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I don't know what sort of Cancer Brooke Burke has, but there is a very real possibility that she is being overdiagnosed. Follow link for complete text:

 

 

 

A story is told by Juan Rosai about an atypical 

melanocytic lesion sent to him in consultation from a patholo- 

gist friend in private practice.

 

 

This is the dilemma that faces the practicing 

pathologist every day. The tendency to “overdiagnose” seems 

to be inevitable as long as there is a surfeit of aggressive, 

unforgiving malpractice attorneys as well as pathology experts 

and a limited risk to the “overdiagnosis.” 

 

This tendency to overdiagnose clearly is accentuated in 

private practice. Fueled by the perception that private practi- 

tioners are not as good as their academic counterparts, cases in 

growing numbers are being referred to the university setting 

for a second opinion, sometimes years after the case originally 

was signed out. If the diagnosis from this second opinion on a 

thyroid nodule is malignant when the original diagnosis was 

benign, the ramifications can be quite devastating. While there 

certainly are benefits to second opinions,1and we are in no 

way arguing against them, the unintended result of this prac- 

tice is to render the private pathologist more vulnerable, more 

prone to litigation, and more likely to overdiagnose. Defensive 

pathology is now so ingrained in the psyche of most private 

pathologists that it has become second nature. 

The purely follicular variant of papillary thyroid carci- 

noma (PTC) described by Lindsay in 19602and later popular- 

ized by Chen and Rosai3and Rosai et al4is now well accepted. 

The nuclear features have become tantamount to papillary 

structures in the diagnosis of PTC. The nuclear features 

include the following: (1) overlapping ground-glass, optically 

clear, or “Orphan Annie” nuclei and (2) nuclear pseudoinclu- 

sions and grooves, which represent cytoplasmic invaginations 

into the nucleus. Despite the universal recognition of this 

variant, it is not well characterized. The conventional PTC is 

classically an invasive tumor even when the majority of it is 

composed of follicles. The purely follicular variant of PTC on 

the other hand is often well circumscribed and encapsulated.4 

What clearly is lacking is a minimal histologic definition of the 

follicular variant of PTC. Is an occasional grooved nucleus 

with pale chromatin in a follicular neoplasm enough to warrant 

a diagnosis of malignancy? Should the nuclear changes be 

uniformly present throughout the nodule? Are the nuclear 

changes that we are seeing significant or are they the “pseudo- 

clear nuclei” described by Hapke and Dehner in the 1970s?5 

At present, there are only a few long-term follow-up 

studies (totaling only 107 patients, as nicely summarized by 

Chan6) of the encapsulated follicular variant of PTC. While it 

is true that only 1 of these 107 patients died of disease,7more 

than 25% of these patients had regional lymph node metas- 

tases. In addition, a recent study by Baloch and LiVolsi8 

described 5 cases in which the encapsulated follicular variant 

of PTC manifested as an occult primary with metastatic 

disease, or in which bone metastases appeared many years 

after resection, and invasion in the primary lesion was subtle 

enough to be overlooked. Another study documented rare 

clinical progression (lymph node metastases) in the macrofol- 

licular variant of PTC despite the fact that the dominant 

cytology and architecture of the primary tumor very closely 

resembled goiter.9In summary, although the follicular variant 

of PTC usually behaves in a very indolent fashion, it rarely 

can cause distal metastasis. Furthermore, the follicular variant...