Skip to main content
SpringerLink
Log in

Morphological and biological observations relating to the development and progression of breast cancer

  • Chapter
Mammary Tumorigenesis and Malignant Progression

Part of the book series: Cancer Treatment and Research ((CTAR,volume 71))

Abstract

Mammary glands are basically modified sweat glands comprising a group of ducts descending from the skin in a radial system of dichotomously branching structures. The human female is unique in that the breast develops fully without the stimulus of copulation or pregnancy. Indeed, there are three overlapping phases of activity that can conveniently be termed structural, functional, and differentiated. The first is associated with puberty, the second with ovulatory menstrual cycles, and only the last with pregnancy and lactation. During the structural phase, the lengthening ducts descend into the fibrous disc below the nipple, extending within and along the contours of the fat spaces, giving rise to an inverted tree-like parenchymal structure. A crucial distinction of the human female from the other members of her species is the virginal development of terminal duct lobular units (TDLUs). These units are spherical or conical in shape due to the compact arrangement of multiple short branchings of the smaller blind-ended ductules, usually enclosed in a specialized stroma (figure 1). They form in groups and individually from the sides and ends of major, intermediate, and small ducts, measure well under 1 mm, and are situated most commonly in the outer third of the breast disc and axillary tail, often amounting to tens of thousands in number. The TDLUs consists of several cell types; the parenchymal branching component is composed of two principal cells, the luminal cuboidal or columnar epithelium and an outer layer of myo-epithelium, all enclosed by a basement membrane; on the opposite stromal side of the membrane lie fibroblasts and a loose textured collagen containing ground substance, traversed by small blood vessels and a variable component of lymphocytes, macrophages, and plasma cells. This intralobular stroma is usually distinguished microscopically from the denser collagen containing extralobular stroma, which is itself surrounded by fat cells. The adipose tissue composes the bulk of the breast, but it is the parenchymal and stromal components that constitute the responsive elements of the basic functioning unit that will become fully differentiated during pregnancy and lactation.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Log in via an institution
Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 169.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 219.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 379.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Russo J, Gusterson BA, Rogers AE, et al. 1990. Comparative studies of human and rat mammary tumorigenisis. Lab Invest 62: 244–277.

    PubMed  CAS  Google Scholar 

  2. Rudland PS. 1991. Histochemical organisation and cellular composition of ductal buds in developing human breast: evidence of cytochemical intermediates between epithelial and myoepithelial cells. J Histochem Cytochem 39: 1471–1484.

    PubMed  CAS  Google Scholar 

  3. McFarland J. 1922. Respiratory lactation assay in the female breast: Their relation to chronic cystic mastitis and malignant disease. Arch Surg 5: 1–64.

    Google Scholar 

  4. Going JJ, Anderson TJ, Battersby S, Maclntyre C. 1988. Proliferative and secretory activity in human breast during natural and artificial menstrual cycles. Am J Pathol 130: 193–204.

    PubMed  CAS  Google Scholar 

  5. Anderson TJ, Battersby S, King RJB, et al. 1989. Oral contraceptive use influences resting breast proliferation. Hum Pathol 20: 1139–1144.

    PubMed  CAS  Google Scholar 

  6. Williams G, Anderson E, Howell A, et al. 1991. Oral contraceptive (OCP) use increases proliferation and decreases oestrogen receptor content of epithelial cells in the normal human breast. Int J Cancer 48: 206–210.

    PubMed  CAS  Google Scholar 

  7. Anderson TJ, Ferguson DJP, Raab GM. 1982. Cell turnover in the ‘resting’ human breast: Influence of parity, contraceptive pill, age and laterality. Br J Cancer 46: 376–382.

    PubMed  CAS  Google Scholar 

  8. Potten CS, Watson RJ, Williams GT, et al. 1988. The effect of age and menstrual cycle upon proliferative activity of the normal breast. Br J Cancer 58: 163–170.

    PubMed  CAS  Google Scholar 

  9. Russo J, Calef G, Roi L, Russo IH. 1987. Influence of age and gland topography on cell kinetics of normal human breast tissue. J Natl Cancer Inst 98: 413–418.

