For more than six decades, radiotherapy has been used for testicular seminoma considering its high radiosensitivity, particularly those in stages I and II. I think that the mechanism(s) by which seminoma is so radiosensitive remains incompletely understood, although seminoma may have better DNA damage repair machinery than non-seminoma. p53 is wild-type in these cells. I am not sure whether Oct4 implicated in chemosensitivity may play a role in radiosensitivity.

https://www.ncbi.nlm.nih.gov/pubmed/18657195

https://www.ncbi.nlm.nih.gov/pubmed/25866027

https://www.ncbi.nlm.nih.gov/pubmed/7893365

https://www.ncbi.nlm.nih.gov/pubmed/24692098

https://www.ncbi.nlm.nih.gov/pubmed/17117392

In contrast to the law of Bergonié and Tribondeau, slowly growing cells are not necessarily more radioresistant than rapidly growing cells. Such examples are discussed in the following paper

https://www.researchgate.net/publication/230628827_The_law_of_Bergonie_and_Tribondeau_A_nice_formula_for_a_first_approximation

Regarding radiosensitivity, we should refer to DNA damage response of the cancer cells.

The DNA damage response of NSGSTs is more efficacious than SGCTs. This may be due to more expression of p53 in NSGSTs in compare with SGSTs.

Resource:

Article Role of DNA repair machinery and p53 in the testicular germ ...