By Hak Choy
Across the world well-known specialists in melanoma biology and scientific study assessment the current prestige of the multimodality method of the administration of stable tumors and speculate on attainable destiny options for chemoradiation remedy. The authors element purposes of mixed modality remedy in lung, esophageal, breast, gastric, pancreatic, colon, and rectal cancers. in addition they express how radiation interacts with such chemotherapeutic brokers because the platinum complexes, taxanes, and gemcitabine within the remedy of malignant gliomas, and head and neck melanoma. A assessment of ways to combine new particular molecular distinctive brokers into multimodality treatment sooner or later.
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Additional info for Chemoradiation in Cancer Therapy (Cancer Drug Discovery and Development)
Several biological mechanisms that have potential to alter sensitization strategies. ment and cellular proliferation (80). High PKC levels have been identified in certain tumor types including carcinoma of the breast, brain, and colon (81–83). Manipulation of cellular PKC levels through transfection and antisense oligonucleotide strategies have indicated a role in carcinogenesis and cellular differentiation. Preclinical studies, which have examined the activity of a reversible inhibitor (PKC412) of certain PKCs including cdk1/cyclin B1, have found that it has substantial antitumor activity in a variety of murine xenografts on its own (84).
Coia et al. (75) reported the results of 57 patients with stage I or II esophageal cancer who received fluorouracil infusion (for 4 d × two cycles, starting on d 2 and 29), and CMT (on d 2) with radiation (60 Gy in 30 fractions). The 3- and 5-yr actuarial survivals were 29% and 18%, respectively. The disease-specific survival was 41% and 30% at 3 and 5 yr, respectively. In a randomized intergroup trial, 121 patients with localized esophageal cancer were administered either 64 Gy of radiation alone or four cycles of fluorouracil and cisplatin plus 50 Gy of radiation.
Sutherland RM. Tumor hypoxia and gene expression—implications for malignant progression and therapy. Acta Oncol 1998; 37(6):567–574. 24. Dachs GU, Tozer GM. Hypoxia modulated gene expression: angiogenesis, metastasis and therapeutic exploitation. Eur J Cancer 2000; 36(13 Spec No):1649–1660. 25. De Vita VT, Hellman S, Rosenberg SA. Cancer. Principles and Practice of Oncology, 5th edition. Lippincott-Raven. 1997. pp. 858–910. 26. Goldie JH, Coldman AJ, Gudauskas GA. Rationale for the use of alternating non-cross-resistant chemotherapy.
Chemoradiation in Cancer Therapy (Cancer Drug Discovery and Development) by Hak Choy