor/self Ag may mandate prior or simultaneous reconstitution of the autoreactive T cell repertoire for this form of immunization to be effective.
  • [MeSH-minor] Animals. Autoantigens / immunology. Disease Models, Animal. Liposomes. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Polymerase Chain Reaction. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / immunology. Transfection

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  • (PMID = 16133108.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA-85307; United States / NCI NIH HHS / CA / R01-CA-89536
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Autoantigens; 0 / Cancer Vaccines; 0 / Liposomes; 0 / RNA, Messenger; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
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14. Schuller HM, Porter B, Riechert A, Walker K, Schmoyer R: Neuroendocrine lung carcinogenesis in hamsters is inhibited by green tea or theophylline while the development of adenocarcinomas is promoted: implications for chemoprevention in smokers. Lung Cancer; 2004 Jul;45(1):11-8
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  • Lung cancer continues to be the leading cause of cancer death in developed countries.
  • With smoking the major etiological factor for lung cancer, there is a great need for the development of chemopreventive treatments that inhibit the progression of initiated cells and premalignant lesions into overt lung cancer in smokers who quit.
  • In turn, the function of such signaling pathways is highly cell type-specific, with a given pathway inhibiting the growth of one cell type while stimulating the growth of others.
  • This hypothesis is based on published evidence that human small cell lung cancer as well as the neuroendocrine hamster tumors are regulated via autocrine signaling pathways that activate Raf-1 and the mitogen-activated (MAP) kinase pathway whereas human pulmonary adenocarcinomas of Clara cell lineage and the hamster model of this cancer type are regulated by a beta-adrenergic pathway involving the activation of cyclic adenosine 3',5'-monophosphate (cAMP) and the arachidonic acid (AA) cascade.
  • In turn, it was hypothesized that theophylline would inhibit Raf-1-dependent tumor progression while promoting cAMP-dependent tumor progression due to its documented ability to inhibit the enzyme cAMP-phophodiesterase.
  • The experimental design simulated chemoprevention in former smokers in that treatments with tea or theophylline started after completion of a 10-week tumor induction period with NNK.
  • Our data show that green tea as well as theophylline significantly inhibited lung tumor multiplicity in the neuroendocrine cancer model whereas identical chemopreventive treatments significantly promoted the lung tumor multiplicity in the adenocarcinoma model.
  • At the current state of knowledge such chemopreventive treatments should only be used as adjuvant to cancer therapy of cancers that have been fully characterized at the pathology and molecular level.
  • [MeSH-major] Adenocarcinoma / etiology. Adenocarcinoma / prevention & control. Bronchodilator Agents / pharmacology. Cell Transformation, Neoplastic / drug effects. Chemoprevention. Lung Neoplasms / etiology. Lung Neoplasms / prevention & control. Neuroendocrine Tumors / etiology. Neuroendocrine Tumors / prevention & control. Smoking / adverse effects. Tea / chemistry. Theophylline / pharmacology
  • [MeSH-minor] Animals. Cricetinae. Disease Models, Animal. Disease Progression. Male. Mesocricetus. Neoplasms, Experimental

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  • [Copyright] Copyright 2004 Elsevier Ireland Ltd.
  • (PMID = 15196729.001).
  • [ISSN] 0169-5002
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA096128
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Bronchodilator Agents; 0 / Tea; C137DTR5RG / Theophylline
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15. Nagamatsu K, Tsuchiya F, Oguma K, Maruyama H, Kano R, Hasegawa A: The effect of small interfering RNA (siRNA) against the Bcl-2 gene on apoptosis and chemosensitivity in a canine mammary gland tumor cell line. Res Vet Sci; 2008 Feb;84(1):49-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effect of small interfering RNA (siRNA) against the Bcl-2 gene on apoptosis and chemosensitivity in a canine mammary gland tumor cell line.
  • The aim of this study was to investigate whether downregulation of Bcl-2 expression by small interfering RNA (siRNA) against the canine Bcl-2 gene would enhance the apoptosis and sensitivity of a canine mammary gland tumor cell line (CF33) to doxorubicin.
  • Sequence-specific downregulation of Bcl-2 expression was measured by semiquantitative RT-PCR and Western blot analysis.
  • This study indicated that downregulation of Bcl-2 expression by siRNA would be useful as a new protocol to increase the effect of doxorubicin on treatment of canine mammary gland tumors, requiring a detailed evaluation of siRNA in vivo.
  • [MeSH-major] Apoptosis / genetics. Doxorubicin / pharmacology. Genes, bcl-2 / genetics. Mammary Neoplasms, Animal / drug therapy. Mammary Neoplasms, Animal / genetics. RNA, Small Interfering / genetics
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cell Line, Tumor. Dogs. Dose-Response Relationship, Drug. Down-Regulation. Gene Expression Regulation, Neoplastic. RNA Interference

