Phylloides tumor of the breast: a rare neoplasm, though not that innocent

Tsaknaki, S; Kontzoglou, Konstantinos; Gogas, J; Kostakis, A.; Safioleas, Michael

doi:10.1186/1477-7800-6-6

Cited by 12 publications

(12 citation statements)

References 24 publications

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“…The TRAMP mouse is also a good model for studying the primary epithelial stromal tumors of seminal vesicles (9, 10), a rare disease in humans (14). In TRAMP mice this tumor develop independently from prostatic lesions (9) and resemble human counterparts observed in seminal vesicles (14), prostate (13) and breast (11). Human primary epithelial-stromal tumors of the seminal vesicles count for a total of 24 documented cases in the literature, and they have been described with different names, including "cystadenoma," "cystic epithelial-stromal tumors," "cystomoma," "Mullerian adenosarcoma-like tumors," "phyllodes tumor," and "cystosarcoma phyllodes" (14).…”

Section: Discussionmentioning

confidence: 99%

“…Along with prostate adenocarcinomas, TRAMP mice also develop spontaneous epithelial-stromal tumors of seminal vesicles (9, 10). These tumors develop as independent clones under the same transgenic SV40 large T antigen oncogene (9, 10) and resemble phyllodes epithelial-stromal tumors observed in seminal vesicles (14), prostate (13), and breast (11) in humans. Therefore, we investigated whether in the above-described cohort of TRAMP mice imatinib exerted any effect on seminal vesicles tumors.…”

Section: Imatinib Treatment Inhibits the Growth Of Pdgfr-b-expressingmentioning

confidence: 98%

“…As in humans, prostate tumors with NE phenotype can arise in about 15% to 20% of C57BL/6J TRAMP mice (7) and the frequency of these cancers increase after castration (8). Moreover, TRAMP mice also develop epithelial-stromal tumors in the seminal vesicles (9,10), which arise independently from prostatic lesions (9) and resemble human phyllodes tumors found in breast (11,12), prostate (13), and seminal vesicles (14). In humans, these rare neoplasms are commonly managed with surgical removal; however, local recurrence is common and metastatic spread associated with a poor prognosis has been reported in some patients (12,14).…”

Section: Introductionmentioning

confidence: 96%

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Imatinib Spares cKit-Expressing Prostate Neuroendocrine Tumors, whereas Kills Seminal Vesicle Epithelial–Stromal Tumors by Targeting PDGFR-β

Jachetti

Rigoni

Bongiovanni

et al. 2017

Molecular Cancer Therapeutics

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Prostate cancer is a leading cause of cancer-related death in males worldwide. Indeed, advanced and metastatic disease characterized by androgen resistance and often associated with neuroendocrine (NE) differentiation remains incurable. Using the spontaneous prostate cancer TRAMP model, we have shown that mast cells (MCs) support in vivo the growth of prostate adenocarcinoma, whereas their genetic or pharmacologic targeting favors prostate NE cancer arousal. Aiming at simultaneously targeting prostate NE tumor cells and MCs, both expressing the cKit tyrosine kinase receptor, we have tested the therapeutic effect of imatinib in TRAMP mice. Imatinib-treated TRAMP mice experience a partial benefit against prostate adenocarcinoma, because of inhibition of supportive MCs. However, they show an unexpected outgrowth of prostate NE tumors, likely because of defective signaling pathway downstream of cKit receptor. Also unexpected but very effective was the inhibition of epithelial-stromal tumors of the seminal vesicles achieved by imatinib treatment. These tumors normally arise in the seminal vesicles of TRAMP mice, independently of the degree of prostatic glandular lesions, and resemble phyllodes tumors found in human prostate and seminal vesicles, and in breast. In both mice and in patients, these tumors are negative for cKit but express PDGFR-β, another tyrosine kinase receptor specifically inhibited by imatinib. Our results imply a possible detrimental effect of imatinib in prostate cancer patients but suggest a promising therapeutic application of imatinib in the treatment of recurrent or metastatic phyllodes tumors. Mol Cancer Ther; 16(2); 365-75. ©2016 AACR.

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Section: Discussionmentioning

confidence: 99%

Section: Imatinib Treatment Inhibits the Growth Of Pdgfr-b-expressingmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 96%

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Imatinib Spares cKit-Expressing Prostate Neuroendocrine Tumors, whereas Kills Seminal Vesicle Epithelial–Stromal Tumors by Targeting PDGFR-β

Jachetti

Rigoni

Bongiovanni

et al. 2017

Molecular Cancer Therapeutics

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“…Initial werden kleinere Tumoren zunächst für Fibroadenome gehalten, wäh-rend größere eher als sarkomatoid interpretiert werden [17]. Eine Biopsie sollte jedoch immer erfolgen, um die Dignität der Läsion zu überprüfen.…”

Section: Diagnostikunclassified

Grenzfälle des Mammakarzinoms

Mundhenke

Schem

2009

Gynäkologe

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In dieser Übersicht werden für die Phylloidestumoren wichtige Eigenheiten der Tumorentität und Empfehlungen für das klinische Management diskutiert. Bei der Betrachtung des CUP-Syndroms liegt der Schwerpunkt auf der Diskussion der zahlreichen Differentialdiagnosen bzw. Ursprünge. Es werden Wege aufgezeigt, ein okkultes Mammakarzinom gezielter diagnostizieren und von nichtmammären Ursachen abgrenzen zu können.

