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These cell lines carry the Epstein‐Barr virus (EBV) genome although only producer cultures synthetize EBV‐specific antigens (virus capsid antigen, VCA and early antigen, EA) detectable by direct and indirect immunofluorescence, usually in less than 5% of the cells. The ACIF test revealed an antigen localized in the nucleus of the lymphoblastoid cells. In contrast to EA and VCA, this antigen was present in over 90% of the cells of both producer and non‐producer cultures. The antigen was shown to be specific for EBV by comparing the reactions of 52 sera in the ACIF test. Sera giving the nuclear reaction contained antibodies to VCA, EA or antigens detectable by complement fixation tests on cell extracts, but sera without EBV antibodies failed to give the reaction. Weak, equivocal or discordant reactions occurred with six sera with low titres in VCA, EA or complement fixation tests. Cell lines derived by transformation of human and primate lymphocytes by EBV gave the nuclear reaction. Control cells with no known association with EBV were non‐reactive. These included foetal lymphocytes transformed by phytohaemagglutinin, cell lines derived from breast cancer, glioma, normal glia, pleuritis maligna and myeloma, and two marmoset lymphoid lines carrying Herpesvirus saimiri (HVS). In preliminary experiments, the ACIF test was used as a tool to trace the EBV genome at the cellular level. Cells from two Burkitt lymphoma biopsies, one tested after biopsy and one after passaging in nude mice, contained an EBV‐specific antigen. Three clones of cells derived from hybrids of mouse somatic cells and a human lymphoblastoid cell line also contained such an antigen, but the number of reactive cells varied from clone to clone. A fourth clone was non‐reactive.\u003C\u002Fjats:p>","\u003Cjats:title>Tóm tắt\u003C\u002Fjats:title>\u003Cjats:p>Kháng thể kháng bổ thể huỳnh quang (ACIF) đã được sử dụng để nghiên cứu các kháng nguyên sửa đổi bổ thể của các dòng tế bào lymphoblastoid người. Các dòng tế bào này mang bộ gen virus Epstein‐Barr (EBV) mặc dù chỉ có các văn hóa sản xuất mới tổng hợp các kháng nguyên đặc hiệu EBV (kháng nguyên vỏ virus, VCA và kháng nguyên sớm, EA) có thể phát hiện được thông qua huỳnh quang trực tiếp và gián tiếp, thường ở mức dưới 5% số tế bào. Thử nghiệm ACIF đã tiết lộ một kháng nguyên nằm trong nhân của các tế bào lymphoblastoid. Trái ngược với EA và VCA, kháng nguyên này có mặt ở trên 90% số tế bào của cả các văn hóa sản xuất và không sản xuất. Kháng nguyên đã được chứng minh là đặc hiệu đối với EBV bằng cách so sánh phản ứng của 52 huyết thanh trong thử nghiệm ACIF. Những huyết thanh tạo ra phản ứng nhân chứa kháng thể chống lại VCA, EA hoặc các kháng nguyên có thể phát hiện qua các thử nghiệm sửa đổi bổ thể trên các chiết xuất tế bào, nhưng các huyết thanh không có kháng thể EBV không tạo ra phản ứng. Các phản ứng yếu, không rõ ràng hoặc không đồng nhất xảy ra với sáu huyết thanh có mức độ thấp trong các thử nghiệm VCA, EA hoặc sửa đổi bổ thể. Các dòng tế bào được thu nhận bằng cách chuyển đổi tế bào lymphocyte người và linh trưởng do EBV gây ra đã cho phản ứng nhân. Các tế bào kiểm soát không có liên kết rõ ràng với EBV thì không có phản ứng. Những tế bào này bao gồm lymphocyte thai nhi được chuyển đổi bằng phytohaemagglutinin, các dòng tế bào từ ung thư vú, glioma, glia bình thường, viêm màng phổi ác tính và đa u tủy, cùng với hai dòng lymphoid marmoset mang virus Herpesvirus saimiri (HVS). Trong các thí nghiệm sơ bộ, thử nghiệm ACIF đã được sử dụng như một công cụ để theo dõi bộ gen EBV ở mức độ tế bào. Các tế bào từ hai mẫu sinh thiết u lympho Burkitt, một mẫu được thử nghiệm sau sinh thiết và một mẫu sau khi được truyền trong chuột nude, đã chứa một kháng nguyên đặc hiệu EBV. Ba dòng tế bào thu được từ các hợp nhất tế bào soma chuột và một dòng tế bào lymphoblastoid người cũng chứa kháng nguyên này, nhưng số lượng tế bào phản ứng khác nhau giữa các dòng. Một dòng thứ tư không có phản ứng.\u003C\u002Fjats:p>",{"EN":114,"VI":115},"Cellular localization of an Epstein‐Barr virus (EBV)‐associated complement‐fixing antigen in producer and non‐producer lymphoblastoid cell lines","Định vị tế bào của một kháng nguyên sửa đổi bổ thể liên quan đến virus Epstein‐Barr (EBV) trong các dòng tế bào lymphoblastoid sản xuất và không sản xuất",{"VOID":117},"4133943",{"VOID":119},"10.1002\u002Fijc.2910110302","PUBLICATION","VERIFIED","2024-09-18T19:27:33.123+00:00","Auto Verify",[125],"EN",[127],"VI","https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fijc.2910110302",[130,165],{"id":131,"sortIndex":25,"researcher":24,"roles":132,"affiliations":133,"properties":160,"displayName":162,"givenName":24,"familyName":24},"c2850ab3-6089-4c1e-a56c-3e7c4babd72d",[],[134,142,151],{"id":135,"sortIndex":25,"affiliation":136,"properties":24},"2fcb477e-9dd8-47bc-ab53-3a36236f57ee",{"id":135,"createTime":24,"updateTime":24,"relativeEntities":137,"slug":24,"properties":138,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":141,"statistic":24},[],{"title":139},{"VI":140},"Department