title: Pleomorphic lobular carcinoma of the breast: its cell kinetics, expression of oncogenes and tumour suppressor genes compared with invasive ductal carcinomas and classical infiltrating lobular carcinomas.
abstract: OBJECTIVE
  The study addresses whether pleomorphic lobular breast carcinomas represent a distinct entity with respect to proliferation and apoptosis as well the expression of the p53, bcl-2 and Her2 protein.
  
  
  RESULTS
  The study included 30 cases of pleomorphic lobular carcinoma (PLC; G2 n=15, G3 n=15). Poorly differentiated invasive ductal carcinomas (IDC; n=15) and well-differentiated infiltrating lobular carcinomas (ILC; n=15) were used as controls. Lymph node metastases were present equally in all groups. MIB-1 labelling was counted as: PLC (G2) 8.36%; PLC (G3) 11.3%; IDC 44.26%; ILC 2.19% (P=0.0001, P=0.004, P=0.001). Apoptotic index was: PLC (G2) 0.82%; PLC (G3) 1.2%; IDC 2.09%; ILC 0.6% (P=0.009, P=0.001). Over-expression of Her2 protein was detected in 53% of PLC (G3) tumours and was present only in scattered cases in the other groups. PLCs and ILCs were strongly positive for bcl-2 and for hormone receptors, while p53+ cells were rare. IDCs exhibited a heterogeneous staining pattern for bcl-2 and for hormone receptors, while p53+ cells occurred considerably more frequently. Stage could not be linked directly to proliferation or apoptosis.
  
  
  CONCLUSIONS
  Our data suggest that more frequent over-expression of Her2 among PLCs (G3) as well as the generally low apoptosis can contribute to their aggressive behaviour.
authors.affiliation: Institute of Clinical Pathology, Department of Pathology, University Hospital Zurich, Zurich, Switzerland.
authors.forename: D
authors.initials: D
authors.lastname: Frolik
authors.forename: R
authors.initials: R
authors.lastname: Caduff
authors.forename: Z
authors.initials: Z
authors.lastname: Varga
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D034961:Antigens, Nuclear; D001053:Apolipoproteins; D053399:Apolipoproteins D; D017209:Apoptosis; D001943:Breast Neoplasms / Q000378:metabolism / Q000473:pathology*; D018270:Carcinoma, Ductal, Breast / Q000378:metabolism / Q000473:pathology*; D018275:Carcinoma, Lobular / Q000378:metabolism / Q000473:pathology*; D002352:Carrier Proteins / Q000032:analysis; D002455:Cell Division; D005260:Female; D006023:Glycoproteins; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D019394:Ki-67 Antigen; D026901:Membrane Transport Proteins; D008875:Middle Aged; D018396:Mucin-1 / Q000032:analysis; D009687:Nuclear Proteins / Q000032:analysis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000096:biosynthesis; D011960:Receptors, Estrogen / Q000032:analysis; D011980:Receptors, Progesterone / Q000032:analysis; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis
chemical_list: D034961:Antigens, Nuclear; D001053:Apolipoproteins; D053399:Apolipoproteins D; D002352:Carrier Proteins; D006023:Glycoproteins; D019394:Ki-67 Antigen; D026901:Membrane Transport Proteins; D018396:Mucin-1; D009687:Nuclear Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D018719:Erb-b2 Receptor Tyrosine Kinases; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016159:Tumor Suppressor Protein p53; C024328:APOD protein, human; C488892:PIP protein, human