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BACKGROUND Telomerase, a ribonucleoprotein complex that maintains telomeric DNA, has been detected in 67–93% of prostate carcinomas by telomeric repeat-amplification protocol assay (involving polymerase chain reaction). One study used in situ hybridization in nine patients; however, to date, no immunohistochemical results have been published. METHODS From two hospitals, the authors compiled data on 62 patients who underwent prostatectomy from January 1996 to May 2001. Representative tissue sections were immunostained with a polyclonal antibody to telomerase reverse transcriptase (TERT), the catalytic subunit of telomerase. Staining was evaluated by two observers and was correlated with grade, stage, and biochemical failure. There were 28 sections from low-grade to intermediate-grade tumors (Gleason score, 3–6), 14 sections with a Gleason score of 3 + 4 = 7, 9 sections with a Gleason score of 4 + 3 = 7, and 11 sections from high-grade tumors (Gleason score, 8–10). RESULTS From low-grade to high-grade tumors, the four groups described above disclosed nuclear reactivity in 64%, 100%, 100%, and 100% of sections, respectively. Mean percentages of 5%, 15%, 40%, and 51% of nuclei were reactive in the respective groups (P < 0.0001) with intratumoral heterogeneity. The percent of reactive tumor nuclei was not correlated with pathologic stage (P = 0.32) or margin status (P = 0.35). The basal cell layer in sections of high-grade prostatic intraepithelial neoplasia (HGPIN) and benign/atrophic acini was reactive; secretory cells were reactive in 13 of 34 HGPIN foci (38%) in 1–20% of nuclei and were never reactive in benign acini. Lymphocytes and skeletal muscle were reactive. Weak, nonspecific, cytoplasmic staining was noted in benign and tumor acini. CONCLUSIONS Like cytokeratin 34βE12, nuclear anti-TERT reactivity is a basal cell marker in nonneoplastic prostatic acini. Anti-TERT reactivity is acquired by secretory cells in tumorigenesis, but consistent reactivity is restricted to high-grade carcinoma (Gleason primary pattern ≥4). This histologic evidence suggests that higher grade tumors have maximally activated telomerase and may be most responsive to antitelomerase therapy. Cancer 2002;95:2487–93. © 2002 American Cancer Society. DOI 10.1002/cncr.10988

During a retrospective analysis of 877 cases of lung cancer, we explored the relationships between cell type, site, cavitation, varying degrees of hemoptysis, and radiation therapy. Massive terminal hemoptysis (29 cases) was found to be significantly associated with cavitated (P less than 0.0001 squamous cell carcinoma (P = 0.0002), ARISING IN EITHER THE RIGHT OR LEFT MAIN BRONCHI (P less than 0.0001). Lesser, nonlethal degrees of hemoptysis (140 cases) were not cell-type associated, occurring in approximately 15% of cases of all major tumor types. Radiotherapy, although employed more frequently in the massive-hemoptysis population, did not appear to be causally related to hemoptysis of any degree. An interesting case, which provoked the above study, is described: a patient with bronchogenic squamous cell carcinoma and terminal hemoptysis due to a tumor fistula between the primary lesion and the left atrial chamber. The forms of cardiac involvement in lung cancer are discussed.

A case of squamous cell carcinoma arising from an esophageal intramural squamous epithelial cyst is reported. Review of the literature reveals no previous reports of malignant transformation of esophageal cysts, although there have been reports of approximately 64 cases of benign esophageal cysts, and 35 cases of carcinoma arising in esophageal diverticula. In the present case, there was a history of increasing dysphagia for 2 months. Esophagram demonstrated a 4.5-cm concentric narrowing of the proximal esophagus just below the superior esophageal ring. Esophagoscopies revealed an esophageal stricture with intact mucosa, and bronchoscopy showed the lesion to be producing tracheal deviation. Multiple esophageal biopsies revealed mild mucosal hyperplasia with deep submucosal inflammatory changes suggesting an underlying lesion. Despite lack of histologic proof of malignancy, the patient underwent radiation therapy and bleomycin chemotherapy on the basis of the highly suggestive radiographic findings, but died with bilateral bronchopneumonia 6 months after admission. Autopsy demonstrated a 1.5-cm long intramural esophageal squamous epithelial cyst, from which arose a locally invasive squamous cell carcinoma, without mucosal involvement or metastases. There was no demonstrable evidence of any associated esophageal diverticulum.

Granulocytic sarcoma (chloroma) was present in 23 of 338 myelogenous leukemia patients autopsied in Hiroshima and Nagasaki during 1949-1969. There was no evidence that granulocytic sarcoma was more frequent among those who received heavy atomic-bomb irradiation, although the incidence of myelogenous leukemia was greatly increased in the heavily irradiated group compared with controls. Granulocytic sarcoma was found in 19 of 237 persons with acute myelogenous leukemia, in 3 of 77 with chronic myelogenous leukemia, and 1 of 24 with chronic myelogenous leukemia with blast crisis. It was distinguished from myelogenous leukemia by: significantly higher frequency in children and young adults; clinical manifestations of pain and tumor formation (often with exophthalmos) followed by paralysis and/or urinary incontinence; slightly shorter survival time; and greater intensity of leukemic infiltration in the pituitary. At autopsy, gross tumors occurred most frequently in bone, ovary, lymph nodes, kidney, dura, lung, arm, and breast. The pathogenesis of tumor formation in leukemia is discussed.