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  • (PMID = 17537469.001).
  • [ISSN] 0034-5288
  • [Journal-full-title] Research in veterinary science
  • [ISO-abbreviation] Res. Vet. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / RNA, Small Interfering; 80168379AG / Doxorubicin
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16. Zusman I: Soluble tumor-associated antigens in cancer detection, prevention and therapy. Med Sci Monit; 2004 Dec;10(12):RA317-24
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  • [Title] Soluble tumor-associated antigens in cancer detection, prevention and therapy.
  • Soluble tumor-associated antigens (sTAA) with molecular mass of 66 and 51 kDa isolated from the serum of cancer patients was shown can be used for cancer detection, prevention and therapy.
  • CANCER DETECTION: Cancer progression is reflected in the relationship between p66 and p51 compared to healthy people or to patients with non-cancer diseases.
  • The method was shown to be highly sensitive (92 to 96%) and moderate specific (42 to 65%) for the detection of different types of cancer, such as of the colon, uterus, ovary, and breast, as well as melanoma.
  • CANCER PREVENTION AND THERAPY: sTAA have both tumor-preventive and tumor-suppressive effects on chemically induced cancers of the colon, skin and mammary glands in rats and mice. sTAA promote suppression of rat mammary tumors by different anticancer drugs, such as cyclophosphamide, tamoxifen and 5-fluorouracil, and decrease the drug's toxic side-effects.
  • CONCLUSIONS: We propose the follow-up after cancer patients in order to verify earlier as soon as possible recurrent cancer and perform preventive therapy of cancer suspect patients with their own sTAA as a kind of autoimmunotherapy.
  • Moreover, in combination with anticancer drugs, sTAA may serve as a new tool in prevention of toxic side-effects of chemotherapy.
  • [MeSH-major] Antigens, Neoplasm / blood. Neoplasms / diagnosis. Neoplasms / therapy
  • [MeSH-minor] Animals. Biomarkers, Tumor / blood. Cancer Vaccines. Humans. Mice. Rats

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  • (PMID = 15567995.001).
  • [ISSN] 1234-1010
  • [Journal-full-title] Medical science monitor : international medical journal of experimental and clinical research
  • [ISO-abbreviation] Med. Sci. Monit.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Cancer Vaccines
  • [Number-of-references] 86
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17. Schuster RK: Opisthorchiidosis--a review. Infect Disord Drug Targets; 2010 Oct;10(5):402-15

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although opisthorchiid flukes live in the bile ducts of the liver and in the gall bladder, they can affect surrounding liver tissue and even other organs.
  • However, the main medical significance is their role in the formation of malignant tumors.
  • Since the clinical symptoms are not specific, a diagnosis must be confirmed by parasitological examination or the detection of antibodies.
  • Apart from coproscopical methods, there are more recent and highly specific assays available, like the detection of coproantigen or the detection of DNA.
  • Praziquantel is the drug of choice for the treatment of opisthorchiidosis.
  • [MeSH-major] Opisthorchiasis / diagnosis. Opisthorchiasis / drug therapy. Opisthorchis
  • [MeSH-minor] Animals. Humans. Praziquantel / therapeutic use

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  • (PMID = 20701569.001).
  • [ISSN] 2212-3989
  • [Journal-full-title] Infectious disorders drug targets
  • [ISO-abbreviation] Infect Disord Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 6490C9U457 / Praziquantel
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18. Bergman PJ: Clinical techniques in small animal molecular oncology. Clin Tech Small Anim Pract; 2003 May;18(2):88-91

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical techniques in small animal molecular oncology.
  • The diagnosis, staging, and treatment of tumors in veterinary as well as human oncology have traditionally incorporated elements of anatomic extent of neoplasia through various clinical and pathologic methods.
  • These clinicopathological methods have been the basis for the development of the tumor, node, and metastasis and grading systems, which have translated into clinically significant advances over the last 20 to 30 years.
  • Unfortunately, there continues to be significant limitations to this system when prognostication and therapeutic decisions need to be made specific to a patient.
  • For example, completely resected and cleanly staged phenotypically identical grade II mast cell tumors in dogs can have opposing clinical outcomes.
  • In addition, dogs or cats with identical stage and grade lymphoma can have significantly divergent responses to the same multi-agent chemotherapy protocol.
  • Numerous nonanatomic neoplastic molecular prognostic factors have been recently identified and have the potential to improve on the presently available tumor, node, and metastasis- and grading-based systems.
  • This review will summarize how to best utilize presently available tumor, node, and metastasis- and grading-based systems, and incorporate newly available molecular prognostic factors.
  • [MeSH-major] Dog Diseases / pathology. Neoplasms / veterinary
  • [MeSH-minor] Animals. Biomarkers, Tumor. Dogs. Immunohistochemistry / veterinary. Neoplasm Invasiveness. Veterinary Medicine

