9 research outputs found
A diagnostic pitfall; small cell carcinoma-like features in basaloid squamous cell carcinoma of the esophagus
Esophageal basaloid squamous cell
carcinoma may resemble small cell carcinoma biopsy
specimens and cause difficulties in pathology diagnosis.
We aimed to clarify the clinicopathological significance
of small cell carcinoma-like morphologies in basaloid
squamous cell carcinoma. Thirty biopsy specimens of
esophageal basaloid squamous cell carcinoma were
reviewed and compared with 13 matched surgical
specimens. Small cell carcinoma-like features, such as
diffuse growth, nuclear molding, or nuclear crush
artifact, were identified in 80% (24/30) of the biopsies
and in 77% (10/13) of the surgery specimens, but in a
proportionally much smaller area in the surgical
specimens than in the biopsy samples. The presence of a
small cell carcinoma-like feature had no impact on
patients´ outcome. Immunohistochemically, synaptophysin and chromogranin A were consistently negative,
while CD56 was expressed in 42% (10/24) of basaloid
squamous cell carcinomas with small cell carcinoma-like
features. p16, a highly sensitive marker for small cell
carcinoma, was also expressed in 8% (2/24). p40 was
expressed in all cases of basaloid squamous cell
carcinoma. In conclusion, small cell carcinoma-like
features are frequent and conspicuous in biopsies, which
are probably caused by exogenous factors such as
friction and external pressure that occur in biopsy
procedure and in the tumor environment. Small cell
carcinoma-like features may lead to a misinterpretation
of a true small cell carcinoma, if CD56 is the only
neuroendocrine marker expressed. p16 expression may
also be detected in basaloid squamous cell carcinoma
p16 in highly malignant esophageal carcinomas: the correlation with clinicopathological factors and human papillomavirus infection
p16 is generally considered to be a surrogate maker of human papillomavirus (HPV) infection and also a predictive marker of favorable clinical outcome of patients with squamous cell carcinoma of the oropharynx. p16 overexpression is also known to be induced by deregulation of RB1 in neuroendocrine carcinomas. In highly malignant esophageal neoplasms, however, the status of p16 has remained largely unknown. We immunolocalized p16 and Rb1 in 82 surgically resected esophageal high-grade squamous cell carcinomas (46 poorly differentiated and 36 basaloid squamous cell carcinomas) and 15 esophageal small-cell carcinomas in order to clarify the clinical and biological significance of p16. p16 immunoreactivity was detected in 7/82 (9%) high-grade squamous cell carcinomas and 15 (100%) small-cell carcinomas. p16 immunoreactivity was significantly associated with Rb1 protein loss in both groups (P < 0.001). HPV was detected in none of the p16-positive cases examined. Clinical outcome of the p16-positive high-grade squamous cell carcinomas was not different from that of the p16-negative counterparts (P = 0.687) but significantly better than those with the small-cell carcinomas (P = 0.023). p16 was therefore considered to be induced through an inactivation of the RB1 signaling pathway and not through HPV infection in highly malignant esophageal neoplasms. Nevertheless, patients' clinical outcome of these neoplasms significantly differs; therefore, small-cell carcinomas have to be carefully differentiated from other neoplasms. In addition, p16 overexpression is not predictive of favorable clinical outcome in high-grade squamous cell carcinomas of the esophagus