Skip to main content
SpringerLink
Log in

Clonality of endocrine proliferative lesions: A critical reappraisal

  • Commentary
  • Published:
Endocrine Pathology Aims and scope Submit manuscript

Abstract

The distinction between nodular hyperplasia and benign tumors of the endocrine system is problematical. Although numerous parameters including lesional size, multicentricity and histological features have been suggested as distinguishing criteria, none of these is absolute. Analyses based on X-chromosome inactivation have provided conflicting results with respect to the clonal origins of these lesions, and at least some lesions conventionally classified as hyperplastic nodules appear to be monoclonal. Although clonality has been generally equated with neoplasia, it is likely that clonal expansion of genetically normal cells can occur in the endocrine system as a result of a variety of growth-promoting stimuli. Multiparametric studies employing markers for X-chromosome inactivation together with methods for identification of unique non-X-linked genetic alterations will be required to resolve the many questions relating to the pathogenesis of endocrine proliferative lesions.

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

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References

  1. Carney JA, Sizemore GW, Sheps SG. Adrenal medullary hyperplasia in multiple endocrine neoplasia, type 2: pheochromocytoma and its precursors. Am J Clin Pathol 66:279–290, 1976.

    PubMed  CAS  Google Scholar 

  2. Masson P.Human tumors. Histology, diagnosis and technique, 2nd ed. (Kobernick SD, translated), Detroit: Wayne State University Press, 1970; pp. 602,603.

    Google Scholar 

  3. Busque I, Gilliland DG. X-inactivation analysis in the 1990s: progress and potential problems. Leukemia 12:128–135, 1998.

    Article  PubMed  CAS  Google Scholar 

  4. Kern SE. Clonality: more than just a tumor— progression model. J Natl Cancer Inst 85: 1020, 1021, 1993.

    Article  PubMed  CAS  Google Scholar 

  5. Nowell P. Mechanisms of tumor progression. Cancer Res 46:2203–2207, 1986.

    PubMed  CAS  Google Scholar 

  6. Vogelstein P, Kinzler KW. The multistepnature of cancer. Trends Genet. 8:138–141, 1993.

    Article  Google Scholar 

  7. Fialkow PJ. Clonal origin of human tumors. Biochim Biophys Acta 458:283–321, 1976.

    PubMed  CAS  Google Scholar 

  8. Baylin SB, Gann DS, Hsu SH. Clonal origin of inherited medullary thyroid carcinoma and pheochromocytomas. Science 193:321–323, 1976.

    Article  PubMed  CAS  Google Scholar 

  9. Fialkow PJ, Jackson CE, Block MA, Greenawald KA. Multicellular origin of parathyroid “adenomas”. N Engl J Med 297:696–698, 1977.

    Article  PubMed  CAS  Google Scholar 

  10. Wainscoat JS, Fey MF. Assessment of clonality in human tumors: A review. Cancer Res 50:1355–1360, 1990.

    PubMed  CAS  Google Scholar 

  11. Willman CL, Busque L, Griffith BB, Favara BE, McClain KL, Duncan MH, et al. Langerhans cell histiocytosis (histiocytosis X)— a clonal proliferative disease. N Engl J Med 331:154–160, 1994.

    Article  PubMed  CAS  Google Scholar 

  12. Aeschimann S, Kopp PA, Kimura ET, Zbaeren J, Tobler A, Fey MF, et al. Morphological and functional polymorphism within clonal rhyroid nodules. J Clin Endocrinol Metab 77:846–851, 1993.

    Article  PubMed  CAS  Google Scholar 

  13. Apel RL, Ezzar S, Bapat BV, Pan N, LiVolsi VA, Asa SL. Clonality of thyroid nodules in sporadic goiter. Diagn Mol Pathol 4:113–121, 1995.

    Article  PubMed  CAS  Google Scholar 

  14. Namba H, Matsuo K, Fagin JA. Clonal composition of benign and malignant human thyroid tumors. J Clin Invest 86:120–125, 1990.

    PubMed  CAS  Google Scholar 

  15. Thomas GA, Williams D, Williams ED. The clonal origin of thyroid nodules and adenomas. Am J Pathol 134:141–147, 1989.