    Google Scholar 

  10. Muir R. 1941. The evolution of carcinoma of the mamma. J Pathol Bacteriol 52: 155–172.

    CAS  Google Scholar 

  11. Foote FW, Stewart FW. 1945. Comparitive studies of cancerous versus non-cancerous breasts. Ann Surg 121: 6–53, 197-222.

    PubMed  CAS  Google Scholar 

  12. Battersby S, Anderson TJ. 1989. Histological changes in breast tissue that characterise recent pregnancy. Histopathology 15: 41–419.

    Google Scholar 

  13. McMahon B, Cole P, Linn TM, et al. 1970. Age at first birth and breast cancer risk. Bull WHO 43: 209–221.

    Google Scholar 

  14. Laron Z, Kanli R, Pertzelan A. 1988. Clinical evidence on the role of oestrogens in the development of the breasts. Proc R Soc Edin 95B: 13–22.

    Google Scholar 

  15. Howell A. 1988. Clinical evidence for the involvement of oestrogen in the development and progression of breast cancer. Proc R Soc Edin 95B: 49–57.

    Google Scholar 

  16. Husseby RA, Thomas LB. 1954. Histological and histochemical alterations in the normal breast tissues of patients with advanced breast cancer being treated with estrogenic hormones. Cancer 7: 54–62.

    Google Scholar 

  17. Stoll BA. 1992. Breast cancer risk in Japanese women with special reference to the growth hormone-insulin-like growth factor axis. Jpn J Clin Oncol 22: 1–5.

    PubMed  CAS  Google Scholar 

  18. Bidlingmaier F, Knorr D. 1978. Oestrogens — Physiological and Clinical Aspects, Pediatric and Adolescent Endocrinology, vol. 4. Karger: Basle, pp 6–81.

    Google Scholar 

  19. Ferenczy A, Bertrand G, Gelfand MM. 1988. Proliferation kinetics of human endometrium during the normal menstrual cycle. Am J Obstet Gynecol 133: 859–867.

    Google Scholar 

  20. Anderson TJ, Battersby S. 1988. The involvement of oestrogen in the development and function of the normal breast; histological evidence. Proc R Soc Edin 95B: 23–32.

    Google Scholar 

  21. King RJB. 1991. A discussion of the roles of oestrogen and progestin in human mammary carcinogenesis. J Steroid Biochem Molec Biol 39(5B): 811–818.

    PubMed  CAS  Google Scholar 

  22. Chalbos D, Escot C, Joyeux C, Tissot-Carayon MJ, Pages A, Rochefort H. 1990. Expression of the progestin-induced fatty acid synthetase in benign mastopathies and breast cancer as measured by RNA in situ hybridization. J Natl Cancer Inst 82: 602–606.

    PubMed  CAS  Google Scholar 

  23. McManus MJ, Welsch CW. 1984. The effect of estrogen, progesterone, thyroxine and human placental lactogen on DNA synthesis of human breast ductal epithelium maintained in athymic nude mice. Cancer 54: 1920–1927.

    PubMed  CAS  Google Scholar 

  24. Laidlaw IJ, Clarke R, Anderson E, Howell A. 1990. Proliferation of normal human breast tissue in nude mice after ovarian hormone stimulation. Br J Surg 77: A1419.

    Google Scholar 

  25. Mauvais-Jarvis P, Kuttenn F, Gompel A. 1986. Antiestrogen action of progesterone in breast cancer. Breast Cancer Res Treat 8: 179–188.

    PubMed  CAS  Google Scholar 

  26. Carpenter S, Georgiade G, McCarty KS Sr, McCarty KS Jr. 1988. Immunohistochemical expression of oestrogen receptor in normal breast tissue. Proc R Soc Edin 95B: 59–66.

    Google Scholar 

  27. Battersby S, Robertson BJ, Anderson TJ, King RJB, McPherson K. 1992. Influence of menstrual cycle, parity and oral contraceptive use on steroid hormone receptors in normal breast. Br J Cancer 65: 601–607.

