Reported imaging agents targeting CA-IX are successful mostly in clear cell renal carcinoma as SKRC-52 and no candidate was approved yet in clinical trials for imaging of CA-IX.
From the clinical point of view, ovarian cancers in LS are mostly endometrioid or clear cell [ 27– 31], and the tumors are less advanced at the time of diagnosis, showing strikingly high stage-specific survival rates [ 24, 32, 33].
The Type II carcinoma, which comprises mostly the serous and clear cell histological subtypes, is known to metastasize more often and to have a worse survival.
In contrast, type II, consisting mostly of serous and clear cell carcinoma, typically arises in atrophic endometrium via a mechanism unrelated to estrogen exposure.
RCC consists mostly of two histological types: clear cell carcinoma (>80 %) and papillary (10%%) [ 7].
Furthermore, wild-type p53 is mostly present and mutations are uncommon in clear cell tumors contrary to Type II tumors, which are genetically unstable and have a high frequency of p53 mutations [ 10, 11].
In contrast, no such association is indicated for clear cell ovarian tumors, which mostly present with a CpG island methylator phenotype (CIMP) but are nevertheless unmethylated at the HNF1B promoter (11).
Contrary to ovarian cancers of the general population or that are HBOC syndrome-related, those related to LS are mostly of the non-serous type, including endometrioid, clear cell and undifferentiated carcinomas [36, 49].
Similarly, others previously identified (mostly truncating) somatic mutations in endometriosis-associated ovarian clear cell and endometrioid carcinomas.
In clear cell carcinoma wild-type p53 is mostly present and mutations are uncommon [ 10, 11].