of Tumor Biology, Karolinska Institutet, S 104 01 Stockholm 60, Sweden",[],{"id":143,"sortIndex":144,"affiliation":145,"properties":24},"7aada013-cee8-4c08-b9b9-116a0d4a5072",1,{"id":143,"createTime":24,"updateTime":24,"relativeEntities":146,"slug":24,"properties":147,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":150,"statistic":24},[],{"title":148},{"EN":149},"Recipient of D.B. Duncan Training Fellowship from the Queensland Cancer Fund",[],{"id":152,"sortIndex":153,"affiliation":154,"properties":24},"59707474-354d-4e58-a27c-6a59b1d490aa",2,{"id":152,"createTime":24,"updateTime":24,"relativeEntities":155,"slug":24,"properties":156,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":159,"statistic":24},[],{"title":157},{"EN":158},"on leave from the Queensland Institute of Medical Research. Present address: c\u002Fo Queensland Institute of Medical Research, Herston Road, Herston, Queensland, Australia 4006.",[],{"title":161,"openalex":163},{"EN":162},"Beverley M. 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W. Miller O. J. Pearson P. L. Klein G. andHarris H. Human chromosomes in 18 man‐mouse somatic hybrid cell lines analyzed by quinacrine fluorescence.J. cell. Sci. in press (1973.)",{"doi":241},"10.1242\u002Fjcs.12.3.809",{"id":24,"text":243,"url":24,"identifiers":244},"Armstrong D., 1966, Complement fixation tests with cell lines derived from Burkitt's lymphoma and acute leukaemias, J. Bact., 91, 1257, 10.1128\u002Fjb.91.3.1257-1262.1966",{"doi":245},"10.1128\u002Fjb.91.3.1257-1262.1966",{"id":24,"text":247,"url":24,"identifiers":248},"Chang R. S., 1971, Cell line initiation from cord blood leukocytes treated with viruses, chemicals and radiation, J. nat. Cancer Inst., 47, 479",{},{"id":24,"text":250,"url":24,"identifiers":251},"10.1002\u002F1097-0142(196706)20:6\u003C926::AID-CNCR2820200603>3.0.CO;2-4",{"doi":250},{"id":24,"text":253,"url":24,"identifiers":254},"Dalton A. J. Heine U. Kondratick J. M. Ablashi D. V. andElizabeth A.Blackhan Ultrastructural and complement fixation studies on suspension cultures derived from human solid tumors.J. nat. Cancer Inst. in press.",{},{"id":24,"text":256,"url":24,"identifiers":257},"De Schryver A., 1969, Epstein‐Barr virus‐associated antibody patterns in carcinoma of the post‐nasal space, Clin. exp. Immunol., 5, 443",{},{"id":24,"text":259,"url":24,"identifiers":260},"10.1002\u002Fijc.2910060315",{"doi":259},{"id":24,"text":262,"url":24,"identifiers":263},"Epstein M. A., 1966, Morphological and virological investigations on cultured Burkitt tumor lymphoblasts (strain Raji), J. nat. Cancer Inst., 37, 547",{},{"id":24,"text":265,"url":24,"identifiers":266},"10.1056\u002FNEJM196811212792101",{"doi":265},{"id":24,"text":268,"url":24,"identifiers":269},"Floyd R., 1971, Fluorescence complement fixation by lymphoblastoid cells, J. nat. Cancer Inst., 46, 383",{},{"id":24,"text":271,"url":24,"identifiers":272},"10.1016\u002F0042-6822(71)90108-5",{"doi":271},{"id":24,"text":274,"url":24,"identifiers":275},"10.1002\u002Fijc.2910070214",{"doi":274},{"id":24,"text":277,"url":24,"identifiers":278},"Goldwasser R. A., 1958, Staining of complement and modifications of fluorescent antibody procedures, J. Immunol., 80, 122, 10.4049\u002Fjimmunol.80.2.122",{"doi":279},"10.4049\u002Fjimmunol.80.2.122",{"id":24,"text":281,"url":24,"identifiers":282},"10.1073\u002Fpnas.68.7.1407",{"doi":281},{"id":24,"text":284,"url":24,"identifiers":285},"10.1128\u002FJB.91.3.1248-1256.1966",{"doi":284},{"id":24,"text":287,"url":24,"identifiers":288},"10.1111\u002Fj.2164-0947.1966.tb02253.x",{"doi":287},{"id":24,"text":290,"url":24,"identifiers":291},"Henle G., 1969, Antibodies to Epstein‐Barr virus in Burkitt's lymphoma and control groups, J. nat. Cancer Inst., 43, 1147",{},{"id":24,"text":293,"url":24,"identifiers":294},"10.1073\u002Fpnas.59.1.94",{"doi":293},{"id":24,"text":296,"url":24,"identifiers":297},"Henle W., 1970, Antibodies to Epstein‐Barr virus in nasopharyngeal carcinoma, other head and neck neoplasms and control groups, J. nat. Cancer Inst., 44, 225",{},{"id":24,"text":299,"url":24,"identifiers":300},"Henle G., 1971, Antibodies to early Epstein‐Barr virus‐induced antigens in Burkitt's lymphoma, J. nat. Cancer Inst., 46, 861",{},{"id":24,"text":302,"url":24,"identifiers":303},"10.1002\u002Fijc.2910080212",{"doi":302},{"id":24,"text":305,"url":24,"identifiers":306},"10.3181\u002F00379727-124-31677",{"doi":305},{"id":24,"text":308,"url":24,"identifiers":309},"Hinuma Y., 1961, Studies on the complement‐fixing antigens of poliomyelitis. III. Intracellular development of antigen, J. Immunol., 87, 367, 10.4049\u002Fjimmunol.87.4.367",{"doi":310},"10.4049\u002Fjimmunol.87.4.367",{"id":24,"text":312,"url":24,"identifiers":313},"Hinuma Y., 1962, Evaluation of the complement method of fluorescent antibody technique with myxoviruses, J. Immunol., 89, 19, 10.4049\u002Fjimmunol.89.1.19",{"doi":314},"10.4049\u002Fjimmunol.89.1.19",{"id":24,"text":316,"url":24,"identifiers":317},"Ikawata S., 1964, Cultivation in vitro of myelobasts from human leukemia, N. Y. State med. J., 64, 2279",{},{"id":24,"text":319,"url":24,"identifiers":320},"Junge U., 1971, Stimulation of peripheral lymphocytes by allogeneic and autochthonous mononucleosis lymphocyte cell lines, J. 