title: Steroid hormone receptor immunohistochemistry and amplification of c-myc protooncogene. Relationship to disease-free survival in breast cancer.
abstract: BACKGROUND
  It is important to develop parameters that aid in prognosticating which patients with breast cancer are more likely to have a rapid disease course and therefore might benefit from early aggressive therapies.
  
  
  METHODS
  Specimens from two groups of women, deliberately selected because their clinical courses differed greatly, were studied to detect amplification of the protooncogenes c-myc, int-2, and C-erbB-2/neu by slot-blot assay, the estrogen receptor (ER), and the progesterone receptor (PR) by both biochemical and immunohistochemical procedures (ERICA and PRICA). One group of 50 patients had a prolonged disease-free interval after initial surgery (mean, 6.4 years); the other group of 52 women had had rapid disease recurrence (mean, 1.4 years) or progression (5 patients died of disease within 1 year of diagnosis). The patients were selected from 1700 consecutively accessioned cases if they fit the study criteria and sufficient tissue was available for oncogene hybridization studies.
  
  
  RESULTS
  The two groups differed statistically by stage, number of involved axillary lymph nodes, ERICA and PRICA results (P = 0.001), and amplification of c-myc (P = 0.003). The percentage of patients with rapid disease recurrence and progression increased from 0-93% when risk factors changed from best case (ERICA and PRICA results, positive; c-myc, not amplified; and axillary nodes, not involved) to worst case (ERICA and PRICA findings, negative; c-myc, amplified; and axillary nodes, involved).
  
  
  CONCLUSIONS
  Women with these worst-case parameters were more likely to have a recurrence sooner and rapidly progressive disease. They might benefit from early aggressive therapeutic measures.
authors.affiliation: Department of Pathology, State University of New York, Health Science Center, Brooklyn.
authors.forename: L P
authors.initials: LP
authors.lastname: Pertschuk
authors.forename: J G
authors.initials: JG
authors.lastname: Feldman
authors.forename: D S
authors.initials: DS
authors.lastname: Kim
authors.forename: K
authors.initials: K
authors.lastname: Nayeri
authors.forename: K B
authors.initials: KB
authors.lastname: Eisenberg
authors.forename: A C
authors.initials: AC
authors.lastname: Carter
authors.forename: W T
authors.initials: WT
authors.lastname: Thelmo
authors.forename: Z T
authors.initials: ZT
authors.lastname: Rhong
authors.forename: P
authors.initials: P
authors.lastname: Benn
authors.forename: A
authors.initials: A
authors.lastname: Grossman
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001943:Breast Neoplasms / Q000737:chemistry / Q000235:genetics / Q000401:mortality* / Q000473:pathology; D016022:Case-Control Studies; D005260:Female; D005784:Gene Amplification; D006801:Humans; D008875:Middle Aged; D009364:Neoplasm Recurrence, Local / Q000737:chemistry / Q000235:genetics / Q000401:mortality* / Q000473:pathology; D011379:Prognosis; D011519:Proto-Oncogenes / Q000235:genetics*; D011960:Receptors, Estrogen / Q000032:analysis*; D011980:Receptors, Progesterone / Q000032:analysis*; D012044:Regression Analysis; D012307:Risk Factors
chemical_list: D011960:Receptors, Estrogen; D011980:Receptors, Progesterone