Bcl-2 downregulation and caspase 3 upregulation coincide in the apoptotic pathway mediated by activated p53, a “classical” signalling pathway. Studies have shown that p53 and its interactional factor, HIF-1a, are major regulators of the cellular response to hypoxia. Interestingly, the high ratio of p53 transcription is a marker of advanced malignancy. The function of HIF-1a is to maintain p53 stabilisation. When cancer cells have lost p53 function, they shift a balance from p53 to HIF transcriptional regulation. However, p53 inhibits HIF-1a expression. Additionally, HIF-1a directly controls the expression of LDHA; HIF-1a and LDH5 are commonly expressed at high levels in cancer cells. We detected that INMAP overexpression decreases LDH5 activity, and it may be deduced that INMAP may regulate the p53- mediated HIF-1a pathway. p53 overexpression may inhibit HIF-1a expression, and HIF-1a might then suppress LDHA expression. In this study, we found that overexpression of INMAP in HeLa cells causes DNA damage/ genomic instability and apoptosis, thereby suppressing tumour growth both in vitro and in vivo. Moreover, a high INMAP level activates key genes associated with DNA damage and apoptosis through p53-medicated signalling pathways. The exact mechanism of p53 signalling pathways triggered by AB1010 excessive expression of INMAP remains to be further studied. These results underscore the crucial role of INMAP in carcinogenesis and tumour growth. In most cancer patients, only tissues from the primary tumors are biopsied or resected for diagnostic and therapeutic purposes. Outside the context of studies clinicians do not biopsy recurrent or metastatic disease, unless it has therapeutic significance. This hampers the molecular comparison of primary and metastatic disease, despite the fact that it is now evident that there is not just intra-tumor heterogeneity but that there are also considerable molecular differences between primary tumors and metastases. Chemotherapeutic and other systemic treatments based on genetic characteristics of the primary tumor may not work effectively on metastases due to changes of molecular targets, such as receptor conversion. Knowing the molecular characteristics of metastases may help to target them specifically. It is, therefore, necessary to pursue molecular research, comparing primary tumors and metastases. Post-mortem investigation is an opportunity to obtain tissue samples from primary tumors and metastases for comparative molecular studies. The so-called “rapid autopsy” is performed soon after death, in order to minimize post-mortem degradation of collected tumor samples and allows for procurement of among others high quality RNA. Unfortunately, autopsies are rarely performed on patients who died of cancer. Bereaved relatives are often not willing to give their consent for conventional autopsy, mainly because they feel that their loved one has suffered enough from the disease and they consider mutilation of the deceased’s body undesirable.