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Identifying tumor‐associated antigens on the surface of intact tumor cells, as opposed to purified proteins, presents a challenge due to the difficulty of preserving complex 3‐D epitopic sites on the cell surface, the variable expression of antigens on different malignant cell types and the stereotactic interference of closely associated proteins on the intact membrane surface limiting accessibility to antigenic sites. A combinatorial Ig library of 10\u003Cjats:sup>10\u003C\u002Fjats:sup> clones was generated from the cDNA of PBMCs derived from patients with breast adenocarcinoma. Following subtractive panning, the library was enriched for Ig (Fab fragment) binding to intact adenocarcinoma cells and the resultant Fabs were screened against a cDNA expression library, itself generated from breast cancer cells. Using this approach, we isolated clones from the cDNA library expressing gC1q‐R, a glycoprotein comprising the major structure of C1, the first component of the complement system. gC1q‐R is a 33 kDa glycoprotein expressed not only on the cell surface but also intracellularly, with motifs that target it to mitochondria and complete homology with HABP and human HeLa cell protein p32, which is copurified with pre‐mRNA SF2. Sequencing of the gene encoding tumor‐associated gC1q‐R did not reveal any consistent tumor‐specific mutations. However, histochemical staining with anti‐gC1q‐R MAb demonstrated marked differential expression of gC1q‐R in thyroid, colon, pancreatic, gastric, esophageal and lung adenocarcinomas compared to their nonmalignant histologic counterparts. In contrast, differential expression was not seen in endometrial, renal and prostate carcinomas. Despite high expression in breast carcinoma, gC1q‐R was also expressed in nonmalignant breast tissue. Although the precise relation of gC1q‐R to carcinogenesis remains unclear, our finding of tumor overexpression and the known multivalent binding of gC1q‐R to not only C1q itself but also a variety of circulating plasma proteins as well as its involvement in cell‐to‐cell interactions suggest that gC1q‐R may have a role in tumor metastases and potentially serve in molecule‐specific targeting of malignant cells. © 2004 Wiley‐Liss, Inc.\u003C\u002Fjats:p>",{"EN":409},"Receptor for the globular heads of C1q (gC1q‐R, p33, hyaluronan‐binding protein) is preferentially expressed by adenocarcinoma cells",{"VOID":411},"15146564",{"VOID":413},"10.1002\u002Fijc.20105","2024-10-14T22:28:34.855+00:00",[125],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fijc.20105",[418,469,492,513,536,561,587,611],{"id":419,"sortIndex":25,"researcher":24,"roles":420,"affiliations":421,"properties":464,"displayName":466,"givenName":24,"familyName":24},"f14039eb-7ccf-4ab6-b834-7045aaab9e67",[],[422,430,438,446,455],{"id":423,"sortIndex":25,"affiliation":424,"properties":24},"74c36ec9-3b02-4f97-967a-134edd3476be",{"id":423,"createTime":24,"updateTime":24,"relativeEntities":425,"slug":24,"properties":426,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":429,"statistic":24},[],{"title":427},{"VI":428},"Cancer Research Center, Boston University School of Medicine, Boston, MA, USA",[],{"id":431,"sortIndex":144,"affiliation":432,"properties":24},"15231a30-a09c-4525-aa55-60140efac3e3",{"id":431,"createTime":24,"updateTime":24,"relativeEntities":433,"slug":24,"properties":434,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":437,"statistic":24},[],{"title":435},{"EN":436},"Daniel B. 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1991, Phagocyte cell molecules that bind the collagen‐like region of C1q. Involvement in the C1q‐mediated enhancement of phagocytosis, J Biol Chem, 366, 20345, 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DA, 1998, Adenovirus core protein V interacts with p32, a protein which is associated with both the mitochondria and the nucleus, J Gen Virol, 79, 1677, 10.1099\u002F0022-1317-79-7-1677",{"doi":856},"10.1099\u002F0022-1317-79-7-1677",{"id":24,"text":858,"url":24,"identifiers":859},"10.1006\u002Fviro.1997.8739",{"doi":858},{"id":24,"text":861,"url":24,"identifiers":862},"10.1128\u002Fjvi.69.5.3017-3023.1995",{"doi":861},{"id":24,"text":864,"url":24,"identifiers":865},"10.1172\u002FJCI10323",{"doi":864},{"id":24,"text":867,"url":24,"identifiers":868},"Dedio J, 1998, The multiligand‐binding protein gC1q‐R putative C1q receptor is a mitochondria protein, J Immunol, 160, 3534, 