Prediction of relapse after lymph node dissection for germ cell tumours: can salvage chemotherapy be avoided?

Berney, Daniel M.; Shamash, Jonathan; Hendry, W. F.; Arora, Amit; Jordan, Suzanne; Oliver, R. T. D.

doi:10.1054/bjoc.2000.1613

Cited by 12 publications

(7 citation statements)

References 30 publications

(24 reference statements)

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“…There is a negative correlation between topo I and II (P=0.004, Fisher's exact test). Ki-67 has been shown to be a useful marker in assesment of likelihood of relapse in metastatic germ cell tumours (Berney et al, 2001b). Comparison of Ki-67 with topo IIa shows a good correlation, indicating that topo IIa levels are a fair indicator of proliferating cells.…”

Section: -100%mentioning

confidence: 98%

DNA topoisomerase I and II expression in drug resistantgerm cell tumours

et al. 2002

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A small number of testicular germ cell tumours are refractory to current chemotherapy regimens. DNA topoisomerase I is the target for several new drugs and a potential candidate treatment for chemorefractory germ cell tumours. DNA topoisomerase IIa is the target for etoposide, which is currently used regularly in germ cell tumour treatment. The expression of DNA topoisomerase I and IIa were therefore assessed immunohistochemically in a range of testicular tumours, especially those with persistent malignant elements on retroperitoneal lymph node dissection. Pre-chemotherapy orchidectomy specimens were matched with postchemotherapy retroperitoneal lymph node dissections to examine changes in expression. There was considerable variation in the expression of topoisomerase I in different tumour types. Both yolk sac tumours and teratoma, mature showed universal expression of topoisomerase I, while 38% of seminomas and 30% of embryonal carcinomas were positive. Strong topoisomerase IIa expression was found in embryonal carcinoma. There was a negative correlation between topoisomerase I and IIa expression (P=0.004) and downregulation of topoisomerase IIa after chemotherapy (P=0.02). Topoisomerase I expression appears to increase in those cases with residual teratoma, mature, but is largely unchanged in those cases remaining as embryonal carcinoma. These results suggest that topoisomerase I inhibitors may be useful in chemorefractory germ cell tumours, especially yolk sac tumours and where there are unresectable residual teratoma, mature deposits.

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Section: -100%mentioning

confidence: 98%

DNA topoisomerase I and II expression in drug resistantgerm cell tumours

et al. 2002

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“…As mentioned above, postchemotherapy teratomas may show areas of immaturity and these tumours have been shown to exhibit no difference in prognosis to those without immature and atypical areas . It may therefore be very challenging to differentiate somatic transformation from immaturity in a mixed tumour with other elements.…”

Section: Trophoblastic Diseasementioning

confidence: 99%

“…Estimations of the volume to retroperitoneal malignancy have usually been estimated by the percentage of viable disease in the resected lymph nodes rather than by more complex volume estimations, but it has been shown in a number of studies that small percentages of viable tissue may be surveilled safely rather than subjecting the patient to further potentially debilitating rounds of chemotherapy. A cut‐off of 10% is used most frequently …”

Section: Other Microscopic Prognostic Factorsmentioning

confidence: 99%

Postchemotherapy changes in testicular germ cell tumours: biology and morphology

Berney

Shamash

et al. 2016

Histopathology

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Advances in modern chemotherapy and targeted treatments have resulted in lengthened survival in a variety of tumour types in the last decade. Increasingly in the 21st century, postchemotherapy resections are considered as a possible mode of treatment. Due to their exquisite chemosensitivity, resection of postchemotherapy masses has long been part of the armamentarium of treatment in testicular germ cell neoplasia, which has resulted in a variety of new morphological variants being described after treatment. Here we discuss the possible reasons for germ cell tumour chemosensitivity and hypotheses on the biological pathways leading to resistance to treatment, as well as an outline of the diverse morphology of those tumours which prove recalcitrant to standard treatment methods. The large range of morphologies and their diagnostic challenges may throw light upon the future problems to be encountered in non-germ cell solid tumour pathology, as the resection of postchemotherapy masses becomes increasingly important in patient management.

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“…Furthermore, pathological review of the resected specimen confirming viable tumour would suggest a significant risk of relapse 42. These patients can be offered further chemotherapy or radiotherapy; however, there is some debate over how beneficial this approach actually is.…”

Section: Intermediate and Poor Prognosis Diseasementioning

confidence: 99%

Testis cancer

Khan

Protheroe

2007

Postgraduate Medical Journal

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Testis cancer is an increasing problem, especially in northern European male populations. However, survival has improved dramatically over one generation. Environmental factors may have a role in the aetiology with high oestrogen concentrations implicated. Testis cancer is subdivided between seminoma and non-seminoma. At presentation, a testicular lump is the most common finding and radical inguinal orchidectomy is recommended for most. Further multidisciplinary management is determined by histological subtype and stage and involves chemotherapy, radiotherapy and surgery, with many patients only undergoing surveillance. There is increasing emphasis on reducing toxicity of treatments in long term survivors. Treatment refractory testis cancer remains a significant challenge.

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Prediction of relapse after lymph node dissection for germ cell tumours: can salvage chemotherapy be avoided?

Cited by 12 publications

References 30 publications

DNA topoisomerase I and II expression in drug resistantgerm cell tumours

DNA topoisomerase I and II expression in drug resistantgerm cell tumours

Postchemotherapy changes in testicular germ cell tumours: biology and morphology

Testis cancer

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