Papillary Thyroid Carcinoma in its Follicular Form

David Rees^*
*Correspondence: David Rees, Department of Diabetes & Endocrinology, ABM University Health Board, Swansea, UK, Email:

Introduction

The identification of genetic, epigenetic and non-genetic factors that contribute to the heterogeneity of these cancers has been advancing as a result of recent advancements in biological technologies. In this review article, we talk about new findings that are making it easier to find new therapeutic targets and expanding our knowledge of the biology of thyroid cancer. Papillary thyroid microcarcinoma (PTMC) is defined as "papillary carcinoma measuring 1.0 cm or less in maximal diameter while other clinicopathological features [1,2].

Description

We also talk about how new discoveries in tumor biology can make it easier to create new targeting therapies for thyroid cancer and how intratumor heterogeneity might be important for understanding therapeutic resistance. The most prevalent malignant thyroid neoplasm is papillary thyroid carcinoma, which is typically identified by its papillary appearance. Based on size (microcarcinoma), several variants of papillary carcinoma have been described.

The risk of lymph node and distant metastases in children between the ages of 2 and 16 is also reported. to be higher in CPTC, the classic form of papillary thyroid cancer; In addition, the presence of the follicular variant of papillary thyroid cancer and other risk factors, such as extrathyroid invasión, would necessitate more aggressive treatment and extended followup than would be the case for patients older than 16 years. In patients with papillary thyroid carcinoma (PTC), central lymph node metastases (CLNM) are thought to be a predictor of local recurrence; however, the significance of prophylactic central lymph node dissection is debatable.

Instead of slavishly attempting to classify a single tumor into a specific variant, it is more important in these situations to comment on the tumor's clinically relevant morphological characteristics. Pathologic and clinical characteristics of papillary carcinoma variants are summarized in this review. 25 percent of medullary thyroid carcinomas (MTCs) are caused by multiple endocrine neoplasia type 2 A and B. Understanding the genetic changes that cause cancer has greatly improved the survival rates of MEN-2 patients.

Several variants of papillary carcinoma have been described; nature of the encapsulated tumor boundaries; architecture (cribriform-morular, solid, micropapillary, macrofollicular and follicular); characteristics of the cell (clear cell, hobnail, tall cell, columnar cell, oncocytic cell); additional tumor components (papillary carcinoma with a focal insular component, spindle and giant cell carcinoma, squamous cell carcinoma and mucoepidermoid carcinoma), stromal characteristics (papillary carcinoma with stroma-like fasciitis); or a combination of the aforementioned features (Warthin-like diffuse sclerosing).

There was no evidence of lymphadenopathy in the postoperative findings, which pointed to a left thyroid nodule. There were no signs of local invasion and the left lobe of the thyroid measured 4-32.5 cm and weighed 14 grams. A follicular adenoma was found in the initial histopathology, but a second histological examination of the thyroid revealed a circumscribed, differentiated neoplasm of thyroid follicular cell origin with tightly packed follicles, some of which were larger and had blunt papillae intraluminally.

Due to erroneous post-translational modifications, the calcitonin antibodies used in immunohistochemistry (IMHC) staining may not be able to recognize the calcitonin molecule, which is another possibility for the normal serum calcitonin levels. The same calcitonin antibodies used for the serum calcitonin assay were used for IMHC staining in all of the cases that were reported and the tumors showed a strong positive staining, ruling out major calcitonin protein abnormalities. Therefore, it appears that these cells retain the capacity to synthesize but do not secrete the calcitonin molecule for unknown reasons. In theory, there are two possible causes of our case's impaired calcitonin secretion, both of which have been described in the literature: During the process of the parafollicular cell dedifferentiating into the MTC cell, there is either a preneoplastic impairment in the parafollicular cell's calcitonin secretion or some abnormality in the secretion of calcitonin. However, despite our belief that this theory may be the most plausible explanation for our situation, the precise mechanism is still unknown and we do not have any evidence to support this.

The high iodine intake-induced BRAF mutation that may be a risk factor for the development of PT may be the cause of the increased incidence of PTC. By interfering with oncogene expression or the mutation of tumor suppressor genes like BRAF, ERK, RAS and p53, it has also been suggested that iodine can stop differentiated thyroid carcinoma from progressing into anaplastic carcinoma. Ultrasound imaging revealed a hyperechoic and hypervascular nodule that measured 4 cm by 2.5 cm in the left lobe of the thyroid. There was no pathological lymphadenopathy in the neck [3-5].

Conclusion

In conclusion, PTC predominated among the histological types of TC, the detection rate of TC significantly increased and female patients' mean age decreased following USI. Under high iodine intake, patients with either nodular goiter or chronic lymphocytic thyroiditis should be followed up.

Acknowledgement

None.

Conflict of Interest

There are no conflicts of interest by author.

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