Indian Journal of Pathology and Microbiology

: 2011  |  Volume : 54  |  Issue : 2  |  Page : 415-

Author's Reply

Ratnadeep Ganguly1, Sumit Mitra2, Asish K Datta3,  
1 Department of Pathology, The Mission Hospital, Durgapur, West Bengal, India
2 Department of Pathology, SSKM Hospital, Kolkata, West Bengal, India
3 Department of Histopathology, Apollo Gleneagles Hospitals, Kolkata, West Bengal, India

Correspondence Address:
Ratnadeep Ganguly
Department of Pathology, The Mission Hospital, Sector-2C, Immon Kalyan Sarani, Durgapur - 713 212, West Bengal

How to cite this article:
Ganguly R, Mitra S, Datta AK. Author's Reply.Indian J Pathol Microbiol 2011;54:415-415

How to cite this URL:
Ganguly R, Mitra S, Datta AK. Author's Reply. Indian J Pathol Microbiol [serial online] 2011 [cited 2020 Aug 6 ];54:415-415
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Full Text


Thank you very much for making the valuable observations and comments [1] about our patient. [2] We will address the issues that came up point by point.

Definitely the downhill differentiation of thyroid tumors has a relationship with the loss of the p53 function. We had thought of it but were limited by our repertoire to do the test then. However, we can do it now on the paraffin blocks but we do not think it will add significantly to our knowledge base.

Regarding the histogenesis of composite thyroid tumors, the collision theory and the hostage theory would be more applicable for the tumors with combined C cell and follicular cell type. In the case presented, all the tumors have a follicular histogenesis; hence in our opinion, it is either a common stem cell origin or any primary follicular cell tumor acquiring more mutations and attaining the anaplastic nature (de-differentiation). In fact it has also been proposed that even the follicular and parafollicular or C-cell-derived tumors have a common origin as suggested by the occurrence of intermediate variants. [3] Still other authors opine that the occurrence of the medullary variety, as a component of composite carcinomas, constitutes a rare subgroup of a separate histogenetic and prognostic significance. [4] I agree that the anaplastic carcinoma was the probable the cause of early mortality in our patient.

We did not, of course, screen the patient for the familial syndromes like Werner's, Cowden's, and Carney's complex before we knew the diagnosis of composite thyroid cancer. Once we had a diagnosis, we went back to her files and ruled them out clinically. Of course, with the patient in a critical condition, the priorities were different then; so we could not do the genetic tests. I agree with the need to get the relatives screened and genetically counseled, if need be and would check with the hospital records if these were done.


1Bhargav PR, Gayathri KB. Comment on: "Synchronous occurrence of anaplastic, follicular and papillary carcinomas with follicular adenoma in thyroid gland". Indian J Pathol Microbiol 2011;54:414-5
2Ganguly R, Mitra S, Datta AK. Synchronous occurrence of anaplastic, follicular and papillary carcinomas with follicular adenoma in thyroid gland. Indian J Pathol Microbiol 2010;53:337-9.
3Ljungberg O. Histogenesis of thyroid carcinoma. Med Hypotheses 1984;14:253-7.
4Merlino G, Barresi G, Tuccari G, Bussolati G. Histogenesis of anaplastic carcinomas of the thyroid, giant cell variety: Immunocytochemical investigation. Appl Pathol 1985;3:150-8.