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10.1182\u002Fblood.V90.10.3819",{"doi":915},"10.1182\u002Fblood.V90.10.3819",{"id":917,"createTime":918,"updateTime":919,"relativeEntities":920,"slug":921,"properties":922,"entityType":120,"verifyStatus":121,"verifyTime":918,"verifyNote":123,"languages":937,"translateLanguages":24,"viewCount":25,"primaryUrl":938,"fullTextUrl":24,"authors":939,"publicationType":180,"publisherRelationship":1063,"citationCount":1113,"citationInfo":1114,"publishDate":1118,"publishYear":1115,"citationAnalyzeStatus":23,"lastCitationAnalyze":919,"indexDatabases":1119,"openAccess":24,"references":1120,"isForceReanalyzing":392},"410fb692-a648-437b-80e8-f39c95d301a6","2024-10-16T22:47:27.109+00:00","2026-05-21T13:59:28.074+00:00",[],"Increased-expression-of-fatty-acid-synthase-and-progesterone-receptor-in-early-steps-of-human-mammary-carcinogenesis",{"mag":923,"gsPaper":925,"openalex":927,"abstract":929,"title":931,"pm":933,"doi":935},{"VOID":924},"1974628766",{"VOID":926},"[\"15144819978737852866\"]",{"VOID":928},"W1974628766",{"EN":930},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Progestins increase the risk of breast cancer in the hormone therapy of menopause, and progesterone receptor‐induced fatty acid synthase (FAS) is a potential therapeutical target of breast cancer. In a first attempt to specify in which lesions at risk of breast cancer progestins might be acting, we have compared the progesterone receptor (PR) and FAS expression in preinvasive breast lesions and in adjacent “normal” mammary glands. We used archive paraffin‐embedded tissues from 116 patients, with 164 lesions of increasing histological risk from nonproliferative “benign” breast disease (BBD) to \u003Cjats:italic>in situ\u003C\u002Fjats:italic> breast carcinomas. Immunostaining using our FAS antibody and a PR antibody from Dako was quantified as continuous variables by computer‐assisted image analysis. FAS level increased (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 10\u003Cjats:sup>−3\u003C\u002Fjats:sup> by the Kruskall–Wallis test) in all lesions, starting from nonproliferative BBD, and was maximal in \u003Cjats:italic>in situ\u003C\u002Fjats:italic> carcinoma. The % of PR‐positive cells increased from nonproliferative BBD and was higher in proliferative atypia (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 10\u003Cjats:sup>−3\u003C\u002Fjats:sup>). It was very low in high‐grade DCIS corresponding to a likely different carcinogenesis pathway. There was a trend for a positive correlation between FAS and PR in normal glands. However, the 2 markers increased independently in BBD and were negatively correlated in \u003Cjats:italic>in situ\u003C\u002Fjats:italic> carcinomas. FAS and PR were positively correlated with Ki67 in BBD. The increased PR level in premalignant steps of mammary carcinogenesis suggests an early increased responsiveness to progestins. The increased FAS expression, in lesions parallel to their increased breast cancer risk, suggests further studies to develop new markers of high‐risk lesions and to prevent breast cancer. © 2006 Wiley‐Liss, Inc.\u003C\u002Fjats:p>",{"EN":932},"Increased expression of fatty acid synthase and progesterone receptor in early steps of human mammary 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pathway are highly expressed in in situ breast carcinoma, Clin Cancer Res, 3, 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21\u002F13 cells, 50 generations from cloning, are transplantable owing to the presence of a small proportion (about 0.001%) of highly tumorigenic variant cells. Non‐tumorigenic cells can easily be isolated from these stocks by recloning. With passage in vitro the proportion of tumorigenic variants can increase to over 90%. This may be due to any or all of three situations: 1) the appearance of many different new tumorigenic variants, 2) the selection of the initially observed variant cells because of their greater capacity for growth in culture, or 3) the presence of a replicating agent transmitted from a variant to other cells. Means by which the increase in the proportion of variants might be minimized are discussed.\u003C\u002Fjats:p>\u003Cjats:p>In contrast to BHK 21\u002F13 cells in early passage, their polyoma‐transformed derivatives are highly tumorigenic. Polyoma virus does not selectively transform existing tumorigenic variant cells; thus, the tumorigenicity of the transformed cells is a consequence of the virus‐cell interaction.