    PubMed  CAS  Google Scholar 

  28. Press MF, Greene GL. 1988. Localization of progesterone receptor with monoclonal antibodies to the human progestin receptor. Endocrinology 122: 1165–1175.

    PubMed  CAS  Google Scholar 

  29. Lippman ME, Dickson RB. 1988. Growth control of normal and malignant breast epithelium. Proc R Soc Edin 95B: 89–106.

    Google Scholar 

  30. Dickson RB, Johnson MD, Bano M, Shi E, et al. 1992. Growth factors in breast cancer: mitogenesis to transformation. J Steroid Biochem Mol Biol 43(l–3): 69–78.

    PubMed  CAS  Google Scholar 

  31. Bano M, Worland P, Kidwell WR, et al. 1991. Receptor-induced phosphorylation by mammary-derived growth factor 1 in mammary epithelial cell lines. J Biol Chem 267: 10389–10392.

    Google Scholar 

  32. Osbournc CK, Clemmons DR, Arteaga CL. 1990. Rcgulation of breast cancer growth by insulin-like growth factors. J Steroid Biochem Mol Biol 37(6): 805–810.

    Google Scholar 

  33. Rosenfield RJ, Furlanetto R, Bock D. 1983. Relationship of somatomedin C concentration to pubertal changes. Pediatrics 103: 723–728.

    CAS  Google Scholar 

  34. Damjanov I, Mildner B, Knowles BB. 1986. Immunohistochemical localisation of epidcrmal growth factor receptor in normal tissues. Lab Invest 55: 588–592.

    PubMed  CAS  Google Scholar 

  35. Perusinghe NP, Monaghan P, O’Hare MJ, Ashley S, Gusterson BA. 1992. Effects of growth factors on proliferation of basal and luminal cells in human breast epithelial expiants in serum-free culture. In Vitro Cell Dev Biol 28A: 90–96.

    CAS  Google Scholar 

  36. Battersby S, Anderson TJ, Miller WR. 1994. Patterns of cyclic AMP binding proteins in normal breast. Breast Cancer Res Treat (in press).

    Google Scholar 

  37. Cho-Chung YS. 1990. Role of cyclic AMP receptor proteins in growth differentiation and suppression of malignancy: new approaches to therapy. Cancer Res 50(22): 7093–7100.

    PubMed  CAS  Google Scholar 

  38. O’Brian CA, Vogel VG, Singletary SE, Ward NE. 1989. Elevated protein kinase C expression in human breast tumor biopsies relative to normal breast tissue. Cancer Res 49: 3215–3217.

    PubMed  Google Scholar 

  39. Hennipman A, van Oirschot BA, Smith J, Rijksen G, Staal GEJ. 1989. Tyrosine kinase activity in breast cancer, benign breast disease and normal breast tissue. Cancer Res 49: 516–521.

    PubMed  CAS  Google Scholar 

  40. Anderson TJ, Wyllie AH. 1989. Neoplasia. In Kyle J, Carey LC (eds), Scientific Foundations of Surgery, 4th ed. Heinemann: London, pp 547–557.

    Google Scholar 

  41. Gallager HS. 1980. The developmental pathology of breast cancer. Cancer 46: 905–907.

    PubMed  CAS  Google Scholar 

  42. Wellings SR, Jensen HM, Marcum RG. 1975. An atlas of subgross pathology of the human breast with special reference to possible precancerous lesions. J Natl Cancer Inst 55: 231–273.

    PubMed  CAS  Google Scholar 

  43. Page DL, Dupont WD, Rogers LW, Landenberger M. 1982. Intraductal carcinoma of the breast: Follow-up after treatment by biopsy only. Cancer 49: 751–758.

    PubMed  CAS  Google Scholar 

  44. Betsill WL, Rosen PP, Lieberman PH, Robbins GF. 1978. Intra ductal carcinoma: Long-term follow-up after treatment by biopsy alone. JAMA 239: 1863–1867.

