Second malignant neoplasms in childhood acute lymphoblastic leukemia: Primitive neuroectodermal tumor of the chest wall with germline p53 mutation as a second malignant neoplasm

Suárez, Carlos; Bertolone, Salvatore; Raj, Ashok; Coventry, Susan

doi:10.1002/ajh.20012

Cited by 11 publications

(7 citation statements)

References 28 publications

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“…Acute lymphoid leukemia (ALL) is the main kind of leukemia that occurs in children. Although about 80% of children diagnosed with ALL can attain complete remission and be long-term survivors with current treatment protocols [12], the prognosis of many individuals, such as those with Philadelphia chromosome positive (Ph + ) ALL and HTLV-I-associated adult T-cell leukemia, is still very poor [13,14]. There-fore, finding new antileukemia drugs and effective therapies for the clinical treatment of myeloid leukemia will remain an important area of research.…”

Section: Discussionmentioning

confidence: 99%

Antiproliferation effects of oridonin on HPB-ALL cells and its mechanisms of action

et al. 2006

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Oridonin, an ent-kaurane diterpenoid derived from the herbal Rabdosia rubescens, has been recently reported to have antitumor effects on a large variety of cancer cells. The present study was undertaken to investigate the in vitro antiproliferation and apoptosis inducing effects of oridonin on HPB-ALL cell lines and its mechanisms of action. HPB-ALL cells in culture medium in vitro were treated with different concentrations of oridonin (16-56 mmol/L). MTT assay was used to detect the cell growth inhibitory rate, and the cell viability was assessed by the trypan blue dye-exclusion method. Cell apoptosis and the mitochondrial membrane potential (Dym) were investigated by flow cytometry (FCM), Hoechst 33258 staining, and DNA fragmentation analysis. The expression of caspase-3 and different apoptosis modulators, including Fas and Bcl-2 family members, was analyzed by Western blotting. The results revealed that oridonin could significantly inhibit the growth of HPB-ALL cells and cause apoptosis, and the suppression was both timeand dose-dependent. After treatment with oridonin for 48 hr, the percentage of disruption of Dym gradually increased in a dose-dependent manner along with marked changes of cell apoptosis, and necrotic cells increased remarkably after the cells were treated with oridonin for 72 hr; Western blotting showed cleavage of the caspase-3 zymogen protein (32 kDa) with the appearance of its 20-kDa subunit when apoptosis occurred; expression of Bcl-2 and Bcl-XL was downregulated remarkably while expression of Bax and Bid was upregulated concurrently after the cells were treated with oridonin for 24 hr. Of note, the expressions of Fas and other Bcl-2 family members including Bak and Bad remained constant before and after apoptosis occurred. We therefore conclude that oridonin has significant antiproliferation effects on HPB-ALL cells by induction of apoptosis as well as directly causing cell necrosis and that oridonin-induced apoptosis on HPB-ALL cells is mainly related to the disruption of Dym and activation of caspase-3 as well as downregulation of anti-apoptotic protein Bcl-2, Bcl-XL, and upregulation of pro-apoptotic proteins Bax and Bid. The results indicate that oridonin may serve as a potential antileukemia reagent. Am.

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Section: Discussionmentioning

confidence: 99%

Antiproliferation effects of oridonin on HPB-ALL cells and its mechanisms of action

et al. 2006

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“…PNETs are rarely observed as SMNs [12,40,41]. To our knowledge, this is the first report of a PNET that developed in pediatric patients treated for hepatoblastoma.…”

Section: Discussionmentioning

confidence: 85%

Sarcoma as Second Cancer in a Childhood Cancer Survivor: Case Report, Large Population Analysis and Literature Review

et al. 2020

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The majority of pediatric patients are cured of their primary cancer with current advanced developments in pediatric cancer therapy. However, survivors often experience long-term complications from therapies for primary cancer. The delayed mortality rate has been decreasing with the effort to reduce the therapeutic exposure of patients with pediatric cancers. Our study investigates the incidence of sarcoma as second cancer in pediatric cancer survivors. We present a 9-year-old male who survived embryonal hepatoblastoma diagnosed at 22 months of age. At 4.5 years of age, he presented with a non-metastatic primitive neuroectodermal tumor (PNET) of the left submandibular area. He has no evidence of recurrence of either cancer for 51 months after finishing all chemotherapy and radiotherapy. We used the Surveillance, Epidemiology, and End Results (SEER) database to identify the current rate of second sarcomas in pediatric cancer survivors. Our literature review and large population analysis emphasize the impact of sarcoma as a second malignancy and provide help to physicians caring for pediatric cancer survivors.

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“…Although a recent study evaluating the prevalence of germline mutations in children with cancer identified TP53 mutations in 4 of 46 patients with Ewing sarcoma, 26 there traditionally has been consensus that these mutations are not associated with Ewing sarcoma (F 1 sarcoma) susceptibility. 5 In our own review of the International Agency for Research on Cancer TP53 database R17 (released November 2013), an online resource providing information regarding the TP53 mutation characteristics and malignancies previously published in TP53 germline mutation carriers, we identified 177 osteosarcomas (approximately 7% of all cancers documented in the database) as opposed to 2 possible cases of Ewing sarcoma (<0.1% of registered cancers): 1 reported case of an Askin tumor with immunohistochemical findings consistent with Ewing sarcoma but no data regarding fusion status 27 and 1 case of Ewing sarcoma reported anamnestically in a family member of a TP53 mutation carrier. 28 Two additional cases of Ewing sarcoma included in the International Agency for Research on Cancer database could not be confirmed by review of the reference publication.…”

Section: Discussionmentioning

confidence: 99%

Second malignancy risk among pediatric, adolescent, and young adult survivors of fusion‐positive and fusion‐negative sarcomas: Results from the SEER database, 1992 through 2012

Lupo

Brown

Hettmer

2016

Cancer

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Second malignant neoplasms in childhood acute lymphoblastic leukemia: Primitive neuroectodermal tumor of the chest wall with germline p53 mutation as a second malignant neoplasm

Cited by 11 publications

References 28 publications

Antiproliferation effects of oridonin on HPB-ALL cells and its mechanisms of action

Antiproliferation effects of oridonin on HPB-ALL cells and its mechanisms of action

Sarcoma as Second Cancer in a Childhood Cancer Survivor: Case Report, Large Population Analysis and Literature Review

Second malignancy risk among pediatric, adolescent, and young adult survivors of fusion‐positive and fusion‐negative sarcomas: Results from the SEER database, 1992 through 2012

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