A bilateral primary yolk sac tumor of the lung associated with chromosome 3 polysomy

Arora, Shitij; Patel, Harish; Mir, Pervez; Mishra, Sneha; Kalra, Amita; Sawhney, Harinder; Duffoo, Frantz; Macera, M.; Abdu, Afaf; Thelmo, William

doi:10.4161/cbt.22624

Cited by 4 publications

(2 citation statements)

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“…A recent study by Sherif and Sultan analysed cav-1 expression in non-cancerous LFS fibroblasts and reported that affected family members showed an 88% down-regulation of cav-1 compared to non-affected family members [37]. This new finding is directly as predicted by our hypothesis and confirms that another key feature of the “two compartment” model, (and one that is also related to characteristics of accelerated host aging), is present in the non-malignant LFS host environment.…”

Section: Telomeres Senescence and Immortalisationmentioning

confidence: 99%

Li Fraumeni syndrome, cancer and senescence: a new hypothesis

Pantziarka

2013

Cancer Cell International

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Li Fraumeni Syndrome (LFS) is a rare autosomal dominant hereditary cancer syndrome characterized by germline mutations in the TP53 tumour suppressor gene. Sufferers are prone to early onset cancers, particularly sarcomas, adrenocortical carcinoma and breast cancer. Cells from LFS sufferers are known to exhibit telomere dysfunction, genomic instability and spontaneous immortalisation. It is hypothesized that these facets of the LFS host are evidence that the host environment is “primed” for carcinogenesis over and above the lack of p53 tumour suppressor function. Further, it is hypothesized that the host presents an ideal environment for "two compartment tumour metabolism" to take place. Evidence from recent studies supports this new view of LFS and suggests that disrupting certain features of the host environment may markedly reduce the incidence of cancer in LFS sufferers.

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Section: Telomeres Senescence and Immortalisationmentioning

confidence: 99%

Li Fraumeni syndrome, cancer and senescence: a new hypothesis

Pantziarka

2013

Cancer Cell International

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“…In contrast to rodents, there are some reports indicating that yolk sac carcinoma occurred in the lung in humans with no evidence of a gonadal lesion 14 , 15 , 16 , 17 , 18 . The origin of pulmonary germ cell tumors in humans is not well known, but it is possible that primordial germ cells remain in the region of the mediastinum or lungs at the time of migration along the gonadal ridge during embryogenesis and become the tumor “seed”, eventually developing extragonadal germ cell tumor 17 , 18 , 19 .…”

mentioning

confidence: 94%

A case report of a metastatic yolk sac carcinoma in the pulmonary artery of a young female Sprague-Dawley rat

et al. 2016

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Yolk sac carcinoma is an extremely rare tumor in rats and is usually found in the genital system of aged animals. We encountered a yolk sac carcinoma in the pulmonary artery of an 18-week-old female Sprague-Dawley rat. In a repeated dosing toxicity study (once weekly for 4 weeks, intraperitoneal), this rat was unexpectedly found dead on the 55th day after the final administration of the test article. At necropsy, grayish white nodules were found on the lung surface. Histopathologically, tumor emboli were observed in the trunk and branch of the pulmonary artery. Tumor cells with slightly basophilic vacuolated cytoplasm and large vesicular nuclei formed nests or clusters and were embedded in a homogenous eosinophilic and periodic acid-Schiff reaction positive matrix. The tumor cells and matrix were immunoreactive for laminin. The embolic tumor resembled yolk sac carcinoma showing a parietal pattern in rodents. Although the primary site was unknown, the tumor was considered to be a metastatic yolk sac carcinoma.

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