    PubMed  Google Scholar 

  45. Haggensen CD, Lane N, Lattes R, Bodian C. 1978. Lobular neoplasia (so called lobular carcinoma in situ) of the breast. Cancer 42: 737–769.

    Google Scholar 

  46. Dupont WD, Page DL. 1985. Risk factors for breast cancer in women with proliferative breast disease. N Engl J Med 312: 146–151.

    PubMed  CAS  Google Scholar 

  47. Rywlin AM. 1984. Perspectives in pathology: Terminology of premalignant lesions in light of the multistep theory of carcinogenesis. Hum Pathol 15: 806–807.

    PubMed  CAS  Google Scholar 

  48. Page DL, Dupont WD. 1990. Anatomic markers of human premalignancy and risk of breast cancer. Cancer 66: 1326–1335.

    PubMed  CAS  Google Scholar 

  49. Anderson TJ. 1991. Genesis and source of breast cancer. Br Med Bull 47: 305–318.

    PubMed  CAS  Google Scholar 

  50. Hutter RVP, et al. 1986. Consensus meeting. Is ‘fibrocystic disease’ of the breast precancerous? Arch Pathol Lab Med 110: 171–173.

    Google Scholar 

  51. Fearon ER, Vogelstein B. 1990. A genetic model for colorectal tumorigenesis. Cell 61: 759–767.

    PubMed  CAS  Google Scholar 

  52. Arends MJ, Wyllie AH, Bird CC. 1990. Papillomaviruses and human cancer. Hum Pathol 21: 686–698.

    PubMed  CAS  Google Scholar 

  53. Chamberlain J. 1982. Screening and natural history of breast cancer. In Baum M (ed), Clinics in Oncology: Breast Cancer, vol. 1(3). Saunders: Philadelphia, pp 679–701.

    Google Scholar 

  54. Anderson TJ. 1989. Breast cancer screening: Principles and practicalities for histopathologists. In Anthony P, MacSween RNM (eds), Recent Advances in Histopathology, vol. 14. Churchill Livingstone: Edinburgh, pp 43–61.

    Google Scholar 

  55. Miller AB. 1984. Biological aspects of natural history and its relevance to screening. In Prorock PC, Miller AB (eds), Screening for Cancer. UICC Technical Report Series 78: 44–54.

    Google Scholar 

  56. Forrest P. 1990. Breast cancer: the decision to screen. Nuffield Provisional Hospital Trust, London, pp 62–103.

    Google Scholar 

  57. Arnerlov C, Emdin SÖ, Lundgren B, et al. 1992. Breast carcinoma growth rate described by mammographic doubling time and s-phase fraction; Correlations to clinical and histopathologic factors in a screened population. Cancer 70: 1928–1934.

    PubMed  CAS  Google Scholar 

  58. Tabar L, Fagerberg G, Day NE, et al. 1992. Breast cancer treatment and natural history; new insights from results of screening. Lancet 339: 412–414.

    PubMed  CAS  Google Scholar 

  59. Hellman S, Harris JR. 1987. The appropriate breast cancer paradigm. Cancer Res 47: 339–342.

    PubMed  CAS  Google Scholar 

  60. Tubiana M, Koscielny S. 1991. Natural history of human breast cancer: Recent data and clinical implications. Breast Cancer Res Treat 18.125–140.

    PubMed  CAS  Google Scholar 

  61. Linell F, Rank F. 1989. Breast Cancer. Comments on Histologic Classifications with Reference to Histogenesis and Prognosis. Universitetsforlaget Dialogos: Lund, pp 18–68.

    Google Scholar 

  62. Anderson TJ, Battersby S. 1985. Radial scars of benign and malignant breasts: comparitive features and significance. J Pathol 147: 23–32.

    PubMed  CAS  Google Scholar 

  63. Andersen JA, Gram JB. 1984. Radial scar in the female breast: a long term follow-up of 32 cases. Cancer 53: 2557–2560.

    PubMed  CAS  Google Scholar 

  64. Andersen JA, Carter D, Linell F. 1986. A symposium on sclerosing duct lesions of the breast. Pathol Annu 21(2): 145–179.

