FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2036703508> ?p ?o ?g. }

• W2036703508 endingPage "24" @default.
• W2036703508 startingPage "10" @default.
• W2036703508 abstract "Collectively, low-grade B-cell malignancies constitute the fifth most common form of potentially lethal cancer in North America and Europe, with chronic lymphocytic leukemia (CLL) and follicular non-Hodgkin's lymphoma (FL) representing the most prevalent of these disorders. Chronic lymphocytic leukemia and FL represent quintessential examples of human malignancies that are caused primarily by defects in programmed cell death (apoptosis). During the early stages of disease, the mature B lymphocytes that comprise most CLLs and FLs are largely quiescent G0 phase cells, which accumulate not because they are dividing more rapidly than normal but because they survive longer than their normal counterparts because of defects in the normal pathways for apoptosis. Defects in apoptosis pathways contribute to chemoresistance, rendering tumor cells less sensitive to the cytotoxic actions of currently available anticancer drugs, and can also promote resistance to cellular immune responses. Several biological agents or their synthetic derivatives show promise as apoptosis modulators, having the potential to place neoplastic cells into a more susceptible state or activating latent programs for cell suicide. These biological response modifiers include monoclonal antibodies such as rituximab (Rituxan; Genentech, Inc, South San Francisco, CA, and IDEC Pharmaceuticals, San Diego, CA) that alter signal transduction pathways, cytokines such as TRAIL (Apo2 ligand), ligands for retinoid/steroid family nuclear receptors, and small-molecule compounds that bind and inhibit protein kinases. Knowledge about the mechanisms by which these agents influence apoptosis pathways in neoplastic diseases may suggest strategies for more effective and less toxic therapies for patients suffering from CLL, FL, and other malignancies. Semin Oncol 29 (suppl 2):10-24. Copyright © 2002 by W.B. Saunders Company." @default.
• W2036703508 created "2016-06-24" @default.
• W2036703508 creator A5000921376 @default.
• W2036703508 creator A5035082589 @default.
• W2036703508 creator A5049032346 @default.
• W2036703508 creator A5059438505 @default.
• W2036703508 date "2002-02-01" @default.
• W2036703508 modified "2023-09-28" @default.
• W2036703508 title "Modulating apoptosis pathways in low-grade B-cell malignancies using biological response modifiers" @default.
• W2036703508 cites W122353466 @default.
• W2036703508 cites W133925001 @default.
• W2036703508 cites W147398146 @default.
• W2036703508 cites W1496387664 @default.
• W2036703508 cites W1499230593 @default.
• W2036703508 cites W1499746632 @default.
• W2036703508 cites W1501301649 @default.
• W2036703508 cites W1535874622 @default.
• W2036703508 cites W1557686543 @default.
• W2036703508 cites W161269271 @default.
• W2036703508 cites W1621124914 @default.
• W2036703508 cites W1624001120 @default.
• W2036703508 cites W1642763135 @default.
• W2036703508 cites W1644953918 @default.
• W2036703508 cites W1678355196 @default.
• W2036703508 cites W180295822 @default.
• W2036703508 cites W1843554028 @default.
• W2036703508 cites W1870720170 @default.
• W2036703508 cites W1915689252 @default.
• W2036703508 cites W1927684145 @default.
• W2036703508 cites W1958512987 @default.
• W2036703508 cites W1962843014 @default.
• W2036703508 cites W1968515578 @default.
• W2036703508 cites W1969783942 @default.
• W2036703508 cites W1975449325 @default.
• W2036703508 cites W1976088592 @default.
• W2036703508 cites W1977499961 @default.
• W2036703508 cites W1978899115 @default.
• W2036703508 cites W1979842763 @default.
• W2036703508 cites W1979995768 @default.
• W2036703508 cites W1981106016 @default.
• W2036703508 cites W1981166298 @default.
• W2036703508 cites W1982661150 @default.
• W2036703508 cites W1985476964 @default.
• W2036703508 cites W1985520226 @default.
• W2036703508 cites W1988508496 @default.
• W2036703508 cites W1990183651 @default.
• W2036703508 cites W1992979608 @default.
• W2036703508 cites W1995891719 @default.
• W2036703508 cites W1996267589 @default.
• W2036703508 cites W1996357925 @default.
• W2036703508 cites W1998826441 @default.
• W2036703508 cites W2002154440 @default.
• W2036703508 cites W2003472250 @default.
• W2036703508 cites W2004487226 @default.
• W2036703508 cites W2007127627 @default.
• W2036703508 cites W2008715871 @default.
• W2036703508 cites W2008898220 @default.
• W2036703508 cites W2013319326 @default.
• W2036703508 cites W2013801793 @default.
• W2036703508 cites W2015588789 @default.
• W2036703508 cites W2015788325 @default.
• W2036703508 cites W2017728303 @default.
• W2036703508 cites W2017985723 @default.
• W2036703508 cites W2021810470 @default.
• W2036703508 cites W2024306318 @default.
• W2036703508 cites W2025128734 @default.
• W2036703508 cites W2028044172 @default.
• W2036703508 cites W2028111124 @default.
• W2036703508 cites W2028526641 @default.
• W2036703508 cites W2030573603 @default.
• W2036703508 cites W2031694725 @default.
• W2036703508 cites W2032531389 @default.
• W2036703508 cites W2035523654 @default.
• W2036703508 cites W2036822121 @default.
• W2036703508 cites W2037665471 @default.
• W2036703508 cites W2041278917 @default.
• W2036703508 cites W2041466047 @default.
• W2036703508 cites W2041980363 @default.
• W2036703508 cites W2043651078 @default.
• W2036703508 cites W2044467049 @default.
• W2036703508 cites W2045086385 @default.
• W2036703508 cites W2046666755 @default.
• W2036703508 cites W2049608177 @default.
• W2036703508 cites W2049873418 @default.
• W2036703508 cites W2054946481 @default.
• W2036703508 cites W2058591356 @default.
• W2036703508 cites W2059126161 @default.
• W2036703508 cites W2062807784 @default.
• W2036703508 cites W2065413461 @default.
• W2036703508 cites W206701898 @default.
• W2036703508 cites W2068240610 @default.
• W2036703508 cites W2070862399 @default.
• W2036703508 cites W2072692243 @default.
• W2036703508 cites W2074451356 @default.
• W2036703508 cites W2079357365 @default.
• W2036703508 cites W2082157761 @default.
• W2036703508 cites W2083560313 @default.
• W2036703508 cites W2083573634 @default.

• next