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“…Benign phyllodes tumor has a 21 % risk of local recurrence, while that of the malignant variety ranges from 20 to 32 %. In patients with malignant phyllodes tumor, the rate of distant metastases ranges from 25 to 40 % [3][4][5][6]. The most frequent sites of distant metastasis include the lungs, bone, heart and liver.…”

mentioning

confidence: 99%

Malignant Phyllodes Tumor of the Breast Metastasizing to the Vulva: 18F-FDG PET-CT Demonstrating Rare Metastasis from a Rare Tumor

Khangembam

Sharma

Singla

et al. 2012

Nucl Med Mol Imaging

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Phyllodes tumors are extremely rare fibroepithelial neoplasms accounting for 0.3 to 0.5 % of all female breast tumors with an incidence of 2.1 per 1 million women [1]. They are classified histologically into benign, borderline and malignant varieties [2]. The majority of them are benign, with only 25 % being malignant. Surgery remains the mainstay of treatment. One characteristic is that although the malignant variety tends to metastasize and recur, the benign form has also been found to behave in a similar manner. Benign phyllodes tumor has a 21 % risk of local recurrence, while that of the malignant variety ranges from 20 to 32 %. In patients with malignant phyllodes tumor, the rate of distant metastases ranges from 25 to 40 % [3][4][5][6]. The most frequent sites of distant metastasis include the lungs, bone, heart and liver. Lymph nodal metastasis is uncommon as this tumor spreads by hematogeneous route [7]. Other sites for distant metastasis have been reported sporadically, including the duodenum, pancreas, brain, nasal cavity, forearm, parotid, skin, oral cavity, skeletal muscle, mandible and maxilla [8][9][10]. We present a rare case of recurrent malignant phyllodes tumor with metastasis to the vulva, which has not been reported in the literature to the best of our knowledge. A 49-year-old female who had undergone lumpectomy and locoregional radiotherapy 1 year previously for malignant phyllodes tumor of the right breast presented with difficulty in breathing and cervical lymphadenopathy. Chest X-ray showed multiple pulmonary nodules suggestive of metastasis. She was referred for restaging with 18F-fluorodeoxyglucose (FDG) positron emission tomography computed tomography (PET-CT) FDG PET-CT (Fig. 1). Maximum intensity projection (MIP) PET images revealed multiple FDG-avid enlarged cervical lymph nodes, bilateral pulmonary nodules along with left pleural effusion and extensive bone marrow metastases (a). The interesting finding was an intensely FDGavid (SUV max -21.4) subcutaneous soft tissue density lesion (measuring 2.0×2.2×2.0 cm) in the vulva, which was later proved to be metastatic from a malignant phyllodes tumor on FNAC (a-g; arrow). However, there was no evidence of local recurrence. This is in agreement with the existing literature on phyllodes tumor, showing that most recurrences with distant metastases occur without evidence of local recurrence, and the two do not seem to be related [11]. In spite of the scarce literature because of the rarity of the disease, there are sporadic reports highlighting the usefulness of FDG PET-CT in phyllodes tumor [12]. However, our case is unique in that over and above the extensive systemic metastases revealed, FDG PET-CT could detect metastatic deposit to the vulva, which is a very rare site for metastasis, even in the case of other common and rapidly metastasizing tumors. FDG PET-CT, thus, is useful in recurrent phyllodes tumor and can demonstrate rare unsuspected sites of metastasis.

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Phylloides tumor of the breast: a rare neoplasm, though not that innocent

Abstract: Background: Cystosarcoma phylloides (CP) is an extremely rare form of breast cancer with an unpredictable clinical course. The histological characteristics of this neoplasm have not proved to offer much in the estimation of prognosis of these patients.

Cited by 12 publications

References 24 publications

Imatinib Spares cKit-Expressing Prostate Neuroendocrine Tumors, whereas Kills Seminal Vesicle Epithelial–Stromal Tumors by Targeting PDGFR-β

Imatinib Spares cKit-Expressing Prostate Neuroendocrine Tumors, whereas Kills Seminal Vesicle Epithelial–Stromal Tumors by Targeting PDGFR-β

Grenzfälle des Mammakarzinoms

Malignant Phyllodes Tumor of the Breast Metastasizing to the Vulva: 18F-FDG PET-CT Demonstrating Rare Metastasis from a Rare Tumor

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