    PubMed  Google Scholar 

  65. Anderson TJ, Lamb J, Donnan P, et al. 1991. Comparative pathology of breast cancer in a randomised trial of screening. Br J Cancer 64: 108–113.

    PubMed  CAS  Google Scholar 

  66. Hawkins RA, Miller WR. 1988. Endogenous sex hormones in cancer development. In Stoll BA (ed), Endocrine Management of Cancer: Biological Basis. Kargel Press: pp 45–60.

    Google Scholar 

  67. Preston-Martin S, Pike MC, Ross RK, Jones PA, Henderson BE. 1990. Increased cell division as a cause of human cancer. Cancer Res 50: 7415–7421.

    PubMed  CAS  Google Scholar 

  68. World Health Organization/ International Agency for Research on Cancer Genetic and Related Effects. 1987. An Updating of Selected IARC Monographs from Vols. 1-42. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Supplement. pp 250–256, 293-295, 369-371, 426-433, 437-443.

    Google Scholar 

  69. Nenci I, Marchetti E, Querzoli P. 1988. Commentary on human mammary preneoplasia: the estrogen receptor promotion hypothesis. J Steroid Biochem 30: 105–106.

    PubMed  CAS  Google Scholar 

  70. Hawkins RA, Tesdale AL, Ferguson WA, Going JJ. 1987. Oestrogen receptor activity in intraduct and invasive breast carcinomas. Breast Cancer Res Treat 9: 129–133.

    PubMed  CAS  Google Scholar 

  71. Alpers CE, Wellings SR. 1985. The prevalence of carcinoma in-situ in normal and cancer-associated breasts. Hum Pathol 16: 796–807.

    PubMed  CAS  Google Scholar 

  72. Dao TL, Sinha DK, Memota T, Patel J. 1982. Effects of estrogen and progesterone on cellular replication of human breast tumours. Cancer Res 42: 359–362.

    PubMed  CAS  Google Scholar 

  73. Miller WR 1990. Endocrine treatment for breast cancers: biological rationale and current progress. J Steroid Biochem Mol Biol 37: 467–480.

    PubMed  CAS  Google Scholar 

  74. Miller WR. 1991. Oestrogens and breast cancer: biological considerations. Br Med Bull 47: 470–483.

    PubMed  CAS  Google Scholar 

  75. Hawkins RA, Roberts MM, Forrest APM. 1980. Oestrogen receptors in breast cancer: Current status. Br J Surg 67: 153–169.

    PubMed  CAS  Google Scholar 

  76. Merkel DE, Osborne CK. 1988. Steroid receptors in relation to response. In Stoll BA (ed), Endocrine Management of Cancer: Biological Basis. Kargel Press: pp 84–89.

    Google Scholar 

  77. Weimer DA, Donegan WL. 1987. Changes in estrogen and progesterone receptor content of primary breast carcinoma during the menstrual cycle. Breast Cancer Res Treat 10: 273–278.

    PubMed  CAS  Google Scholar 

  78. Press MF, Nousek-Goebi N, King WJ, Herbst AL, Greene GL. 1984. Immunohisto-chemical assessment of estrogen receptor distribution in the human endometrium throughout the menstrual cycle. Lab Invest 51: 495–503.

    PubMed  CAS  Google Scholar 

  79. Santen RJ, Marini A, Harvey H, Richmond C. 1990. Endocrine treatment of breast cancer in women. Endocrine Rev 2: 221–265.

    Google Scholar 

  80. Horwitz KB, Freidenberg GR. 1985. Growth inhibition and increase of insulin receptors in antiestrogen-resistant T47DCO human brcast canccr cells by progcstins; implications for endocrine therapies. Cancer Res 45:167–173.

    PubMed  CAS  Google Scholar 

  81. Clark JH, Peck EJ Jr. 1979. Female sex steroids. Receptors and Function. Springer: Berlin, pp 99–113.

    Google Scholar 

  82. King RJB. 1990. Role of oestrogen and progestin in human mammary carcinogenesis. In Goldhirsch A (ed), Endocrine Therapy of Breast Cancer IV. Springer-Verlag: Berlin, pp 3–8.

