Torsion of the testis: a new risk factor for testicular cancer

Chilvers, Clair; Pike, Malcolm C.; Peckham, M. J.

doi:10.1038/bjc.1987.21

Cited by 62 publications

(14 citation statements)

References 4 publications

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“…In clinical practice, necrotic testes are usually removed to avoid contralateral testicular injury potentially reducing fertility rates, and the risk of atrophy-related testicular cancer. 4 Our results showed that the ischemic injury produced by 1,080-degree torsion of the spermatic cord did not result in significant macroscopic or histological testicular necrosis after 1 to 4 hours of torsion, suggesting there may be persistent blood flow to the testis and testicular viability even with this degree of testicular torsion. In humans, these testes would be considered for preservation through operative detorsion and orchidopexy.…”

Section: Discussionmentioning

confidence: 66%

“…3 Further, testicular atrophy following torsion of the spermatic cord has been reported to increase the risk of testicular cancer. 4 Experimental models of testicular torsion are valuable tools to evaluate the relationship between the degree and duration of torsion with the blood flow and resultant damage to the torsed testes. The results, however, have been conflicting.…”

Section: Introductionmentioning

confidence: 99%

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Ipsilateral testicular necrosis and atrophy after 1,080-degree torsion of the spermatic cord in rats

et al. 2009

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PURPOSE: To assess the incidence of testicular necrosis/atrophy immediately after 1 to 4 hours of 1,080-degree torsion of the spermatic cord, and 60 days after detorsion of the spermatic cord. METHODS: 42 rats were divided in 7 groups. Except for the control group, surgical torsion of the right spermatic cord was performed in all groups (T0). After 1, 2, or 4 hours of torsion, each group underwent either ipsilateral orchiectomy (groups OT1, OT2, and OT4), or detorsion of the spermatic cord and observation for 60 days (groups DT1, DT2, and DT4), before they were evaluated for the presence of testicular necrosis/atrophy. RESULTS: Only one rat (5.5%) in groups OT1, OT2, and OT4 had testicular necrosis, in comparison with six rats (33.3%) in groups DT1, DT2, and DT4 (p=0.04). The incidence of testicular necrosis/atrophy was not different between subgroups T1, T2, and T4, and the control group (p>0.05). There was, however, a tendency toward greater incidence of necrosis/atrophy in the rats in group DT4. CONCLUSION: The incidence of testicular necrosis/atrophy immediately after 1 to 4 hours of 1,080-degree torsion of the spermatic cord is 5.5%, in comparison with 33.3% sixty days after detorsion of the spermatic cord.

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Section: Discussionmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 99%

Ipsilateral testicular necrosis and atrophy after 1,080-degree torsion of the spermatic cord in rats

et al. 2009

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“…Contrarily, results of the study done by Puri et al [16] supports that torsion of the testis does not affect fertility. In a cohort study, it is also calculated that the patients who had testicular torsion in their history have threefold increased risk for testicular malignancy [8].…”

Section: Discussionmentioning

confidence: 99%

Histological evaluation of the testicular nubbins in patients with nonpalpable testis: assessment of etiology and surgical approach

et al. 2006

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There is a controversy in the literature whether testicular nubbins carry malignancy risk and excision of the nubbin is necessary in patients with nonpalpable testis. It is also controversial whether vanishing testis has the same etiopathogenesis and risk with true undescended testis. The aim of this study is to investigate the histological findings of testicular nubbins in patients with nonpalpable testis and to question etiology and surgical indications for vanishing testis. We reviewed the histopathological results of 44 testicular nubbins in 40 patients (mean age: 4.1 years, range 1-13 years) with nonpalpable testis between 1992 and 2004, retrospectively. Exploration revealed 5 intraabdominal and 39 inguinal testicular nubbins. Of 44 specimens only 5 (11.3%) from inquinal testicular nubbins were found to have seminiferous tubules. Two of the five had seminiferous tubule structures with viable germ cells showing maturation correlating with age. The other two with scarce seminiferous tubules were seen on only a single area and one had Sertoli cells only. None of the excised tissue had malignant degeneration. The vas deferens was identified in 23 (52.2%), vessels in 26 (59%), calcification in 14 (31.8%) and hemosiderin in 12 (27.2%) of excised tissue. Presence of calcification in one-third of the nubbins supports vascular accident thesis in the etiopathogenesis of vanishing testis. The possibility for the presence of seminiferous tubules and viable germ cells in the testicular nubbin is low. These facts decrease theoritical risk of malingnancy. Therefore, an inguinal exploration for testicular nubbin in patients with vas deferens and vessels entering into the inquinal canal diagnosed at laparoscopy can be postponed untill testicular prosthesis implantation and the nubbin can be removed at this operation.

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“…This increased clustering will also generate frequently DNA damage that is more complex than that induced by low-LET radiations, in the sense that it will comprise more lesions within one or two turns of the DNA helix. It constitutes what is sometimes called clustered damage sites (CDS) or multiply damaged sites (50,65). Although CDS is generated by low-LET radiation, such as X-rays, it occurs more frequently after exposure to high-LET radiations and is implicated in their enhanced biological effects.…”

Section: Systematic Analysis Of Dsb Complexity Levelsmentioning

confidence: 99%

DNA double-strand-break complexity levels and their possible contributions to the probability for error-prone processing and repair pathway choice

Schipler

Iliakis

2013

Nucleic Acids Research

240

232

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Although the DNA double-strand break (DSB) is defined as a rupture in the double-stranded DNA molecule that can occur without chemical modification in any of the constituent building blocks, it is recognized that this form is restricted to enzyme-induced DSBs. DSBs generated by physical or chemical agents can include at the break site a spectrum of base alterations (lesions). The nature and number of such chemical alterations define the complexity of the DSB and are considered putative determinants for repair pathway choice and the probability that errors will occur during this processing. As the pathways engaged in DSB processing show distinct and frequently inherent propensities for errors, pathway choice also defines the error-levels cells opt to accept. Here, we present a classification of DSBs on the basis of increasing complexity and discuss how complexity may affect processing, as well as how it may cause lethal or carcinogenic processing errors. By critically analyzing the characteristics of DSB repair pathways, we suggest that all repair pathways can in principle remove lesions clustering at the DSB but are likely to fail when they encounter clusters of DSBs that cause a local form of chromothripsis. In the same framework, we also analyze the rational of DSB repair pathway choice.

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Torsion of the testis: a new risk factor for testicular cancer

Cited by 62 publications

References 4 publications

Ipsilateral testicular necrosis and atrophy after 1,080-degree torsion of the spermatic cord in rats

Ipsilateral testicular necrosis and atrophy after 1,080-degree torsion of the spermatic cord in rats

Histological evaluation of the testicular nubbins in patients with nonpalpable testis: assessment of etiology and surgical approach

DNA double-strand-break complexity levels and their possible contributions to the probability for error-prone processing and repair pathway choice

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