    PubMed  CAS  Google Scholar 

  16. Arnold A. Molecular basis of primary hyperparathyproidism. In:The parathyroids. Basic and clinical concepts. Bilezekian JP, Marcus R, Levine MA, eds. New York: Raven, 1994; pp. 407–422.

    Google Scholar 

  17. Arnold A, Brown MF, Urena P, Gaz RD, Sarfarti E, Drueke TB. Monoclonality of parathyroid tumors in chronic renal failure and in primary parathyroid hyperplasia. J Clin Invest 95:2047–2053, 1995.

    Article  PubMed  CAS  Google Scholar 

  18. Shan L, Nakamura M, Nakamura Y, Inoue D, Morimoto S, Yokoi T, et al. Comparative analysis of clonality and pathology in primary and secondary hyperparathyroidism. Virchows Arch 430:247–251, 1997.

    Article  PubMed  CAS  Google Scholar 

  19. Peng H, Du M, Diss TC, Isaccson PG, Pan L. Clonality analysis in tumors of women by PCR amplification of X-linked genes. J Pathol 181:223–227, 1992.

    Article  Google Scholar 

  20. Bonner RF, Emmert-Buck M, Cole K, Pohida T, Chuaqui R, Goldstein S, et al. Laser capture microdissection: molecular analysis of issue. Science 278:1481, 1997.

    Article  PubMed  CAS  Google Scholar 

  21. Benditt EP, Benditt JM. Evidence for a monoclonal origin of human atherosclerotic plaques. Proc Natl Acad Sci USA 70:1753–1756, 1973.

    Article  PubMed  CAS  Google Scholar 

  22. Chung I-M, Schwartz SM, Murry CE. Clonal architecture of normal and atherosclerotic aortas. Implications for atherogenesis and vascular development. Am J Pathol 152:913–923, 1998.

    PubMed  CAS  Google Scholar 

  23. Tsai YC, Simoneau AR, Spruck CH, Nichols PW, Steven K, Buckley JD, et al. Mosaicism in human epithelium: macroscopic monoclonal patches cover the urothelium. J Urol 153:1697–1700, 1995.

    Article  PubMed  CAS  Google Scholar 

  24. Tsai Y, Lu Y, Nichols PW, Zlornikov P, Jones PA, Smith HS. Contiguous patches of normal human mammary epithelium derived from a single stem cell: Implications for breast carcinogenesis. Cancer Res 56:402–404, 1996.

    PubMed  CAS  Google Scholar 

  25. Thomas GA, Williams D, Williams ED. The demonstration of tissue clonality by X-linked enzyme histochemistry. J Pathol 155:101–108, 1988.

    Article  PubMed  CAS  Google Scholar 

  26. Collins RD. Is clonality equivalent to malignancy: specifically, is immunoglobulin gene rearrangement diagnostic of malignant lymphoma? Hum Pathol 28:757–759, 1997.

    Article  PubMed  CAS  Google Scholar 

  27. Studer H, Peter HJ, Gerber H. Natural heterogeneity of thyroid cells. The basis for understanding thyroid function and nodular goiter growth. Endocrine Rev 10:125–135, 1989.

    Article  CAS  Google Scholar 

  28. Ferraris AM, Mangerini R, Gaetani GF, Romei C, Pinchera A, Pacini F. Polyclonal origin of medullary carcinoma of the thyroid in multiple endocrine neoplasia type 2. Hum Genet 99:202–205, 1997.

    Article  PubMed  CAS  Google Scholar 

  29. Ewing J. Pathological aspects of some problems of experimental cancer research. J Cancer Res 1:71–86, 1916.

    Google Scholar 

Download references

Author information

Author notes

  1. Ronald A. DeLellis MD

    Present address: Department of Pathology, The New York Hospital-Cornell Medical Center, New York, NY

Authors and Affiliations

  1. Department of Pathology, The New England Medical Center and Tutis University School of Medicine, Boston, MA

    Arthur S. Tischler MD

Authors
  1. Ronald A. DeLellis MD
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Arthur S. Tischler MD
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Ronald A. DeLellis MD.

Rights and permissions

Reprints and permissions

About this article

Cite this article

DeLellis, R.A., Tischler, A.S. Clonality of endocrine proliferative lesions: A critical reappraisal. Endocr Pathol 9, 281–285 (1998). https://doi.org/10.1007/BF02739687

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF02739687

Key Words

Search

Navigation