Objective. There is increasing evidence in support of an association between systemic lupus erythematosus (SLE) and malignancy, but in earlier studies the association could not be quantified precisely. The present study was undertaken to ascertain the incidence of cancer in SLE patients, compared with that in the general population.Methods. We assembled a multisite (23 centers) international cohort of patients diagnosed as having SLE. Patients at each center were linked to regional tumor registries to determine cancer occurrence. Standardized incidence ratios (SIRs) were calculated as the ratio of observed to expected cancers. Cancers expected were determined by multiplying person-years in the cohort by the geographically matched age, sex, and calendar year-specific cancer rates, and summing over all person-years.Results. The 9,547 patients from 23 centers were observed for a total of 76,948 patient-years, with an average followup of 8 years. Within the observation interval, 431 cancers occurred. The data confirmed an Dr.

In our SLE sample, age > or = 65, damage, and tobacco exposure were associated with cancer risk. Though immunosuppressive therapy may not be the principal driving factor for overall cancer risk, it may contribute to an increased risk of haematological malignancies. Future studies are in progress to evaluate independent influence of medication exposures and disease activity on risk of malignancy.

Background: Recent evidence supports an association between systemic lupus erythematosus (SLE) and nonHodgkin's lymphoma (NHL). Objectives: To describe demographic factors, subtypes, and survival of patients with SLE who develop NHL. Methods: A multi-site cohort of 9547 subjects with definite SLE was assembled. Subjects at each centre were linked to regional tumour registries to determine cancer cases occurring after SLE diagnosis. For the NHL cases ascertained, descriptive statistics were calculated, and NHL subtype frequency and median survival time of patients determined.Results: 42 cases of NHL occurred in the patients with SLE during the 76 948 patient-years of observation. The median age of patients at NHL diagnosis was 57 years. Thirty six (86%) of the 42 patients developing NHL were women, reflecting the female predominance of the cohort. In the patients, aggressive histological subtypes appeared to predominate, with the most commonly identified NHL subtype being diffuse large B cell (11 out of 21 cases for which histological subtype was available). Twenty two of the patients had died a median of 1.2 years after lymphoma diagnosis. Conclusions: These data suggest aggressive disease in patients with SLE who develop NHL. Continuing work should provide further insight into the patterns of presentation, prognosis, and aetiology of NHL in SLE.

Background: Eighty percent of all breast cancers and almost 90% of breast cancer deaths occur among post-menopausal women. We used a nested case control design to examine the association between nonsteroidal anti-inflammatory drug (NSAID) use and breast cancer occurrence among women over 65 years of age. The cyclooxygenase (COX)-2 enzyme is expressed more in breast cancers than in normal breast tissue. COX-2 inhibition may have a role in breast cancer prevention.

A history of STDs and use of OCs were associated with abnormal Pap reports in this SLE sample. Immunosuppressive exposure may confer further risk to women with SLE.

Purpose Long-term (LT) androgen suppression (AS) with RT is a standard treatment for high-risk, localized prostate cancer (PCa). RTOG 9902 was a randomized trial testing the hypothesis that adjuvant combination chemotherapy (CT) with paclitaxel, estramustine, and oral etoposide (TEE) + LT AS+ RT would improve overall survival (OS). Materials and Methods High-Risk PCa patients (PSA 20–100 and Gleason score (GS) ≥7 or clinical stage ≥T2 and GS ≥8) were randomized to RT and AS (AS+RT) alone or with adjuvant CT (AS+RT+CT). CT was four 21-day (d) cycles, delivered beginning 28d after 70.2 Gy RT. AS was: LHRH for 24 months (mo) beginning 2 mo prior to RT plus oral anti-androgen for 4 mo before and during RT. The study was designed based on a 6% improvement in OS from 79% to 85% at 5 years, with 90% power and a 2-sided alpha of 0.05. Results 397 patients (380 eligible) were randomized. The patients had high-risk PCa, 68% having Gleason Score 8–10, and 34% T3–T4 tumors, and median PSA of 22.6 ng/ml. Median follow-up is 9.2 years. The trial closed early because of excess thromboembolic toxicity in the CT arm. 10-year results for all randomized patients revealed no significant difference in AS+RT vs. AS+RT+CT in OS (65% vs. 63%; p=0.81); Biochemical Failure (BF) (58% vs. 54%; p=0.82); Local Progression (LP) (11% vs. 7%; p=0.09); Distant Metastases (DM) (16% vs. 14%; p=0.42); or Disease-Free Survival (DFS) (22% vs. 26%; p=0.61). Conclusions NRG Oncology RTOG 9902 showed no significant difference in OS, BF, LP, DM, or DFS with the addition of adjuvant CT to LT AS + RT. The trial provides valuable data regarding the natural history of high-risk PCa treated with LT AS + RT, and has implications for the feasibility of clinical trial accrual and tolerability utilizing CT in PCa.

SummaryBackground: Several studies have reported that patients who present with idiopathic deep vein thrombosis (DVT) have an increased risk of subsequently developing cancer. A clinical trial had previously been conducted examining the optimal duration of oral anticoagulant therapy following initial heparin treatment in patients with proximal DVT.Methods: A historical cohort study was performed on patients enrolled in the duration of anticoagulant trial. Patients known to have cancer at the time of entry into the trial were excluded. The qualifying DVTs were classified as idiopathic (no known associated risk factors) or secondary without knowledge of subsequent recurrent venous thrombosis or cancer. The patients were then followed for the development of cancer.Results: Thirteen (8.6%) of the 152 patients in the idiopathic cohort subsequently developed cancer compared to eight (7.1%) of 112 patients in the secondary cohort, P = 0.86. Two (5.4%) of 37 patients with recurrent venous thromboembolism and 19 (8.4%) of 227 patients without recurrent thromboembolism developed cancer, P = 0.7.Conclusion: Our study did not detect an increased risk of subsequent cancer in patients presenting with idiopathic DVT compared to secondary DVT; nor did we detect an increased incidence of cancer in patients with recurrent venous thromboembolism. Further studies are required prior to pursuing a policy of aggressive screening for cancer in patients with idiopathic venous thromboembolism.

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