Question: Which oncogenes are able to induce cellular senescence?

Context:
ROS-generating oxidases Nox1 and Nox4 contribute to oncogenic Ras-induced premature senescence
Activated oncogenes induce premature cellular senescence, a permanent state of proliferative arrest in primary rodent and human fibroblasts. Recent studies suggest that generation of reactive oxygen species (ROS) is involved in oncogenic Ras-induced premature senescence.
these findings suggest that Nox1- and Nox4-generated ROS play an important role in Ras-induced premature senescence
A role for c-Abl in cell senescence and spontaneous immortalization
Here, we report an important role for c-Abl in replicative senescence and immortalization by regulating the expression of two tumor suppressors that induce cellular senescence, p53 and p16(INK4a).
The role for c-Abl in regulating cell senescence and immortalization might explain some of the developmental defects in c-Abl (-/-) mice and how BCR-ABL transforms cells.
Ras/Raf-prototypic oncogenes induce cellular senescence, a terminal cell-cycle arrest, as a default cellular safeguard program
oncogene-induced senescence, Myc style
We review and discuss here evidence for Myc-induced senescence - which is detectable to a limited degree as a cell-autonomous, direct response to Myc action, but occurs predominantly in a non-cell-autonomous fashion via crosstalk of the oncogene-driven cell population with non-neoplastic bystanders, namely cells of the host immune system, prompting them to release pro-senescent cytokines that strike back onto adjacent proliferating tumor cells.
genetic Skp2 inactivation evokes cellular senescence even in oncogenic conditions in which the p19(Arf)-p53 response is impaired, whereas a Skp2-SCF complex inhibitor can trigger cellular senescence in p53/Pten-deficient cells and tumour regression in preclinical studies.
Activated RAS/BRAF oncogenes induce cellular senescence as a tumor-suppressive barrier in early cancer development, at least in part, via an oncogene-evoked DNA damage response (DDR).
Cdk2 suppresses cellular senescence induced by the c-myc oncogene
Loss of Cdk2 also caused sensitization to Myc-induced senescence in pancreatic beta-cells or splenic B-cells in vivo
Myc also causes senescence in cells lacking the DNA repair protein Wrn.
In MEFs, Myc-induced senescence was genetically dependent on the ARF-p53-p21Cip1 and p16INK4a-pRb pathways, p21Cip1 and p16INK4a being selectively induced in Cdk2-/- cells.
We have found that expression of such an oncogene, Akt, causes senescence in primary mouse hepatoblasts in vitro.
hyperproliferative signaling through AKT might be a driving force of the senescence in activated hepatic stellate cells.
oncogenic RAS expression, which causes genotoxic stress and senescence in normal cells,
Here we report that the suppression of the c-Myc (MYC) oncogene induces cellular senescence in diverse tumor types including lymphoma, osteosarcoma, and hepatocellular carcinoma.
Cellular senescence is an important mechanism of tumor regression upon c-Myc inactivation
MYC inactivation was associated with prototypical markers of senescence
only after lymphomas were repaired for p53 expression did MYC inactivation induce robust senescence and sustained tumor regression.
Replicative senescence due to telomere shortening can, for example, be induced by a dominant negative version of telomerase, premature senescence by the overexpression of oncogenic ras, or p16.
knockdown of HDAC2 induced cellular senescence.
MYC overexpression is thought to initiate tumorigenesis by inducing cellular proliferation and growth and to be restrained from causing tumorigenesis by inducing cell cycle arrest, cellular senescence, and/or apoptosis.
Several conditions, including oncogenic Ras over-expression and inappropriate culture conditions, also induce senescence without telomere shortening.
We demonstrate that p38 mitogen-activated protein kinase (MAPK) plays important causative roles in senescent cells following telomere shortening, Ras-Raf activation, oxidative stress or inappropriate culture conditions.
Mitogen-activated protein kinase p38 defines the common senescence-signalling pathway
These results indicate that p38 comprises the senescence-executing pathway in response to diverse stimuli.
this p38-activating condition appears to be defined quantitatively as a sum of continuous and low-level stresses, and remains even after the initial stimuli are withdrawn, which may explain the well-known irreversible nature of cellular senescence. We also show that papilloma virus E7 abolishes the p38-induced growth arrest but not other senescence-associated phenotypes, indicating the differential role of pRb in the downstream of p38.
Expression of caveolin-1 induces premature cellular senescence in primary cultures of murine fibroblasts
Here, we demonstrate that mouse embryonic fibroblasts transgenically overexpressing caveolin-1 show: 1) a reduced proliferative lifespan; 2) senescence-like cell morphology; and 3) a senescence-associated increase in beta-galactosidase activity. These results indicate for the first time that the expression of caveolin-1 in vivo is sufficient to promote and maintain the senescent phenotype.
Interestingly, premature senescence induced by hydrogen peroxide is greatly reduced in NIH 3T3 cells harboring antisense caveolin-1. Importantly, induction of premature senescence is recovered when caveolin-1 levels are restored.
these results clearly indicate a central role for caveolin-1 in promoting cellular senescence
Oncogenic activation of the mitogen-activated protein (MAP) kinase cascade in murine fibroblasts initiates a senescence-like cell cycle arrest that depends on the ARF/p53 tumor suppressor pathway.
In contrast, coexpression of oncogenic ras or activated mek1 with p53 enhanced both p53 levels and activity relative to that observed for p53 alone and produced an irreversible cell cycle arrest that displayed features of cellular senescence.
our results indicate that oncogenic activation of the MAP kinase pathway in murine fibroblasts converts p53 into a senescence inducer through both quantitative and qualitative mechanisms.
Myc-evoked apoptosis serves as a signal for macrophage attraction and activation, followed by the secretion of TGF-β as a cytokine that is capable of terminally arresting Myc-driven lymphoma cells without causing further DNA damage and without launching a senescence-associated, pro-inflammatory, and, therefore, potentially detrimental cytokine response in the target population.
The suppression of oncogenic levels of MYC is sufficient to induce sustained tumor regression associated with proliferative arrest, differentiation, cellular senescence, and/or apoptosis, a phenomenon known as oncogene addiction.

Answer: Cellular senescence can be induced through activation or inactivation of a number of oncogenes, such as Ras, c-Abl, Raf, Myc, Skp2, BRAF, AKT, HDAC2, p38 MAPK, Caveolin-1 and Mek1.
Exact answer: Ras, c-Abl, Raf, Myc, Skp2, BRAF, AKT, HDAC2, p38 MAPK, Caveolin-1, Mek1