Metastatic renal cell carcinoma with undetectable renal mass presenting as lymphadenopathy

Fayaz, Mohamed Salah; AlQaderi, A.; El-Sherify, Mustafa

doi:10.1007/s13730-016-0239-9

Cited by 7 publications

(11 citation statements)

References 16 publications

(24 reference statements)

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“…Renal cell carcinoma is the most common malignant tumor of the kidney, accounting for almost 3% of all human malignancies ( 1 ). Insensitivity to radiotherapy and chemotherapy are a great obstacle for the treatment of metastatic renal cell carcinoma.…”

Section: Introductionmentioning

confidence: 99%

HMGA2 facilitates epithelial-mesenchymal transition in renal cell carcinoma by regulating the TGF-β/Smad2 signaling pathway

et al. 2017

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High-mobility group AT-hook 2 (HMGA2), a member of the high mobility group family, has been reported to correlate with cancer progression. However, there is no report concerning the correlation between HMGA2 and metastasis in renal cell carcinoma. In the present study, we found that HMGA2 was highly expressed in five renal cell carcinoma cell lines compared with that in the normal renal tubular epithelial HK2 cell line. Additionally, HMGA2 facilitated cell migration and invasion of renal cell carcinoma cells, as evidenced by wound healing and Transwell assays. Subsequently, our results revealed that the E-cadherin level was upregulated, while N-cadherin, Twist1 and Twist2 expression were downregulated in HMGA2-depleted ACHN cells. In contrast, overexpression of HMGA2 in 786-O cells enhanced epithelial-mesenchymal transition (EMT). In addition, analysis of the database Cancer Browser further validated the positive correlation between HGMA2 and Twist1 or Twist2 in renal cell carcinoma. Meanwhile, Kaplan-Meier analysis indicated that low HMGA2 expression was closely associated with an increased overall survival in renal cell carcinoma patients. To confirm the underlying mechanism of HMGA2-regulated EMT, our results revealed that silencing of HMGA2 downregulated the mRNA and protein levels of TGF-β and Smad2, while HMGA2 overexpression had the opposite effect. Furthermore, TGF-β overexpression could partially reverse the anti-metastatic effect and mesenchymal-epithelial transition (MET) by HMGA2 loss, while TGF-β deficiency impeded the pro-metastatic phenotype and high expression of EMT markers induced by HMGA2 overexpression. In summary, our results demonstrated that HMGA2 facilitated a metastatic phenotype and the EMT process in renal cell carcinoma cells in vitro through a TGF-β-dependent pathway. In addition, these data strongly suggest that HGMA2 may serve as a potential therapeutic target and prognostic biomarker against renal cell carcinoma in the future.

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Section: Introductionmentioning

confidence: 99%

HMGA2 facilitates epithelial-mesenchymal transition in renal cell carcinoma by regulating the TGF-β/Smad2 signaling pathway

et al. 2017

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“…Seven patients had surgery to treat a solitary metastatic lesion, with no additional systemic treatment provided. 8,9,11,[15][16][17] Eleven patients described in 8 case reports received targeted therapies with sunitinib (n ¼ 6), 6,7,10,18,19 pazopanib (n ¼ 2), 14,19 temsirolimus (n ¼ 2), 12 and everolimus (n ¼ 1). 13 Efficacy data showed that 8 (72%) of 11 patients responded to treatment, and 9 (82%) of 11 were alive when the cases were reported, surviving between 6 weeks and 36 months.…”

Section: Discussionmentioning

confidence: 99%

“…Several of the above-mentioned case reports used molecular diagnostic tools after inconclusive IHC diagnostic assessment and identified the tissue of origin, thereby enabling treatment with TT. 10,[12][13][14]19 Molecular profiling is not yet part of standard diagnostic assessment at most institutions. 1 It is unknown why the primary tumor was not found in the kidneys at the time of diagnosis.…”

Section: Anders Overby Et Almentioning

confidence: 99%

“…This entity has only rarely been described in the literature. [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] Renal-cell carcinoma (RCC) is a group of cancers arising from the nephron, where 70% of RCC are clear-cell RCC. Because of mutation in the Von Hippel-Lindau gene, a high amount of vascular endothelial growth factor (VEGF) is produced, resulting in increased angiogenesis, cell growth, metabolism, and immunesuppression.…”

Section: Introductionmentioning

confidence: 99%

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Carcinoma of Unknown Primary Site (CUP) With Metastatic Renal-Cell Carcinoma (mRCC) Histologic and Immunohistochemical Characteristics (CUP-mRCC): Results From Consecutive Patients Treated With Targeted Therapy and Review of Literature