\u003C\u002Fjats:p>",{"EN":1234},"The basis of the tumorigenicity of BHK 21 cells",{"VOID":1236},"4302087",{"VOID":1238},"10.1002\u002Fijc.2910030514",[125],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fijc.2910030514",[1242,1259],{"id":1243,"sortIndex":25,"researcher":24,"roles":1244,"affiliations":1245,"properties":1254,"displayName":1256,"givenName":24,"familyName":24},"b8247db5-f062-4fa5-9b63-334a0d48a719",[],[1246],{"id":1247,"sortIndex":25,"affiliation":1248,"properties":24},"71f58637-ee4f-47db-b60c-e5431b970c60",{"id":1247,"createTime":24,"updateTime":24,"relativeEntities":1249,"slug":24,"properties":1250,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1253,"statistic":24},[],{"title":1251},{"VI":1252},"Institute of Virology University of Glasgow Scotland",[],{"title":1255,"openalex":1257},{"EN":1256},"Oswald Jarrett",{"VOID":1258},"A5054683249",{"id":1260,"sortIndex":144,"researcher":24,"roles":1261,"affiliations":1262,"properties":1269,"displayName":1273,"givenName":24,"familyName":24},"f6937a99-ce7e-4798-834f-68e3394861e0",[],[1263],{"id":1247,"sortIndex":25,"affiliation":1264,"properties":24},{"id":1247,"createTime":24,"updateTime":24,"relativeEntities":1265,"slug":24,"properties":1266,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1268,"statistic":24},[],{"title":1267},{"VI":1252},[],{"orcid":1270,"title":1272,"openalex":1274},{"VOID":1271},"https:\u002F\u002Forcid.org\u002F0000-0002-7925-3515",{"EN":1273},"I. 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Cancer Inst., 30, 795",{},{"id":24,"text":1360,"url":24,"identifiers":1361},"10.1016\u002F0042-6822(64)90301-0",{"doi":1360},{"id":24,"text":1363,"url":24,"identifiers":1364},"10.1016\u002F0042-6822(62)90290-8",{"doi":1363},{"id":24,"text":1366,"url":24,"identifiers":1367},"McGee‐Russell S. M., 1964, Observations on virus ascites‐cell systems in Third European Regional Conf. Electron Microscope, 367",{},{"id":24,"text":1369,"url":24,"identifiers":1370},"Montagnier L., 1966, An epithelioid variant of the BHK 21 hamster fibroblast line and its transformation by polyoma virus, J. nat. Cancer Inst., 36, 503",{},{"id":24,"text":1372,"url":24,"identifiers":1373},"10.1073\u002Fpnas.60.1.126",{"doi":1372},{"id":24,"text":1375,"url":24,"identifiers":1376},"10.1084\u002Fjem.103.2.273",{"doi":1375},{"id":24,"text":1378,"url":24,"identifiers":1379},"10.1016\u002FS0074-7696(08)60556-2",{"doi":1378},{"id":24,"text":1381,"url":24,"identifiers":1382},"Sanford K. K., 1967, Search for “indicators” of neoplastic conversion in vitro, J. nat. Cancer Inst., 39, 705",{},{"id":24,"text":1384,"url":24,"identifiers":1385},"10.1016\u002F0042-6822(62)90071-5",{"doi":1384},{"id":24,"text":1387,"url":24,"identifiers":1388},"10.1101\u002FSQB.1962.027.001.035",{"doi":1387},{"id":24,"text":1390,"url":24,"identifiers":1391},"10.1016\u002F0042-6822(61)90320-8",{"doi":1390},{"id":24,"text":1393,"url":24,"identifiers":1394},"10.1038\u002F2031355a0",{"doi":1393},{"id":24,"text":1396,"url":24,"identifiers":1397},"Todaro G. J., 1963, Growth properties of polyoma virus‐induced hamster tumor cells, Cancer Res., 23, 825",{},{"id":24,"text":1399,"url":24,"identifiers":1400},"10.1073\u002Fpnas.49.2.171",{"doi":1399},{"id":24,"text":1402,"url":24,"identifiers":1403},"10.1038\u002F1811407a0",{"doi":1402},{"id":1405,"createTime":1406,"updateTime":1407,"relativeEntities":1408,"slug":1409,"properties":1410,"entityType":120,"verifyStatus":121,"verifyTime":1406,"verifyNote":123,"languages":1426,"translateLanguages":24,"viewCount":25,"primaryUrl":1427,"fullTextUrl":24,"authors":1428,"publicationType":180,"publisherRelationship":1580,"citationCount":1630,"citationInfo":1631,"publishDate":1634,"publishYear":1632,"citationAnalyzeStatus":707,"lastCitationAnalyze":1635,"indexDatabases":1636,"openAccess":24,"references":1637,"isForceReanalyzing":392},"46750629-d2e1-45bd-8103-bcfbfb21959d","2024-08-31T00:21:33.971+00:00","2026-05-01T16:13:37.418+00:00",[],"Human-V%CE%B32V%CE%B42-T-cells-limit-breast-cancer-growth-by-modulating-cell-survival-apoptosis-related-molecules-and-microenvironment-in-tumors",{"mag":1411,"gsPaper":1413,"pmc":1414,"openalex":1416,"abstract":1418,"title":1420,"pm":1422,"doi":1424},{"VOID":1412},"1608402399",{"VOID":403},{"VOID":1415},"3939063",{"VOID":1417},"W1608402399",{"EN":1419},"\u003Cjats:p>Innate immune system has been known to play an important role in inhibiting the malignant transformation, tumor progression and invasion. However, the mechanistic basis remains ambiguous. Despite polyclonality of human γδ T cells, Vγ2Vδ2 T cell subset was shown to recognize and limit the growth of various tumors at various degrees. The differential recognition of the tumor cells by Vγ2Vδ2 T cells are yet to be defined. Our study reveals that γδ T cells limit \u003Cjats:italic>in vitro\u003C\u002Fjats:italic> growth of most breast tumor cells, such as SkBr7 (HER2+), MCF7 (ER+) and MDA‐MB‐231 (ER−) by inhibiting their survival and inducing apoptosis, except BrCa‐MZ01 (PR+) cells. To investigate detail mechanisms of antineoplastic effects, we found that cell death was associated with the surface expression levels of MICA\u002FB and ICAM1. Molecular signaling analysis demonstrated that inhibition of cell growth by γδ T cells was associated with the lower expression levels of cell survival‐related molecules such as AKT, ERK and concomitant upregulation of apoptosis‐related molecules, such as PARP, cleaved caspase 3 and tumor suppressor genes PTEN and P53. However, opposite molecular signaling was observed in the resistant cell line after coculture with γδ T cells. \u003Cjats:italic>In vivo\u003C\u002Fjats:italic>, antineoplastic effects of γδ T cells were also documented, where tumor growth was inhibited due to the downregulation of survival signals, strong induction of apoptotic molecules, disruption of microvasculature and increased infiltration of tumor associated macrophages. 