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K-P Dieckmann

Publications and source records attributed to K-P Dieckmann.

6 recordsLinked to original sources

Single agent carboplatin for CS IIA/B testicular seminoma. A phase II study of the German Testicular Cancer Study Group (GTCSG).

BACKGROUND: The aim was to investigate the use of single agent carboplatin in patients with seminoma stage IIA/B. PATIENTS AND METHODS: In a prospective phase II trial, single agent carboplatin at a dose of AUC 7 mg.min/ml every 4 weeks for three cycles in stage IIA (n=51) or four cycles in stage IIB (n=57) was given to 108 patients with previously untreated seminoma stage IIA/B. Patients with residual masses of >or=3 cm were scheduled to receive secondary surgery. RESULTS: A complete response (CR) was achieved by 88/108 (81%) patients, 17/108 (16%) achieved a partial response (PR), two of 108 (2%) showed no change, and one patient progressed. In all patients with PR the residual disease was <or=3 cm; yet in two of 17 patients with PR, in two of two patients with NC and in one patient with disease progression residual tumor resection was performed demonstrating vital seminoma. Toxicity was acceptable with grades 3 and 4 myelosuppression, nausea and vomiting in less than 10% of patients each. After a median follow-up of 28 months (range 1-68 months) 14/108 (13%) patients relapsed, all after having achieved a CR. All relapses occurred in the retroperitoneum. One patient died from an unrelated cause. The overall failure rate was 19/108 patients (18%). The overall and disease specific survival was 99% and 100%, respectively. CONCLUSIONS: Four cycles of single agent carboplatin AUC 7 do not safely eradicate retroperitoneal metastases in patients with stage IIA/B seminoma.

Adult↗

[Aftercare in testicular cancer is worthwhile. Recurrences are curable].

Patients with germ cell tumours of the testis can have an extremely favourable chance of cure when compared to other malignancies. Therapeutic problems may arise with recurrent disease. High tumour burden can result when relapses are diagnosed too late and the prognosis will deteriorate, consecutively, even in spite of intensified therapeutic endeavours. Apart from early detection of recurrent disease, the follow-up schedule of germ cell cancer aims to identify and manage treatment-related morbidities, e.g. vascular problems and second neoplasms, respectively. Follow-up examinations should be tailored to the individual situation taking into account the particular risk of relapse based on histology, stage and treatment previously applied. In light of the rarity of the disease and according to the complexity of managing this malignancy, follow-up should be conducted by particularly experienced institutions.

Aftercare↗

Clinical epidemiology of testicular germ cell tumors.

Clinical epidemiology is sometimes called the basic science of clinical medicine. In terms of the pathogenesis of testicular germ cell tumors (GCTs), clinical epidemiology analyzes suspected risk factors. The present review highlights the risk factors established so far and briefly summarizes those factors currently under investigation. In analogy to the methods of evidence based medicine, this review attributes levels of evidence to each of the putative risk factors. Level I represents highest quality of evidence while level V denotes the lowest level. So far, undescended testis (UDT), contralateral testicular GCT and familial testis cancer are established risk factors attaining high levels of evidence (levels I-III a). In a meta-analysis of 21 studies exploring the association of UDT with GCT risk, an over-all relative risk (RR) of 4.8 (95% confidence interval 4.0-5.7) was found. Contralateral testicular GCT involves a roughly 25-fold increased RR of GCT, while familial testis cancer constitutes a RR of 3-10. Infertility, testicular atrophy, and twin-ship represent risk factors with lesser levels of evidence (level III a). There is also some evidence for HIV infection being a predisposing factor for GCT (level IV a). Scrotal trauma is probably not associated with GCT risk. The estrogen excess theory implies high estrogen levels during the first trimester of pregnancy. As a consequence, primordial germ cells lose track of the normal developmental line and transform into premalignant cells that later become testicular intraepithelial neoplasia (TIN), the precursor of full-blown testicular GCT. Surrogate parameters for high gestational estrogen levels are investigated in case control studies. Such factors are maternal age >30 years, first-born, low birth weight, maternal breast cancer, high sex-ratio of siblings. So far, the sum of evidence is promising but still conflicting (especially for level III b). Another novel theory is the childhood nutrition hypothesis. This concept postulates a modulating or "catalyzing" effect by high dietary intake during childhood on the pathogenesis of testicular GCT. A surrogate parameter of early childhood nutrition is adult height. So far, 12 controlled studies have looked to the possible association of attained height and GCT risk of which six demonstrated a significant association. Thus, the sum of evidence corresponds to level III b. This concept is appealing because it would explain several hitherto unexplained epidemiological features of GCT.

