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Qesem Cave, 12 km east of the Mediterranean coast, is excavated by A. Gopher and R. Barkai since 2001 on behalf of Tel Aviv University. The cave reveals 7 meters of anthropogenic sediments all assigned to the late Lower Paleolithic period (200-400 thousand years ago). It is very rich in finds which are outstandingly well preserved, enabling a detailed look at lithic finds and faunal remains. Prehistoric research throughout the world in the last decade emphasizes aspects of what is called "Modern Human Behavior" found in Lower Paleolithic sites. The Qesem Cave finds provide a wealth of information related to such behaviors concerning the habitual use of fire, hunting techniques and patterns of meet sharing, the organization of space (activity areas) and the production of flint blades using an efficient and innovative technology. The cave also provides some human remains, mainly teeth that indicate a long history of Homo sapience in this part of the world.

Aggressive transformed features caused by concomitant expression of oncogenic Ras and mutant p53 are well documented. However, the mechanisms by which the various mutant p53 categories cooperate with Ras remain largely obscure. In this study, we report on several molecular mechanisms that underlie the crosstalk between the H-RasG12V oncogene (H-RasV12) and several hot spot p53 mutants in inducing a previously described cancer-related gene signature (CGS) and tumorigenicity. The different molecular mechanisms are attributed to a specific mutant p53 category. While the DNA-contact p53 mutants (p53R248Q and p53R273H) exhibited the highest level of CGS expression by cooperating with the NF-κB gene, the Zn+2 region conformational p53 mutants (p53R175H and p53H179R) induced the CGS by elevating H-Ras activity. In contrast, the L3 loop region conformational mutant (p53G245S) did not affect the CGS expression. A similar pattern of CGS expression was observed in Head & Neck human tumors expressing mutated p53 proteins. Finally, a strong correlation between the capability of a specific mutant p53 to induce the CGS and malignant phenotypes was observed, thus further supporting the notion of a tailor-made p53-based therapy.