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  • (PMID = 12831067.001).
  • [ISSN] 1096-2867
  • [Journal-full-title] Clinical techniques in small animal practice
  • [ISO-abbreviation] Clin Tech Small Anim Pract
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 15
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19. Safe S, McDougal A: Mechanism of action and development of selective aryl hydrocarbon receptor modulators for treatment of hormone-dependent cancers (Review). Int J Oncol; 2002 Jun;20(6):1123-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mechanism of action and development of selective aryl hydrocarbon receptor modulators for treatment of hormone-dependent cancers (Review).
  • Ligand-activated receptors are extensively used as targets for developing tissue-selective drugs for treatment of multiple diseases including cancers.
  • The high affinity ligand TCDD induces several AhR-mediated changes in gene expression, tissue/species-specific toxicities, and both tumorigenic and anticarcinogenic responses including inhibition of estrogen-dependent mammary and uterine tumor formation and growth.
  • Research in this laboratory has demonstrated that TCDD inhibits E2-induced responses in the rodent uterus and mammary tumors (growth inhibition) and in breast and endometrial cancer cell lines through complex inhibitory AhR-estrogen receptor (ER) crosstalk.
  • These compounds are relatively non-toxic and inhibit ER-positive and ER-negative mammary tumor growth, and synergize with tamoxifen to inhibit breast cancer growth and block tamoxifen-induced estrogenic activity in the uterus.
  • SAhRMs represent a novel class of drugs for treatment of hormone-dependent cancers, and combined therapies of SAhRMs with tamoxifen and other selective ER modulators (SERMs) provides a new approach for treating women with breast cancer.
  • [MeSH-major] Neoplasms, Hormone-Dependent / drug therapy. Receptors, Aryl Hydrocarbon / drug effects
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Female. Humans. Male. Receptors, Estrogen / analysis. Receptors, Estrogen / antagonists & inhibitors. Receptors, Estrogen / drug effects. Selective Estrogen Receptor Modulators / therapeutic use. Tetrachlorodibenzodioxin / pharmacology

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  • (PMID = 12011988.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA64081; United States / NIEHS NIH HHS / ES / ES04176; United States / NIEHS NIH HHS / ES / ES09106
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Receptors, Aryl Hydrocarbon; 0 / Receptors, Estrogen; 0 / Selective Estrogen Receptor Modulators; DO80M48B6O / Tetrachlorodibenzodioxin
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20. Vanderlaag K, Su Y, Frankel AE, Burghardt RC, Barhoumi R, Chadalapaka G, Jutooru I, Safe S: 1,1-Bis(3'-indolyl)-1-(p-substituted phenyl)methanes induce autophagic cell death in estrogen receptor negative breast cancer. BMC Cancer; 2010 Dec 03;10:669
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  • However, treatment of MDA-MB-231 and MDA-MB-453 cells with C-DIMs resulted in accumulation of LC3-II compared to LC3-I protein, a characteristic marker of autophagy, and transient transfection of green fluorescent protein-LC3 also revealed that treatment with C-DIMs induced a redistribution of LC3 to autophagosomes after C-DIM treatment.
  • In addition, the autofluorescent drug monodansylcadaverine (MDC), a specific autophagolysosome marker, accumulated in vacuoles after C-DIM treatment, and western blot analysis of lysates from cells treated with C-DIMs showed that the Beclin 1/Bcl-2 protein ratio increased.
  • CONCLUSION: The results suggest that C-DIM compounds may represent a new mechanism-based agent for treating drug-resistant ER-negative breast tumors through induction of autophagy.

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  • (PMID = 21129193.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01CA108718
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 1,1-bis(3'-indolyl)-1-(4-biphenyl)methane; 0 / 1,1-bis(3'-indolyl)-1-(4-t-butylphenyl)methane; 0 / Amino Acid Chloromethyl Ketones; 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / BECN1 protein, human; 0 / Biomarkers, Tumor; 0 / Caspase Inhibitors; 0 / Cysteine Proteinase Inhibitors; 0 / Indoles; 0 / Macrolides; 0 / Membrane Proteins; 0 / Microtubule-Associated Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Estrogen; 0 / Recombinant Fusion Proteins; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 88899-55-2 / bafilomycin A1; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC3003661
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