Papillary tumor of the pineal region (PTPR) is a recently described tumor entity thought to arise from the specialized ependyma of the subcommissural organ. Whereas histologic features of PTPR are well defined, data on the prognostic value of PTPR remain scarce. We therefore investigated clinicopathologic features, including data on progression-free survival and overall survival, in a retrospective series of 31 PTPR. The age of the 14 males and 17 females ranged from 5 to 66 years (median age, 29 years). Histologically, all tumors were characterized by an epithelial-like growth pattern in which the vessels were covered by layers of columnar or cuboidal tumor cells forming perivascular pseudorosettes. Most of the tumor cells showed strong expression of neuron-specific enolase, cytokeratins (particularly CK18), S-100 protein, and vimentin. Most PTPRs examined also expressed microtubule-associated protein-2. Expression of synaptophysin, epithelial membrane antigen, transthyretin, neural cell adhesion molecule, and nestin was encountered in some tumors. Gross total resection could be achieved in 21 of 31 cases; 15 patients received radiotherapy on resection of the primary tumor. Nevertheless, the majority of patients experienced recurrences; 5-year estimates for overall survival and progression-free survival were 73% and 27%, respectively. To conclude, the clinical course of PTPR is characterized by frequent local recurrence, and the value of radiotherapy on disease progression will need to be investigated in future prospective trials.

Because of the increasing incidence of primary central nervous system lymphoma (PCNSL), it is essential to recognize this disease in order to start appropriate treatment. We present the characteristic CT and MRI features of this tumour. The findings of 32 CT and 31 MR of 37 immunocompetent patients with biopsy-proved PCNSL are reviewed. The main features are presented and analysed, and are discussed in comparison with proven literature data. Primary central nervous system lymphoma presents as supratentorial solitary lesions in approximately 80% of the patients and multiple lesions in 20%. In contrast to classical data, the lesions are located in deep structures only in one-third of the cases, and involve posterior fossa in 10% of cases. Most of the lesions are hyperdense or isodense (92%) on CT, hypointense or isointense on T1-weighted images, and only about 40% are hyperintense on T2-weighted images. Nearly all the lesions enhance, except after corticosteroid administration. They produce mild oedema and mass effect. Meningeal or ventricular enhancement are rare but suggestive. Calcification, haemorrhage or necrosis are scarce. Although PCNSL in immunocompetent patients have a variable CT and MR appearance, the imaging data often suggest the diagnosis.

Papillary tumors of the pineal region constitute a rare entity, with a difficult diagnosis, an uncertain prognosis, and a high risk of local recurrence; they must be treated by a combination of surgery and radiotherapy. The only identified prognostic factor is the complete or incomplete nature of surgical resection.

Aims:  To analyse the expression pattern of the semaphorin 3A (Sema3A) pathway, including the receptor neuropilin 1 (NRP1) and its ligands the ‘antitumoral’ Sema3A and the ‘protumoral’ vascular endothelial growth factor (VEGF)in prostatic cancer. Methods and results:  tissues were obtained from 120 patients treated by prostatectomy for clinically localized prostatic cancer, and 31 hormone‐refractory prostatic cancer (HRPC) samples. Immunohistochemistry was performed on tissue microarrays using antibodies directed against Sema3A, NRP1 and VEGF. Moreover, real‐time reverse transcriptase‐polymerase chain reaction was performed on frozen prostatic tissue, including normal prostate, clinically localized tumours and HPRC. Sema3A immunoreactivity of the membrane of cancer cells was closely associated with NRP1 expression in clinically localized prostatic cancer, but not in HRPC. In clinically localized cancer, Sema3A expression correlated with lower preoperative prostate‐specific antigen (PSA) and pathological stage; NRP1 reactivity was associated with lower PSA and Gleason score, and VEGF reactivity with higher PSA and Gleason score. HRPC displayed higher expression of NRP1 compared with clinically localized cancer, and lower Sema3A immunoreactivity. Conclusions:  These results support the hypothesis that dysregulation of the Sema3A pathway plays a key role in prostatic cancer progression, and suggest a loss of the inhibitory Sema3A autocrine loop in HRPC.

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