    Google Scholar 

  83. King RJB. 1992. Progression from steroid sensitive to insensitive state in breast tumours. Cancer Surv 14: 131–146.

    PubMed  CAS  Google Scholar 

  84. Isaacs JT. 1988. Clinical heterogeneity in relation to response. In Stoll BA (ed), Endocrine Management of Cancer: Biological Basis. Pub Kargel Press: pp 125–145.

    Google Scholar 

  85. Hamon JT, Allegra JC. 1988. Loss of hormonal responsiveness in cancer. In Stoll BA (ed), Endocrine Management of Cancer: Biological Basis. Kargel Press: pp 61–71.

    Google Scholar 

  86. Allegra JC, Barlock A, Huff KK, Lippman ME. 1980. Changes in multiple or sequential estrogen receptors in breast cancer. Cancer 45: 792–794.

    PubMed  CAS  Google Scholar 

  87. Hawkins RA, Tesdale A, Anderson L, et al. 1990. Does the oestrogen receptor concentration of a breast cancer change during system therapy. Br J Cancer 61: 877–880.

    PubMed  CAS  Google Scholar 

  88. McGuire WL, Chamness GC, Fuqua SAW. 1992. Abnormal estrogen receptors in clinical breast cancer. J Steroid Biochem Mol Biol 43: 243–247.

    PubMed  CAS  Google Scholar 

  89. Klijn JGM, Berns PMJJ, Bontenbal M, Alexieva-Figusch J, Foeckens JA. 1992. Clinical breast cancer, new developments in selection and endocrine treatment of patients. J Steroid Biochem Mol Biol 43: 211–221.

    PubMed  CAS  Google Scholar 

  90. Allred DC, Clark GM, Molina R, Tandon AK, Schnitt SJ, Gilchrist KW, Osborne CK, Tormey DC, McGuire WL. 1992. Overexpression of HER-2/neu and its relationship with other prognostic factors change during the progression of in situ to invasive breast cancer. Hum Pathol 23: 974–979.

    PubMed  CAS  Google Scholar 

  91. Bates SE, Davidson NE, Valverius EM, Dickson RB, Freter CE, Tarn JP, Kudlow JE, Lippman ME, Salomon DS. 1988. Expression of transforming growth factor alpha and mRNAin human breast cancer: Its regulation by oestrogen and its possible functional significance. Mol Endocrinol 2: 543–555

    PubMed  CAS  Google Scholar 

  92. Travers MR, Barrett-Lee PJ, Berger U, Luqmani YA, Gazet J-C, Powles TJ, Coombes R. 1988. Growth factor expression in normal, benign and malignant breast tissue. Br Med J 296: 1621–1630.

    CAS  Google Scholar 

  93. Gregory H, Thomas CE, Willshire IR, Young JA, Anderson H, Baildan A, Howell A. 1989. Epidermal and transforming growth factor x in patients with breast tumours. Br J Cancer 59: 605–609.

    PubMed  CAS  Google Scholar 

  94. Dickson RB, Lippman ME. 1986. Hormonal control of human breast cancer cell lines. Cancer Surv 5: 617–624.

    PubMed  CAS  Google Scholar 

  95. King RJB, Wang DY, Daly RJ, Darbre PDJ. 1989. Approaches to studying the role of growth factors in the progression of breast tumours from the steroid sensitivity in insensitive state. J Steroid Biochem 34: 133–138.

    PubMed  CAS  Google Scholar 

  96. Knabbe C, Lippman ME, Wakefield LM, Flanders K, Hanoi A, Derynck R, Dickson RB. 1987. Evidence that TGFβ is a hormonally regulated growth factor in human breast cancer. Cell 48: 417–428.

    PubMed  CAS  Google Scholar 

  97. Coombes RC, Barrett-Lee P, Lugnani Y. 1990. Growth factor expression in breast tissue. J Steroid Biochem Mol Biol 37: 833–836.

