Papillary and follicular thyroid carcinomas are recognized entities of differentiated thyroid carcinomas (DTC’s) which are derived from thyroglobulin-secreting follicular cells . Collectively, they make up 80–95% of all thyroid cancers, the remaining variants being, poorly differentiated thyroid carcinoma, anaplastic carcinoma (AC) and medullary thyroid carcinoma (MTC) [10–12]. The simultaneous occurrences of these different histological thyroid cancers have been reported previously but mainly of PTC and MTC or a combination with other forms of cancers [13–18]. Despite the first reporting of a collision tumour of PTC and FTC almost a decade ago by Plauche et.al, data on this phenomenon is still lacking. [4, 5, 7].
The terms “collision tumours”, “synchronous tumours”, “mixed tumours” and “composite tumours” have been used to describe the simultaneous existence of different forms of malignant cells in an organ. Collision tumours are described as two independent tumours with distinct morphology which occur concurrently at the same site but having a distinct border [19, 20], whereas in synchronous tumours, these primaries are anatomically separated . The term “mixed tumours” is used when there is histological admixture of two tumours in the same organ with the same precursor cells while in “composite tumours”, the tumour contains two discrete cell populations .
A simultaneous occurrence of tumours pose a diagnostic challenge as FNA could miss the more sinister locus harboring malignancy as demonstrated in our case where the cytology of the right gland revealed cyst content while AUS was seen in the left gland. AUS carries a 6–18% risk of malignancy and the customary management is either a repeat FNA after an appropriate time interval, molecular studies or a surgical lobectomy, which was the initial proposed management in this case . Surprisingly, HPE of the right thyroid lobe in our case revealed a nodule of follicular neoplastic cells with capsular and vascular invasion – indicating FTC and another adjacent nodule with malignant cells arranged in papillary architecture exhibiting dispersed chromatin nuclei, ground glass appearance, nuclear pseudoinclusions and nuclear grooves consistent with PTC. These two nodules occurring in the same thyroid lobe, each with different malignant cells and having a distinct border allows its categorization as a “collision tumour”. In addition to that, the histopathological specimen of the left thyroid lobe also revealed PTC, further adding a concern on the potential aggressive nature of collision tumours. As per consensus with the oncologist, the patient was treated with radioiodine (131I) and was also subjected to thyroxine suppression therapy to treat both the PTC and FTC.
A number of theories have been proposed concerning the pathogenesis of these tumours but none could completely explain this phenomenon. In their retrospective review of 53 patients, Kim et al proposed that concurrent occurrences of thyroid carcinomas could simply be coincidental but did recognize the various theories related to this event which includes – stem cell theory, collision theory, hostage theory, tumourigenic stimulus and divergent differentiation theory [7, 23–26]. Genetic mutations were detected in studies of collision tumours and several genes have been implicated, namely BRAF, RAS and RET protooncogenes [27–29]. The use of molecular markers have shown promising results in the detection, prognostication and guidance of the therapeutic regime . Fundamentally, the concept of triple assessment by clinical examination, radiological imaging and cyto-histopathological confirmation that is usually performed for the investigation of thyroid lesions may miss these “collision tumours”. The addition of molecular markers as an investigative tool may be useful in selected cases.