scholarly journals Surgical controversies in the management of post-chemotherapy nonretroperitoneal residual disease in metastatic nonseminomatous germ cell tumors

2016 ◽  
Vol 05 (01) ◽  
pp. 20-22 ◽  
Author(s):  
Durgatosh Pandey ◽  
Pankaj Kumar Garg ◽  
Mukur Dipi Ray ◽  
Ashutosh Mishra

AbstractFollowing the advent of platinum-based chemotherapy, Surgery, excepting orchidectomy, has become an adjunct treatment in the management of metastatic non-seminomatous germ cell tumors (NSGCT). Role of surgery comes into play in metastatic NSGCT when residual disease persists following standard chemotherapy. Surgical excision of all post chemotherapy residual disease at all places, whenever surgically feasible with acceptable morbidity and mortality, should be undertaken. As histopathological examination of the excised postchemotherapy residue shows only necrosis and fibrosis in significant number of patients; surgical exercise in this group of patients seems futile and unwarranted retrospectively. This issue becomes more contentious when surgeons are confronted with multiple nonretroperitoneal post chemotherapy residues. This article aims to deal with the management of postchemotherapy nonretroperitoneal residues in metastatic NSGCT.

1995 ◽  
Vol 81 (4) ◽  
pp. 299-301 ◽  
Author(s):  
Alfredo Berruti ◽  
Enrica Pazè ◽  
Enrica Fara ◽  
Gabriella Gorzegno ◽  
Luigi Dogliotti

The demonstrated association with hematologic neoplasms may partially account for the poor survival of patients with mediastinal nonseminomatous germ cell tumors (MNSGCT) compared to patients with testicular and retroperitoneal counterparts. It has been shown that the median interval from the diagnosis of MNSGCT to the diagnosis of the hematologic disorders is 6 months, which contrasts sharply with the average time of 2 to 3 years for the development of therapy-related leukemias. The 2 cases herein described, 1 male and 1 female, developed acute M2 leukemia 4 and 2 years after the diagnosis of MNSGCT. In the second patient (the first female ever described), we cannot exclude a pathogenetic role of the PEB regimen (platinum, etoposide, bleomicin), even though the total dose of etoposide administred has been demonstrated to have a mild leukemogenic potential. This is not the case of the first patient, who did not receive adjuvant chemotherapy after the radical resection of primary MNGSCT and developed the hematologic disorder a few months after local recurrence. In conclusion, the time elapsed from chemotherapy administration does not discriminate the hematologic neoplasms associated to MNGSCT from those related to therapy.


1982 ◽  
Vol 33 (4) ◽  
pp. 333-339 ◽  
Author(s):  
Nicholas J. Vogelzang ◽  
Derek Raghavan ◽  
Robert W. Anderson ◽  
Juan Rosai ◽  
Seymour H. Levitt ◽  
...  

1991 ◽  
Vol 9 (1) ◽  
pp. 62-69 ◽  
Author(s):  
A Horwich ◽  
D P Dearnaley ◽  
J Nicholls ◽  
G Jay ◽  
M Mason ◽  
...  

The combination of carboplatin, etoposide, and bleomycin (CEB) was evaluated as initial chemotherapy in 76 patients with good-prognosis metastatic nonseminomatous germ cell tumors (NSGCT) between 1984 and 1988. The classification of eligible patients included Royal Marsden Hospital (RMH) stages IM, IIA, IIB, IIC, IIIA, IIIB, IV0ABCL1, and IV0ABL2. Four courses of combination chemotherapy were administered in a 21-day cycle, and surgical excision of residual mass was performed in 27 cases (23 laparotomies and four thoracotomies). At the time of analysis, median follow-up was 24 months from start of chemotherapy (range, 6 to 54 months). The 2-year cause-specific survival probability was 98.5%, the single cause-related mortality being caused by bleomycin pneumonitis. Five patients failed CEB chemotherapy, but all have been successfully salvaged with a combination of surgery and intensive chemotherapy, follow-up from completion of all treatment being 35 to 44 months. The toxicity of CEB included bone marrow suppression and alopecia in all patients but no significant neurotoxicity or ototoxicity, and minimal renal toxicity. Only four (5%) patients had a decrease in the glomerular filtration rate greater than 15%. In 51% of patients, the hemoglobin fell below 10 g/dL. The WBC count nadir was less than 1,500/microL in 11% of treatment cycles and in 16% the platelet nadir fell below 50,000/microL. Decreases in the WBC and platelet counts were of very brief duration. Only one of 310 CEB cycles was complicated by neutropenic sepsis, and there were no episodes of thrombocytopenic purpura or bleeding. We conclude that the CEB combination represents an effective alternative to cisplatin-based chemotherapy in good-prognosis NSGCT and that the replacement of cisplatin by carboplatin leads to reduced toxicity.