Animals↗

False-negative biopsies for the diagnosis of testicular intraepithelial neoplasia (TIN)--an update.

PURPOSE: Testicular intraepithelial neoplasia (TIN; or carcinoma in situ of the testis) is the precursor of testicular germ-cell tumours (GCT). It is detected by conventional surgical biopsy of the testis. To date, only little information is available in regard to the accuracy of the biopsy. False-negative biopsies have been reported only sporadically. PATIENTS AND METHODS: Twenty-one patients who developed a testicular GCT despite a testicular biopsy negative for TIN were analysed clinically and histologically. The median age of the patients is 34 years. The median interval from biopsy to the clinical appearance of GCT is 39 months. Four of the 21 patients had their biopsy done within a previously reported multicentric study (n=1859 cases with negative biopsy including five cases with false-negative biopsy hitherto known). All of the biopsy specimens were re-examined immunohistologically. In 15 cases, the orchiectomy specimens were re-examined for the presence of TIN in the tumour-surrounding tissue. RESULTS: In five cases, TIN was found in the biopsy specimen upon re-examination. In all of the 15 orchiectomy specimens there was evidence of TIN in the tissue adjacent to the tumour. In three biopsy specimens there were microcalcifications in the seminiferous tubules. Severe impairment of the spermatogenesis was observed histologically in only 3 of the 21 patients. The relative proportion of false-negative biopsies is 0.5% (95% confidence intervals (CI): 0.22%; 0.92%). The sensitivity of the biopsy to detect TIN is 0.914 (95% CI: 0.842; 0.959) and the overall accuracy is 0.995 (95% CI: 0.991; 0.9979). A total of 44 false-negative biopsies are reported to date. CONCLUSIONS: False-negative biopsies for TIN do occur but the proportion is only 0.5%. There is no clear-cut clinical nor histological feature associated with false-negative biopsies. However, young age (i.e. <18 years) and intratubular microcalcifications should increase the clinician's and pathologist's vigilance. The majority of false-negative biopsies are caused by the non-random distribution of TIN in the testis while some few cases are caused by technical problems. Two-site biopsies would probably increase the accuracy of the biopsy in high risk cases.

Adolescent↗

Testicular microlithiasis--one case and four points to note.

A 38-year-old man with non-specific scrotal complaints was found to have bilateral testicular microlithiasis (TM) sonographically. MRI of the testes failed to depict microlithiasis. Bilateral double biopsies of the testes revealed testicular intraepithelial neoplasia (TIN; carcinoma in situ of the testis) in only one of the two biopsies from the right testis. At the request of the patient the biopsies were repeated, with the same histological result. A right-sided orchiectomy was performed. Histology disclosed TIN in only some tubules of the lower pole of the testis. This case highlights four interesting points: (i) TM may be associated with testicular malignancy; (ii) MRI does not depict TM; (iii) TIN is arranged focally within the testis; and (iv) a two-site biopsy may increase the sensitivity of the diagnosis of TIN.

Adult↗

Testicular germ cell cancer despite previous local radiotherapy to the testis.

BACKGROUND: Testicular intraepithelial neoplasia (TIN, also carcinoma in situ of the testis) is the uniform precursor of testicular germ cell cancer. Local radiotherapy to the testis with dosages of 18-20 Gy has been found to safely eradicate TIN and germ cells, too. Thus, the general assumption is that the development of invasive germ cell tumours can be prevented by this radiotherapy. PATIENTS AND METHODS: Herein, we report two patients with one-sided testicular tumour and biopsy-proven contralateral TIN. Both of them developed germ cell neoplasms in the remaining testis although local radiotherapy with 20 Gy had been applied to the testis. RESULTS: One patient developed pure seminoma 7 years after completion of radiotherapy, the other developed a combined tumour consisting of embryonal carcinoma and seminoma after 5 years. Treatment consisted of orchiectomy in each of the cases. Histologically, both had TIN in the testicular tissue surrounding the new growths. CONCLUSIONS: Pathogenetically, a small fraction of radioresistent TIN cells overcoming irradiation and progressing to full-blown germ cell cancer in the later course may be the histogenetic clue to explain these unexpected events. Other explanations, though less probable, could be technical radiotherapeutic failure due to targeting problems and a pre-existing radioresistent germ cell tumour in the irradiated testicle.

Adolescent↗