Complete response after treatment with imatinib in pretreated disseminated testicular seminoma with overexpression of c-KIT

Pedersini, Rebecca; Vattemi, Emanuela; Mazzoleni, Guido; Graiff, Claudio

doi:10.1016/s1470-2045(07)70344-3

Cited by 57 publications

(34 citation statements)

References 11 publications

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“…In this case, any known mutations in the KIT could not be detected. Currently, imatinib is being examined for refractory KIT-positive germ-cell tumors in a salvage setting with or without chemotherapy after the third line [4,5]. …”

mentioning

confidence: 99%

Possible alternative strategy for stage I imatinib-sensitive testicular seminoma; lessons from a case associated with Philadelphia chromosome-positive acute lymphoblastic leukemia

et al. 2010

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confidence: 99%

Possible alternative strategy for stage I imatinib-sensitive testicular seminoma; lessons from a case associated with Philadelphia chromosome-positive acute lymphoblastic leukemia

et al. 2010

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“…Mutations result in ligand-independent permanent activation of the KIT tyrosine kinase and are often seen in GIST tumors [Corless et al, 2011]. Importantly, it has been shown that Imatinib, a tyrosine kinase inhibitor, has potent effects on the progression of GISTs and results in dramatic prolongation of the median survival [ESMO/European Sarcoma Network Working Group, 2014] and also in a case of extragonadal seminoma [Pedersini et al, 2007]. It remains to be shown whether the present patient would benefit from Imatinib or other tyrosine kinase inhibitors should she suffer a relapse.…”

Section: Discussionmentioning

confidence: 99%

A Rare Case of Embryonal Carcinoma in a Patient with Turner Syndrome without Y Chromosomal Material but Mutations in KIT, AKT1, and ZNF358 Demonstrated Using Exome Sequencing

Gravholt¹,

Dollerup²,

Duval³

et al. 2017

Sex Dev

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Gonadoblastoma and malignant transformations thereof can occur in females with Turner syndrome (TS) and Y chromosomal material. However, in females with TS and no Y chromosomal material, this is rarely seen. We report a female with an apparent 45,X karyotype (in blood and tumor) who was diagnosed with a metastatic embryonal carcinoma. Exome sequencing of blood and the tumor was done, and no Y chromosomal material was detected, while predicted deleterious mutations in KIT (likely driver), AKT1, and ZNF358 were identified in the tumor. The patient was treated with chemotherapy (first-line: cisplatin, etoposide, and bleomycin; second-line: paclitaxel and gemcitabine), and after that surgical debulking was performed. She is currently well and without signs of relapse. We conclude that embryonal carcinoma can apparently occur in 45,X TS without signs of Y chromosomal material.

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“…The interaction of these two molecules negatively regulates immune responses. Of major interest is that inhibition of the interaction between PD1 and PD-L1 can enhance T cell responses in vitro and mediates relevant antitumor activity in a variety of tumors [46][47][48][49][50][51][52][53]. In one of our own tissue microarray studies, PD-L1 expression was found in 73 % of all seminomas, and in 64 % of all non-seminomas [38].…”

Section: Pd-l1/pd-1 Immunotherapymentioning

confidence: 99%

“…Particularly in choriocarcinoma and teratocarcinoma subtypes, the expression is low or completely absent [46][47][48][49][50][51]. The efficacy of the c-kit inhibitor imatinib in GCT was studied, but only one case report described a complete remission and a disease-free survival of 2 years [52]. Another case report described a patient treated concomitantly with imatinib, paclitaxel, oxaliplatin, and gemcitabine, leading to a complete remission.…”

Section: Stem Cell Growth Factor Receptormentioning

confidence: 99%

Emerging Therapeutic Targets for Male Germ Cell Tumors

et al. 2015

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Male germ cell tumors (GCTs) are curable cancers, yet 10-15 % of patients with metastatic disease fail cisplatin-based first-line treatments. While therapeutic options have increased for various other cancers, little progress has been made in the management of GCT in the last decades. A better understanding of the molecular alterations underlying the disease and identification of new therapeutic targets are needed. Several phase I/II studies with promising new agents are ongoing or have been completed, but most of those trials have been small and have not included translational research. Therefore, molecular profiles predictive for response or new agents have not been identified in male GCT so far. The purpose of this review is to highlight emerging targets and therapies with the potential to improve systemic treatment of metastatic male GCT and to develop strategies for future clinical trials.

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Complete response after treatment with imatinib in pretreated disseminated testicular seminoma with overexpression of c-KIT

Cited by 57 publications

References 11 publications

Possible alternative strategy for stage I imatinib-sensitive testicular seminoma; lessons from a case associated with Philadelphia chromosome-positive acute lymphoblastic leukemia

Possible alternative strategy for stage I imatinib-sensitive testicular seminoma; lessons from a case associated with Philadelphia chromosome-positive acute lymphoblastic leukemia

A Rare Case of Embryonal Carcinoma in a Patient with Turner Syndrome without Y Chromosomal Material but Mutations in <b><i>KIT</i></b>, <b><i>AKT1</i></b>, and <b><i>ZNF358</i></b> Demonstrated Using Exome Sequencing

Emerging Therapeutic Targets for Male Germ Cell Tumors

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