2003 ◽  
Vol 1 (5) ◽  
pp. S254
Author(s):  
J.T. Hartmann ◽  
O. Rick ◽  
K. Oechsie ◽  
T. Gauler ◽  
P. Schoeffski ◽  
...  

2021 ◽  
Vol 22 (21) ◽  
pp. 11774
Author(s):  
Dennis M. Timmerman ◽  
Thomas F. Eleveld ◽  
Ad J. M. Gillis ◽  
Carlijn C. Friedrichs ◽  
Sanne Hillenius ◽  
...  

Germ cell tumors (GCTs) are considered to be highly curable; however, there are major differences in the outcomes related to histology and anatomical localization. GCTs originating from the testis are, overall, sensitive to platinum-based chemotherapy, whereas GCTs originating from the mediastinum show a worse response, which remains largely unexplained. Here, we address the differences among GCTs from two different anatomical locations (testicular versus mediastinal/extragonadal), with a specific focus on the role of the P53 pathway. It was recently shown that GCTs with TP53 mutations most often localize to the mediastinum. To elucidate the underlying mechanism, TP53 knock-out lines were generated in cisplatin-sensitive and -resistant clones of the representative 2102Ep cell line (wild-type TP53 testicular GCT) and NCCIT cell line (hemizygously mutated TP53, mutant TP53 mediastinal GCT). The full knock-out of TP53 in 2102Ep and resistant NCCIT resulted in an increase in cisplatin resistance, suggesting a contributing role for P53, even in NCCIT, in which P53 had been reported to be non-functional. In conclusion, these results suggest that TP53 mutations contribute to the cisplatin-resistant phenotype of mediastinal GCTs and, therefore, are a potential candidate for targeted treatment. This knowledge provides a novel model system to elucidate the underlying mechanism of clinical behavior and possible alternative treatment of the TP53 mutant and mediastinal GCTs.


1986 ◽  
Vol 4 (4) ◽  
pp. 528-536 ◽  
Author(s):  
P J Loehrer ◽  
L H Einhorn ◽  
S D Williams

Forty-eight evaluable male patients with germ cell tumors (GCT) failing to be cured with first-line therapy were treated with VP-16 (75 mg/m2), ifosfamide (1.2 g/m2), and cisplatin (20 mg/m2) (VIP), all given daily for 5 consecutive days every 3 weeks. All patients either achieved an unresectable partial remission as their best response to induction chemotherapy (Group A), relapsed from complete remission (CR) less than or equal to 2 months after induction therapy (Group B), or had received cisplatin plus VP-16 as previous salvage therapy (Group C). Nine (19%) had extragonadal GCT, and 37 (77%) had advanced disease. Twenty-three (48%) of the patients had greater than or equal 2 prior treatment regimens. Sixteen of 48 (33%) achieved CR with VIP treatment alone or following surgical excision of residual disease. Six of 22 (27%), three of seven (43%), and seven of 19 (37%) patients from groups A, B, and C, respectively, attained a CR. The median survival time of all patients was 7 months (range 0 to 28+) with seven patients remaining continuously free of disease (four patients greater than 1 year). Myelosuppression was significant with a median WBC nadir of 900/mm2 and platelet nadir of 24,000/mm2. Fourteen (26%) had granulocytopenic fever, and renal insufficiency developed in 15%. VIP combination chemotherapy demonstrates activity in this highly unfavorable population of patients with germ cell tumors. The actual contribution of ifosfamide in this regimen is unclear, but these results compare favorably to our experience with similar patients treated with cisplatin plus VP-16 alone. Further studies with VIP as initial salvage therapy for patients with GCT are planned.


2019 ◽  
Vol 27 (2) ◽  
pp. 98-104 ◽  
Author(s):  
Ashwani Kumar Sachdeva ◽  
Prasanth Penumadu ◽  
Pavneet Kohli ◽  
Biswajit Dubashi ◽  
Hemachandren Munuswamy

Background Growing teratoma syndrome is a rare phenomenon seen in nonseminomatous germ cell tumors after chemotherapy, where the tumor grows paradoxically despite normalization of tumor markers. It has been found in various locations, most commonly, the retroperitoneum in association with metastatic disease. The occurrence of growing teratoma syndrome in a mediastinal primary is very rare and there are only a few reports in the literature. Methods In a retrospective review, out of 12 patients with mediastinal involvement by a germ cell tumor, 5 had a primary from the mediastinum. We present a series of 3 cases of primary germ cell tumor of the mediastinum, which after chemotherapy, fulfilled the criteria for growing teratoma syndrome and were managed with surgical excision. Conclusion Development of growing teratoma syndrome in a primary mediastinal germ cell tumor is extremely rare. Its awareness and early detection can lead to successful surgical excision and long-term cure.


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