Desmoid tumors in adults: The role of radiotherapy in their management

Batalni, Jean Pierre; Belloir, C; Mazabraud, A; Pilleron, J P; Cartigny, Aude; Jaulerry, C; Ghossein, Nemetallah Ā.

doi:10.1016/s0002-9610(88)80037-0

Cited by 83 publications

(32 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…RT has a long tradition in the treatment of desmoids: In 1928, James Ewing, who was the first to propose RT as a treatment option, described that desmoid lesions respond ‘slowly but satisfactorily' to RT [19]. These observations were confirmed by several studies that demonstrated high local control rates after RT [9,12,16,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43]. …”

Section: Discussionmentioning

confidence: 99%

Radiotherapy Is Effective for Desmoid Tumors (Aggressive Fibromatosis) - Long-Term Results of a German Multicenter Study

et al. 2014

View full text Add to dashboard Cite

Background: Desmoids (aggressive fibromatosis) are defined as benign neoplasms of the connective tissue that arise from the deep muscle fascia, aponeurosis, tendons, and scar tissue. Recurrence rates between 40 and 80% were reported after surgery alone. We addressed the impact of radiation therapy (RT) in the management of aggressive fibromatosis. Patients and Methods: A large literature review was performed, and the data was compared with the results of a multicenter study of the German Cooperative Group on Radiotherapy for Benign Diseases (GCG-BD). Results: This analysis included 52 patients treated with RT. 37 patients received postoperative RT (20 patients after R2 resection and 17 patients after R1 resection). 15 patients received RT alone (6 patients with inoperable primary tumor and 9 patients with inoperable recurrent tumor). In the case of postoperative RT, a median dose of 50 Gy (range 50-60 Gy) was used; for definitive RT, a median dose of 55 Gy (range 55-65 Gy) was used. The local control rate was 79% for the whole group. The median follow-up was 44 month (range 8-62 months). Conclusion: Given the large number of patients, these data show that RT is highly effective in the treatment of desmoid tumors. RT is an attractive alternative to mutilating surgery.

show abstract

Section: Discussionmentioning

confidence: 99%

Radiotherapy Is Effective for Desmoid Tumors (Aggressive Fibromatosis) - Long-Term Results of a German Multicenter Study

et al. 2014

View full text Add to dashboard Cite

show abstract

“…This would be consistent with the observation that in some patients complete regression of prostatic tumors can take more than a year after completing radiation therapy. 46 To gain the above perspective, it was critical that each major p53-dependent determinant of cell fate be collectively evaluated within a common cell population after exposure to any given dose of IR. Since cell cycle arrest is critical for allowing time for DNA repair, G 1 and G 2 checkpoints were evaluated.…”

Section: Discussionmentioning

confidence: 99%

A Dominant Role for p53-Dependent Cellular Senescence in Radiosensitization of Human Prostate Cancer Cells

Lehmann

McCubrey²,

Jefferson³

et al. 2007

Cell Cycle

106

View full text Add to dashboard Cite

ACKnoWLeDgeMenTSSupported in part by grants from the NIH (R01098195 to J.A.M.) and the Brody Brothers Foundation Endowment (#997729 to J.A.M. and D.M.T.). ReportA Dominant Role for p53-Dependent Cellular Senescence in Radiosensitization of Human Prostate Cancer Cells ABSTrACT Because p53 inactivation may limit the effectiveness of radiation therapy for localized prostate cancer, it is important to understand how this gene regulates clonogenic survival after an exposure to ionizing radiation. Here, we show that premature cellular senescence is the principal mode of cell death accounting for the radiosensitivity of human prostate cancer cell lines retaining p53 function. Alternative stress response pathways controlled by this tumor suppressor, including cell cycle arrest, DNA damage repair, mitotic catastrophe and apoptosis, contributed significantly less to radiation-induced clonogenic death. Using a dominant negative C-terminal fragment of p53, we present the first evidence that a complete loss of endogenous p53 function is sufficient to limit the irradiation-induced senescence and clonogenic death of prostate cancer cells. Conversely, inheritance of wild-type p53 by prostate cancer cells lacking a functional allele of this gene (i.e., DU145) significantly increases clonogenic death through p53-dependent cellular senescence and apoptotic pathways. Our data provide evidence that mutations of even one p53 allele may be sufficient to alter their clonogenic fate. In addition, they support the idea that the p53 pathway can be used as a specific target for enhancing the radiosensitivity of prostate cancer cells. Activation of p53 by the drug nutlin-3 is shown to be an effective radiosensitizer of prostate cancer cells retaining functional alleles of p53 and this effect was entirely attributable to an increased induction of p53-dependent cellular senescence.

show abstract

“…In particular, complete regression of prostate cancers was reported in some patients to take more than a year after radiation treatment (Cox and Kline, 1983), whereas regression of desmoid tumors took up to 2 years (Bataini et al, 1988). This slow response seems most consistent with radiation-induced senescence.…”

Section: Implications Of Senescence For Cancer Therapymentioning

confidence: 96%