DuCLOX-2/5 inhibition: a promising target for cancer chemoprevention
Abstract Cancer is a leading cause of death and major health concern worldwide. The animal and human studies support the presumption that inflammation directs the cancer initiation and progression. Cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) are the key players in the inflammatory cascade contributing towards the angiogenesis, tumor cell invasiveness, and disruption in the pathways of cellular proliferation/apoptosis. Contemporary studies have particularized a promising role of COX-2 and 5-LOX inhibitors in cancer chemoprevention. The present review is a pursuit to define implications of dual COX-2 and 5-LOX (DuCLOX-2/5) inhibition on various aspects of cancer augmentation and chemoprevention..
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2016 |
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Erschienen: |
2016 |
Enthalten in: |
Zur Gesamtaufnahme - volume:24 |
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Enthalten in: |
Breast cancer - 24(2016), 2 vom: 24. Aug., Seite 180-190 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Gautam, Swetlana [VerfasserIn] |
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Links: |
Volltext [lizenzpflichtig] |
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Themen: |
Angiogenesis |
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Anmerkungen: |
© The Japanese Breast Cancer Society 2016 |
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doi: |
10.1007/s12282-016-0723-2 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
SPR024770051 |
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520 | |a Abstract Cancer is a leading cause of death and major health concern worldwide. The animal and human studies support the presumption that inflammation directs the cancer initiation and progression. Cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) are the key players in the inflammatory cascade contributing towards the angiogenesis, tumor cell invasiveness, and disruption in the pathways of cellular proliferation/apoptosis. Contemporary studies have particularized a promising role of COX-2 and 5-LOX inhibitors in cancer chemoprevention. The present review is a pursuit to define implications of dual COX-2 and 5-LOX (DuCLOX-2/5) inhibition on various aspects of cancer augmentation and chemoprevention. | ||
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700 | 1 | |a Kaithwas, Gaurav |4 aut | |
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