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opisthorchiasis caused by \u003Cjats:italic>Opisthorchis viverrini\u003C\u002Fjats:italic> infection is characterized by advanced periductal fibrosis leading to hepatobiliary diseases (HBD), including cholangiocarcinoma (CCA). We aimed to determine fibrotic markers to differentiate HBD status including opisthorchiasis, benign biliary disease (BBD) and CCA. Candidate fibrotic markers in plasma of healthy individuals (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 14) and patients with opisthorchiasis (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 32, pre‐ and post‐treatment with praziquantel), BBD (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 31), CCA (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 37) and other types of tumors (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 14) were measured by ELISA and zymography. Plasma levels of hydroxyproline (HYP), collagen I, MMP‐7 and TIMP2 in opisthorchiasis patients were significantly higher than those in healthy individuals, and MMP9\u002FTIMP2 balance may be associated with tissue resorption after praziquantel treatment. HYP and TIMP‐2 levels were significantly correlated with periductal fibrosis status evaluated by ultrasonography. Plasma HYP level of CCA patients was the highest among HBD patients (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.05). ROC curves revealed HYP, MMP‐7 and collagen I levels significantly distinguished opisthorchiasis, BBD and CCA (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.001). Odd ratio (OR) analysis demonstrated these markers in opisthorchiasis were predictable for BBD risk (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.05; OR = 28.50, 10.12 and 4.63 for collagen I, MMP‐7 and HYP, respectively), and the risk was reduced by praziquantel treatment. Interestingly, only plasma HYP level in BBD was predictable for CCA risk (OR = 3.69; \u003Cjats:italic>p\u003C\u002Fjats:italic> = 0.020). 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breast is particularly vulnerable to carcinogenic influences during adolescence due to rapid proliferation of mammary cells and lack of terminal differentiation. We investigated consumption of adolescent red meat and other protein sources in relation to breast cancer risk in the Nurses' Health Study II cohort. We followed prospectively 44,231 women aged 33–52 years who, in 1998, completed a detailed questionnaire about diet during adolescence. Relative risks (RR) and 95% confidence intervals (95%CI) were estimated using Cox proportional hazard regression. We documented 1132 breast cancer cases during 13‐year follow‐up. In multivariable Cox regression models with major breast cancer risk factors adjustment, greater consumption of total red meat in adolescence was significantly associated with higher premenopausal breast cancer risk (highest \u003Cjats:italic>vs\u003C\u002Fjats:italic>. lowest quintiles, RR, 1.43; 95%CI, 1.05–1.94; \u003Cjats:italic>P\u003C\u002Fjats:italic>\u003Cjats:sub>trend\u003C\u002Fjats:sub> = 0.007), but not postmenopausal breast cancer. Adolescent intake of poultry was associated with lower risk of breast cancer overall (RR, 0.76; 95%CI, 0.60–0.97; for each serving\u002Fday). Adolescent intakes of iron, heme iron, fish, eggs, legumes and nuts were not associated with breast cancer. Replacement of one serving\u002Fday of total red meat with one serving of combination of poultry, fish, legumes, and nuts was associated with a 15% lower risk of breast cancer overall (RR, 0.85; 95%CI, 0.74–0.96) and a 23% lower risk of premenopausal breast cancer (RR, 0.77; 95%CI, 0.64–0.92). In conclusion, higher consumption of red meat during adolescence was associated with premenopausal breast cancer. 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The monoclonal antibody (MAb) Ki‐67 was used as a marker for proliferating cells and a polyclonal antibody directed against human von‐Willebrand factor to identify blood vessels. The proportion of Ki‐67‐labelled cells varied from 1% to 20%, the number of small blood vessels from 4.4\u002Fmm\u003Cjats:sup>2\u003C\u002Fjats:sup> to 57.6\u002Fmm\u003Cjats:sup>2\u003C\u002Fjats:sup>. Within single histological sections of individual tumours the percentage of proliferating cells was not related to the number of small blood vessels. However, after evaluation of 5 sections of each tumour, the average values showed that tumours with high grade of vascularization had a higher percentage of Ki‐67‐positive cells than poorly vascularized samples. The influence of vascular density on cell proliferation was investigated in a selected area of one of the tumours (in 2‐dimensions) and with regard to the over‐ and underlying sections (in 3‐dimensions). 