Zobrazeno 1 - 6
of 6
pro vyhledávání: '"Angela M. Sosin"'
Autor:
Ayad Al-Katib, Sophia Z Shalhout, Dania Haddad, Thomas C. Holland, Alberto Martin, Angela M. Sosin, Ashok S. Bhagwat
Publikováno v:
Molecular and cellular biology. 34(21)
Activation-induced deaminase (AID) converts DNA cytosines to uracils in immunoglobulin genes, creating antibody diversification. It also causes mutations and translocations that promote cancer. We examined the interplay between uracil creation by AID
Autor:
Ramzi M. Mohammad, Judith Abrams, Ayad Al-Katib, Angelika M. Burger, Angela M. Sosin, Aisha Siddiqi
Publikováno v:
Journal of Hematology & Oncology
Journal of Hematology & Oncology, Vol 5, Iss 1, p 57 (2012)
Journal of Hematology & Oncology, Vol 5, Iss 1, p 57 (2012)
Background Lymphomas frequently retain wild-type (wt) p53 function but overexpress HDM2, thereby compromising p53 activity. Therefore, lymphoma is a suitable model for studying the therapeutic value of disrupting the HDM2-p53 interaction by small-mol
Autor:
Anwar N. Mohamed, Frances W.J. Beck, Angela M. Sosin, Ramzi M. Mohammad, Peter G. Smith, Ayad Al-Katib, Alan A. Arnold, Amro Aboukameel
Publikováno v:
Molecular Cancer, Vol 9, Iss 1, p 228 (2010)
Molecular Cancer
Molecular Cancer
Background IKK-2 is an important regulator of the nuclear factor-κB (NF-κB) which has been implicated in survival, proliferation and apoptosis resistance of lymphoma cells. In this study, we investigated whether inhibition of IKK-2 impacts cell gro
Publikováno v:
Cancer Research. 71:594-594
Mutations in TP53 occur in 50% of all cancers but are far less common in hematological malignancies. The activity of wild-type p53 (wt-p53) is frequently compromised in lymphomas by overexpression of MDM2. Small-molecule inhibitors (SMIs) that can di
Publikováno v:
Cancer Research. 70:4516-4516
The p53 tumor suppressor protein function is impaired in over 50% of all cancers via inactivating mutations. However, the frequency of p53 mutations is much lower in hematological malignancies. Most lymphomas have wild-type (wt) p53, mutant (mt) p53
Autor:
Shaomeng Wang, Dajun Yang, Ramzi M. Mohammad, Angela M. Sosin, Amro Aboukameel, Ayad Al-Katib, Jack Wu, Sherwin Wu, Asfar S. Azmi
Publikováno v:
Molecular Cancer
Molecular Cancer, Vol 8, Iss 1, p 115 (2009)
Molecular Cancer, Vol 8, Iss 1, p 115 (2009)
Background MI-319 is a synthetic small molecule designed to target the MDM2-P53 interaction. It is closely related to MDM2 antagonists MI-219 and Nutlin-3 in terms of the expected working mechanisms. The purpose of this study was to evaluate anti-lym