A senescence program controlled by p53 and p16INK4a contributes to the outcome of cancer therapy.

By C. Schmitt, J. Fridman, Meng Yang, Soyoung Lee, E. Baranov, R. Hoffman, Scott W. Lowe. Cell, 2002

1,074 citations recorded by the source corpus.

Subfields: Hematology, Oncology, Physiology

View Paper: https://www.semanticscholar.org/paper/08b2333193ea779da8664dbbbcf59bd814134f9c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Hematology

1. Scott W. Lowe

In Oncology

1. J. Campisi
2. Scott W. Lowe
3. Manuel Serrano
4. C. Sherr
5. M. Collado
6. R. DePinho
7. N. Bardeesy
8. T. Mak

In Physiology

1. J. Campisi
2. Manuel Serrano
3. M. Demaria
4. Jesús Gil
5. Scott W. Lowe
6. M. Collado
7. D. Peeper
8. T. Kuilman

Citations in the corpus

• The RB and p53 pathways in cancer. (2002, background): “Loss of p53 portends a poorer prognosis, since p53 is required for both apoptosis and cytostasis (Schmitt et al., 2002).”
• Survival signalling by Akt and eIF4E in oncogenesis and cancer therapy (2004, methodology): “Here, animals harbouring Arf -null lymphomas were used as controls, as these lymphomas are also highly aggressive but remain chemosensitiv”
• The multiple uses of fluorescent proteins to visualize cancer in vivo (2005, background): “Moreover, whole-body imaging shows that MYC-driven GFP-expressing lymphomas with p53 or INK4A and ARF mutations, or that overexpress BCL2, respond poorly to cyclophosphamide therapy in vivo compared with wild-type cell”
• Senescence and apoptosis: dueling or complementary cell fates? (2014, neutral): “One of the first studies to report an apoptosis-independent function to p53 in cancer showed that murine lymphomas overexpressing Bcl-2 undergo p53/p16-dependent senescence rather than apoptosis in response to cyclophosphamide [91].”
• Pathways of apoptotic and non-apoptotic death in tumour cells (2004, background): “This hypothesis has been confirmed in an elegant study of anticancer-drug responses in a transgenic mouse model of lymphomagenesi”
• The essence of senescence. (2010, background): “Furthermore, DNA damage-inducing drugs can cause senescence of tumor cells in vitro and in vivo, a phenomenon termed drug-induced senescence, which may be exploited for the treatment of cancer (Wang et al. 1998; Chang et al. 1999; Berns 2002; Schmitt et al. 2002; te Poele et al. 2002; Roninson 2003)”
• The Cell-Cycle Arrest and Apoptotic Functions of p53 in Tumor Initiation and Progression. (2016, background): “Treatment of established lymphomas with cyclophosphamide caused p53-dependent senescence and tumor regression (Schmitt et al. 2002).”
• Targeting p53 pathways: mechanisms, structures and advances in therapy (2023, background): “Various internal or external stressors trigger the DNA damage response pathway, activating the p53 and/or p16INK4A pathways.(84) p16INK4A inactivates Cdk4/6, phosphorylates Rb accumulation and inactivates E2F transcription, leading to cell cycle arrest or senescence.”
• Directed elimination of senescent cells by inhibition of BCL-W and BCL-XL (2016, neutral): “In addition, senescence has been shown to contribute to the cytotoxicity of anti-cancer agents and to support tissue repair by limiting excessive proliferation of cells 5–10 .”
• Nuclear structure in cancer cells (2004, background): “In fact, anticancer drugs used in chemotherapy can induce senescenc”
• The proliferation gene expression signature is a quantitative integrator of oncogenic events that predicts survival in mantle cell lymphoma. (2003, background): “Whereas the proliferation rate of the malignant B cells ex vivo (Eischen et al., 1999; Schmitt et al., 2002).”
• Therapy-induced senescence in cancer. (2010, background): “Experimental evidence indicates that there are benefits to the induction of senescence in immunocompetent patients (20,21).”