    PubMed  CAS  Google Scholar 

  98. Delvenne CG, Winkler-Gol RA, Piccard MJ, Hustin J, Michaux D, Leclercq G, Nogaret JM, Autier Ph. 1992. Expression of c-erbB2, TGF-ßl and pS2 genes in primary human breast cancers. Eur J Cancer 28: 700–705.

    PubMed  CAS  Google Scholar 

  99. Butta A, macLennan K, Flanders KC, et al. 1992. Induction of transforming growth factor ßl in human breast cancer in vivo following tamoxifen treatment. Cancer Res 52: 4261–4264.

    PubMed  CAS  Google Scholar 

  100. Pekonen F, Partanen S, Makinen T, Rutanen EM. 1988. Receptors for epidermal growth factor and insulin growth factor 1 and their relation to steroid receptors in human breast cancer. Cancer Res 1343–1347.

    Google Scholar 

  101. Jammes H, Peyrat JP, Ban E, Vilain MO, Haour F, Djiane J, Bonneterre J. 1992. Insulinlike growth factor — receptors in human breast tumor — localization and quantification by histo-autoradiographic analysis. Br J Cancer 66(N2): 248–253.

    PubMed  CAS  Google Scholar 

  102. Cantley LC, Auger KR, Carpenter C, Duckworth B, Granziani A, Kapeller R, Soltoff. 1991. Oncogenes and signal transduction. Cell 64: 281–302.

    PubMed  CAS  Google Scholar 

  103. Ullrich A, Schlessinger J. 1990. Signal transduction by receptors with tyrosine kinase activity. Cell 61: 203–212.

    PubMed  CAS  Google Scholar 

  104. Waterfield MD. 1989. Growth factor receptors. Br Med Bull 45: 541–553.

    PubMed  CAS  Google Scholar 

  105. Ottenhoff-Kaff, AE, Rijksen G, van Beurden EACM, Hennipman A, Michels AA, Staal GEJ. 1992. Characterization of protein tyrosine kinases from human breast cancer: Involvement of the c-src oncogene product. Cancer Res 52: 4773–4778.

    Google Scholar 

  106. O’Brian CA, Ward NE. 1989. Biology of the protein kinase C family. Cancer Metastasis Rev 8: 199–214.

    PubMed  Google Scholar 

  107. Miller WR, Elton RA, Dixon JM, Chetty U, Watson DMA. 1990. Cyclic AMP binding proteins and prognosis in breast cancer. Br J Cancer 61: 263–266.

    PubMed  CAS  Google Scholar 

  108. Miller WR, Hulme MJ, Cho-Chung Y-S, Elton RA. In press. Types of cyclic AMP binding proteins in human breast cancers. Eur J Cancer.

    Google Scholar 

  109. Cho-Chung YS, Clair T, Tortora G, et al. 1991. Role of site-selective cAMP analogs in the control and reversal of malignancy. Pharmacol Ther 50: 1–33.

    PubMed  CAS  Google Scholar 

  110. Page DL, Dupont WD. 1992. Indicators of increased breast cancer risk in humans. J Cell Biochem Suppl 16G: 175–182.

    PubMed  CAS  Google Scholar 

Download references

Authors
  1. Thomas J. Anderson
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. William R. Miller
    View author publications

    You can also search for this author in PubMed Google Scholar

Editor information

Editors and Affiliations

  1. Lombardi Cancer Research Center, Georgetown University School of Medicine, Washington, DC, USA

    Robert B. Dickson  & Marc E. Lippman  & 

Rights and permissions

Reprints and permissions

Copyright information

© 1994 Springer Science+Business Media New York

About this chapter

Cite this chapter

Anderson, T.J., Miller, W.R. (1994). Morphological and biological observations relating to the development and progression of breast cancer. In: Dickson, R.B., Lippman, M.E. (eds) Mammary Tumorigenesis and Malignant Progression. Cancer Treatment and Research, vol 71. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2592-9_1

Download citation

  • DOI: https://doi.org/10.1007/978-1-4615-2592-9_1

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-6109-1

  • Online ISBN: 978-1-4615-2592-9

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics

Search

Navigation