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Zymographic analysis of conditioned medium from 2 highly invasive squamous‐cell‐carcinoma cell lines indicated large amounts of an enzyme which was indistinguishable, in size (92 kDa) from the MMP‐9 pro‐enzyme. Conversion of the 92‐kDa gelatinase into a lower‐molecular‐weight species (84 kDa), identical in size to the activated gelatinase, was evident when both cell lines, which are avid secretors of urokinase, were cultured in the presence of plasminogen. Penetration of an extracellular‐matrix‐coated filter was dramatically reduced in the presence of the collagenase inhibitor, tissue inhibitor of metalloproteinase‐2, suggesting a critical role for MMP‐9 in the invasive process. Immunohistochemical studies demonstrating the presence of MMP‐9 in tumor cells of resected squamous‐cell cancers suggested that secretion of this collagenase by cells in vitro was reflective of the in vivo setting. Since several phorbol‐ester response elements are present in the MMP‐9 promoter, we determined the role of protein‐kinase‐C pathways in the regulation of MMP‐9 expression in cultured SCC. Treatment of cells with PMA resulted in a more‐than‐20‐fold increase in the level of protein and mRNA. Conversely, culturing of cells in the presence of the protein‐kinase‐C inhibitor, calphostin‐C, led to a dose‐dependent decrease in the amount of MMP‐9 mRNA and protein, suggesting that the constitutive expression of this collagenase reflects activation of this signal transduction pathway. In summary, our data suggest that, for a sub‐population of squamous‐cell carcinomas, secreted MMP‐9 is an important determinant of the invasive phenotype, and that the expression of this metalloproteinase is regulated by protein‐kinase‐C pathways. © 1993 Wiley‐Liss, Inc.\u003C\u002Fjats:p>",{"EN":2730},"Role and regulation of expression of 92‐kDa type‐IV collagenase (MMP‐9) in 2 invasive squamous‐cell‐carcinoma cell lines of the oral cavity",{"VOID":2732},"7688350",{"VOID":2734},"10.1002\u002Fijc.2910550104",[125],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fijc.2910550104",[2738,2755,2774,2793,2810,2829,2846],{"id":2739,"sortIndex":25,"researcher":24,"roles":2740,"affiliations":2741,"properties":2750,"displayName":2752,"givenName":24,"familyName":24},"88e85c24-c496-4188-b663-95b12e3cce8c",[],[2742],{"id":2743,"sortIndex":25,"affiliation":2744,"properties":24},"149b4cbe-47d3-4516-947c-ba083f39d5c3",{"id":2743,"createTime":24,"updateTime":24,"relativeEntities":2745,"slug":24,"properties":2746,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2749,"statistic":24},[],{"title":2747},{"VI":2748},"University of Texas MD Anderson Cancer Center",[],{"title":2751,"openalex":2753},{"EN":2752},"Jose Juarez",{"VOID":2754},"A5065154328",{"id":2756,"sortIndex":144,"researcher":24,"roles":2757,"affiliations":2758,"properties":2767,"displayName":2771,"givenName":24,"familyName":24},"c3c09d5c-2c9e-436e-875f-f8d5e434ef4b",[],[2759],{"id":2760,"sortIndex":25,"affiliation":2761,"properties":24},"3ba119e5-ab77-460f-9827-5faf4fc8c906",{"id":2760,"createTime":24,"updateTime":24,"relativeEntities":2762,"slug":24,"properties":2763,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2766,"statistic":24},[],{"title":2764},{"VI":2765},"Head & Neck Surgery",[],{"orcid":2768,"title":2770,"openalex":2772},{"VOID":2769},"https:\u002F\u002Forcid.org\u002F0000-0002-2746-0387",{"EN":2771},"Gary L. 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Chem, 264, 17213, 10.1016\u002FS0021-9258(18)71480-4",{"doi":3010},"10.1016\u002FS0021-9258(18)71480-4",{"id":3012,"createTime":3013,"updateTime":3013,"relativeEntities":3014,"slug":3015,"properties":3016,"entityType":120,"verifyStatus":121,"verifyTime":3013,"verifyNote":123,"languages":3029,"translateLanguages":24,"viewCount":25,"primaryUrl":3030,"fullTextUrl":24,"authors":3031,"publicationType":180,"publisherRelationship":3128,"citationCount":2374,"citationInfo":3177,"publishDate":3180,"publishYear":3178,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":3181,"openAccess":24,"references":3182,"isForceReanalyzing":392},"409d5718-bfd8-4b7f-a311-1cdfa5851836","2025-02-10T15:51:31.561+00:00",[],"New-short-chain-analogs-of-a-substance-P-antagonist-inhibit-proliferation-of-human-small-cell-lung-cancer-cells-i-in-vitro-and-in-vivo-i-",{"openalex":3017,"mag":3019,"abstract":3021,"title":3023,"pm":3025,"doi":3027},{"VOID":3018},"W2073825587",{"VOID":3020},"2073825587",{"EN":3022},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Human small‐cell lung‐cancer cells (SCLC) produce and secrete gastrin‐releasing peptide (GRP), the mammalian equivalent of bombesin (BN). There is some evidence to suggest that GRP is an autocrine regulator of SCLC cell growth. In the search for potent BN antagonists, several substance‐P (SP) analogs were found to inhibit the growth of SCLC cells. We found that a known short‐chain SP antagonist, pHOPA‐DTrp‐Phe‐DTrp‐Leu‐Leu‐NH\u003Cjats:sub>2\u003C\u002Fjats:sub> (NY3238), inhibits