We present here the first report of an adult patient with simultaneous LCH and AML with t(9;11).5.

How pathologists communicate an error is complicated by the absence of a direct physician-patient relationship. Using 2 examples, we elaborate on how other physician colleagues routinely play an intermediary role in our day-to-day transactions and in the communication of a pathologist error to the patient. The concept of a "dual-hybrid" mind-set in the intermediary physician and its role in representing the pathologists' viewpoint adequately is considered. In a dual-hybrid mind-set, the intermediary physician can align with the patients' philosophy and like the patient, consider the smallest deviation from norm to be an error. Alternatively, they might embrace the traditional physician philosophy and communicate only those errors that resulted in a clinically inappropriate outcome. Neither may effectively reflect the pathologists' interests. We propose that pathologists develop strategies to communicate errors that include considerations of meeting with the patients directly. Such interactions promote healing for the patient and are relieving to the well-intentioned pathologist.

Craniopharyngioma is an epithelial tumor of the sellar region with a high survival rate but a high rate of recurrence, especially in children. Hypothalamic involvement, tumor recurrence, and multiple treatments result in clinical deterioration and impaired quality of life. Using immunohistochemistry, we investigated the expression pattern of osteonectin, a marker of tumor invasion and aggressive behavior, in 43 cases of craniopharyngioma. We observed a positive correlation of osteonectin expression in connective-type stromal tissue surrounding the epithelial tumor cells of craniopharyngioma with the extent of central nervous system infiltration and recurrence rate (P < .001). Given the previous success of chemotherapeutic agents that target the tumor microenvironment, our findings on osteonectin expression in stroma of craniopharyngiomas might, hopefully, be a guide to find newer prognostic markers capable of estimating the risk of progression or recurrence. They may also aid in the development of therapeutics that target tumor microenvironment to improve patient outcome.

The rare reports of primary, nonneuroendocrine small cell carcinomas of the thyroid have not provided enough evidence to support the recognition of these tumors as an entity or to understand their etiopathogenesis. We report the second case of a primary, nonneuroendocrine small cell carcinoma of the thyroid displaying diffuse expression of cytokeratins, CD99, and p63, in the absence of vimentin expression, in a 24-year-old male who is alive without any signs of disease 13 years after total thyroidectomy and radioactive iodine. The tumor disclosed the EWSR1-FLI1 rearrangement, and we propose to designate it as a carcinoma of the thyroid with Ewing family tumor elements.

We evaluated clinical parameters, histomorphology, and thyroid transcription factor 1 (TTF-1) immunoreactivity in 40 epidermal growth factor receptor (EGFR) mutation- and anaplastic lymphoma kinase (ALK) rearrangement-negative invasive pulmonary adenocarcinomas. Tumors were histomorphologically quantitated by a pulmonary pathologist and TTF-1 immunohistochemistry applied. EGFR mutation and ALK rearrangement status was determined with polymerase chain reaction/DNA sequencing and fluorescence in situ hybridization, respectively. Treatment response was related to type of treatment (P < .005) and clinical stage (P = .001). EGFR mutation- and ALK rearrangement-negative pulmonary adenocarcinomas containing papillary/micropapillary histology showed greater morphologic heterogeneity (P < .001), greater TTF-1 immunoreactivity (P = .004), and were more common in treatment responders (P < .05). These findings support that patients with pulmonary adenocarcinomas that are subject to nontargeted therapies may respond to treatment as a function of tumor cell differentiation with TTF-1 as a potential biomarker of this response.

An unusual granular variant of ameloblastoma presenting as a mandibular mass in a 43-year-old woman is described. These visually striking tumors display unusual and inconsistent immunohistochemical staining patterns although differential diagnosis from other granular cell lesions of the head and neck is usually not problematic.

Primary hepatic and hepatosplenic diffuse large B-cell lymphomas (DLBCLs) are rare cancers and form nodules in most instances. However, very rare cases can diffusely infiltrate the whole liver without nodules. The general clinicopathological features of these lymphomas have not been reported to date. In our current study, we attempted to elucidate the features of these lesions through our direct observations and by reviewing the current literature. We describe the characteristics of 2 patients with hepatic and hepatosplenic DLBCL by autopsy. The lymphoma cells showed diffuse infiltration of the liver, red pulp of the spleen, and bone marrow with intrasinusoidal and interstitial lymphomatous infiltration of the organs. We discuss our observations in relation to previously reported DLBCLs with a similar pathology.