Øverby

Duval

Ladekarl

et al. 2019

Clinical Genitourinary Cancer

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Diagnostic assessment occasionally presents carcinoma of unknown primary site (CUP) with metastatic renalcell carcinoma (mRCC) histologic and immunohistochemical characteristics (CUP-mRCC). We reviewed our single-institution experience and searched the PubMed database, and identified 10 patients treated at our institution; 60% were poor risk patients. Objective response rate was 40%, progression-free survival was 2.5 months, and overall survival was 5.7 months; and the literature search identified 42 CUP-mRCC cases, for a total of 52 cases of CUP-mRCC. Vascular endothelial growth factoretargeted therapy is valid, feasible, and safe in CUP-mRCC, and these patients should thus be identified among CUP patients for specific renal-cell carcinoma therapy. Background: Carcinoma of unknown primary site (CUP) is a heterogenous group of metastatic cancer with no detectable primary tumor site. Diagnostic assessment occasionally presents CUP with metastatic renal-cell carcinoma (mRCC) histologic and immunohistochemical characteristics (CUP-mRCC). Efficacy and toxicity data for vascular endothelial growth factor inhibitor therapies in CUP-mRCC patients are few. Patients and Methods: We retrospectively reviewed consecutive patients with CUP-mRCC at a single institution between 2007 and 2018. Treatment outcomes were assessed from initiation of renal-cell carcinomaespecific therapy, including response rate, progression-free survival, and overall survival. Results: Ten patients with CUP-mRCC were identified. Median age was 64 years. Histologies were clear-cell (30%), papillary type II (20%), and unclassified renal-cell (50%) carcinoma. International Metastatic Renal Cell Carcinoma Database Consortium risk group were favorable, intermediate, and poor in 0, 40%, and 60%, respectively. One patient received empiric first-line chemotherapy. Targeted treatments were pazopanib (n ¼ 7), sunitinib (n ¼ 2), and sorafenib (n ¼ 1). Objective response rate was 40%, progression-free survival was 2.5 months (95% confidence interval, 1.2-3.8), and overall survival was 5.7 months (95% confidence interval, 0-24.0). Stratified for International Metastatic Renal Cell Carcinoma Database Consortium risk, overall survival in intermediate versus poor risk group were 18.6 months and 2.3 months, respectively. Second-line therapy did not result in disease control. No new or unexpected toxicities were observed. Conclusion: CUP-mRCC treated with vascular endothelial growth factoretargeted therapy is valid, feasible, and safe even though these patients had several negative prognostic factors. CUP-mRCC patients should be identified among CUP patients for specific renal-cell carcinoma therapy.

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“…В литературе этому вопросу посвящены ограниченные сообщения в виде описания единичных случаев [8][9][10][11][12][13]. Локализация метастазов при этом весьма разнообразна.…”

Section: Introductionunclassified

Metastatic renal cell carcinoma of unknown primary site. Clinical follow-up

Огнерубов

Antipova²,

Гумарева

2020

J. Mod. Onco.

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Renal cell cancer metastases without evidence of a primary tumor are extremely rare. These variants are usually showed as a spontaneous description of single clinical cases. Aim.This contribution is a clinical follow-up of synchronous renal cell cancer metastases of unknown primary site. Results.A 52-year-old patient U. with a history of increased blood pressure, up to 170/100 mmHg for the last 5 years, who had undergone many instrumental examinations, including ultrasound examination, because of this disease. The computed tomography of the abdomen showed a 4975 mm heterogeneous tumor in the right adrenal gland in October 2017. The combined positron emission and X-ray computed tomography showed a 795441 mm mass in the right adrenal gland, associated with elevated fluorodeoxyglucose metabolic activity SUVmax 7.25. Focal accumulation of the radiopharmaceutical SUVmax 4.31 in a 171124 mm mass was detected in the space of bifurcation in the mediastinum. The lytic lesion (1015 mm) was found in right superior L3 articular process. The patient underwent retroperitoneoscopic adrenalectomy and thoracoscopic removal of mediastinal tumor in November 2017 because of the oligometastatic nature of the process. The histological study identified clear-cell carcinoma with areas of papillary structure in the right adrenal gland. The immunohistochemical study showed carcinoma cells intensively expressing CD10, and some other cells RCC. The immune phenotype of the tumor was identified as clear-cell renal cell carcinoma. The immunohistological and immunohistochemical analysis reviled the metastases of the same variant of renal cell carcinoma in one of 9 lymph nodes. The patient was treated with pazopanib. The primary renal tumor was not detected during the dynamic observation, including the application of annual combined positron emission and X-ray computed tomography. The patient is alive without disease progression with a follow-up of 32 months. Conclusion.Metastases of clear-cell renal cell carcinoma, including adrenal gland, without evidence of a primary site are extremely rare. The main method of treatment is a combination of surgery and targeted therapy, providing long-term local control of the course of the disease.

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Metastatic renal cell carcinoma with undetectable renal mass presenting as lymphadenopathy

Cited by 7 publications

References 16 publications

HMGA2 facilitates epithelial-mesenchymal transition in renal cell carcinoma by regulating the TGF-β/Smad2 signaling pathway

HMGA2 facilitates epithelial-mesenchymal transition in renal cell carcinoma by regulating the TGF-β/Smad2 signaling pathway

Carcinoma of Unknown Primary Site (CUP) With Metastatic Renal-Cell Carcinoma (mRCC) Histologic and Immunohistochemical Characteristics (CUP-mRCC): Results From Consecutive Patients Treated With Targeted Therapy and Review of Literature

Metastatic renal cell carcinoma of unknown primary site. Clinical follow-up

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