the binding of \u003Cjats:sup>125\u003C\u002Fjats:sup>l‐Tyr\u003Cjats:sup>4\u003C\u002Fjats:sup>‐BN on Swiss 3T3 cell line expressing BN receptors, as well as the proliferation of NCI‐H69 SCLC cells. In this study we tested several analogs of NY3238 and we found that NY3521 and NY3460 are more effective in inhibition of proliferation of SCLC cells but less potent in inhibition of binding of \u003Cjats:sup>125\u003C\u002Fjats:sup>l‐Tyr\u003Cjats:sup>4\u003C\u002Fjats:sup>‐BN on Swiss 3T3 cells than NY3238. Furthermore, we detected specific binding of radiotabelled NY3238 even below I nM on NCI‐H69 cells that could have been inhibited by SP and NY3460 rather than by BN. In addition to these \u003Cjats:italic>in vitro\u003C\u002Fjats:italic> studies, NY3460 proved to be effective in inhibiting the growth of NCI‐H69 SCLC xenografts in nude mice \u003Cjats:italic>in vivo.\u003C\u002Fjats:italic> These analogs of NY3238 could be promising therapeutic agents in the treatment of SCLC. © 1995 Wiley‐Liss, Inc.\u003C\u002Fjats:p>",{"EN":3024},"New short‐chain analogs of a substance‐P antagonist inhibit proliferation of human small‐cell lung‐cancer cells \u003Ci>in vitro and in vivo\u003C\u002Fi>",{"VOID":3026},"7529212",{"VOID":3028},"10.1002\u002Fijc.2910600112",[125],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fijc.2910600112",[3032,3049,3066,3081,3096,3113],{"id":3033,"sortIndex":25,"researcher":24,"roles":3034,"affiliations":3035,"properties":3044,"displayName":3046,"givenName":24,"familyName":24},"0f29bb7b-1465-4801-976f-76c919b3decc",[],[3036],{"id":3037,"sortIndex":25,"affiliation":3038,"properties":24},"77b85dbf-0a8f-4173-a5e3-48fdaf35ee87",{"id":3037,"createTime":24,"updateTime":24,"relativeEntities":3039,"slug":24,"properties":3040,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3043,"statistic":24},[],{"title":3041},{"EN":3042},"Biochemical Department of National Korányi Institute for TBC and Pulmonology, Budapest, Hungary.",[],{"title":3045,"openalex":3047},{"EN":3046},"Antal Orosz",{"VOID":3048},"A5111771264",{"id":3050,"sortIndex":144,"researcher":24,"roles":3051,"affiliations":3052,"properties":3061,"displayName":3063,"givenName":24,"familyName":24},"d1bc8449-2fd5-484c-974b-c030f02cdb15",[],[3053],{"id":3054,"sortIndex":25,"affiliation":3055,"properties":24},"2f23f701-84c1-4255-9774-8a9fe12addf6",{"id":3054,"createTime":24,"updateTime":24,"relativeEntities":3056,"slug":24,"properties":3057,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3060,"statistic":24},[],{"title":3058},{"EN":3059},"Biochemical Department of National Korányi Institute for TBC and Pulmonology",[],{"title":3062,"openalex":3064},{"EN":3063},"János Schrett",{"VOID":3065},"A5029468907",{"id":3067,"sortIndex":153,"researcher":24,"roles":3068,"affiliations":3069,"properties":3076,"displayName":3078,"givenName":24,"familyName":24},"1103b663-bde9-462e-9ed4-ffc457716f88",[],[3070],{"id":3054,"sortIndex":25,"affiliation":3071,"properties":24},{"id":3054,"createTime":24,"updateTime":24,"relativeEntities":3072,"slug":24,"properties":3073,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3075,"statistic":24},[],{"title":3074},{"EN":3059},[],{"title":3077,"openalex":3079},{"EN":3078},"Józscf Nagy",{"VOID":3080},"A5037276946",{"id":3082,"sortIndex":448,"researcher":24,"roles":3083,"affiliations":3084,"properties":3091,"displayName":3093,"givenName":24,"familyName":24},"8545b37a-0368-45e7-ac3c-d50c50c50b93",[],[3085],{"id":3054,"sortIndex":25,"affiliation":3086,"properties":24},{"id":3054,"createTime":24,"updateTime":24,"relativeEntities":3087,"slug":24,"properties":3088,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3090,"statistic":24},[],{"title":3089},{"EN":3059},[],{"title":3092,"openalex":3094},{"EN":3093},"László Bartha",{"VOID":3095},"A5006221538",{"id":3097,"sortIndex":457,"researcher":24,"roles":3098,"affiliations":3099,"properties":3108,"displayName":3110,"givenName":24,"familyName":24},"5e878dc3-96a2-4dd1-b1c0-9a7df8197481",[],[3100],{"id":3101,"sortIndex":25,"affiliation":3102,"properties":24},"7b788ad8-d801-474c-8018-0f1d5261c5df",{"id":3101,"createTime":24,"updateTime":24,"relativeEntities":3103,"slug":24,"properties":3104,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3107,"statistic":24},[],{"title":3105},{"VI":3106},"Chemical Works of Gedeon Richter Ltd., Budapest, Hungary",[],{"title":3109,"openalex":3111},{"EN":3110},"István Schön",{"VOID":3112},"A5079550606",{"id":3114,"sortIndex":563,"researcher":24,"roles":3115,"affiliations":3116,"properties":3123,"displayName":3125,"givenName":24,"familyName":24},"dede4f46-884a-4a2b-b5bc-a44082755bf5",[],[3117],{"id":3101,"sortIndex":25,"affiliation":3118,"properties":24},{"id":3101,"createTime":24,"updateTime":24,"relativeEntities":3119,"slug":24,"properties":3120,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3122,"statistic":24},[],{"title":3121},{"VI":3106},[],{"title":3124,"openalex":3126},{"EN":3125},"O. 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