PRESURGICAL INTRAVENOUS NUTRITION AND RECTAL CANCER

癌症治疗中营养治疗的早期假说 如果宿主的营养状况能够保持或改善， 那么宿主的存活率也应该会提高。几项临床试验 旨在测试这一假设，并发现总 肠外营养(TPN)不能增加患者的存活率 全身性治疗多种肿瘤疾病的临床研究 化疗。积极的营养治疗失败了 患者存活率的提高可能归因于 宿主和肿瘤组织中的营养物质。而TPN可以保持或 改善宿主营养状况，消耗肿瘤营养素 可导致肿瘤进行性生长，导致早期宿主 正如一些调查人员所建议的那样死亡。尽管TPN- 最近还没有观察到诱导人类肿瘤生长的现象 有证据表明，TPN可能会刺激肿瘤生长。 因为多胺的生物合成是细胞所必需的 增殖，我们的发现是红细胞多胺增加 在接受TPN的癌症患者中出现的水平而不是在 接受类似治疗的非癌症患者建议肿瘤增强 成长。需要进一步的研究才能提供直接的证据 TPN诱导的RBC多胺增加与 肿瘤的生长速度明显加快。初步研究 已经表明，TPN在平台期刺激肿瘤生长 Gompertzian曲线的相位。对照研究是 有必要确定这种肿瘤生长增加是否 与红细胞多胺水平升高有关。多胺 生物合成途径可能是设计的一个重要焦点 选择性地将营养物质转移到宿主的治疗性制造商 组织和远离肿瘤细胞。假设是这样的 在TPN期间应用多胺抑制剂可能会抑制 肿瘤营养物质的利用，改善宿主营养。 二氟甲基鸟氨酸(DFMO)是一种特殊的不可逆性物质 鸟氨酸脱羧酶抑制剂及其对宿主肿瘤的影响 对营养素的竞争将进行研究。的具体目标 这项研究是为了确定TPN是否会产生显著的 红细胞多胺水平和肿瘤大小的增加 非指数增长阶段，b)以确定 在TPN期间管理DFMO可提高主机利用率 营养成分，同时抑制肿瘤生长，以及c)决定 DFMO联合细胞毒性化疗药物 将产生肿瘤消退，进一步提高宿主利用率 外源营养素。

A early hypothesis of nutritional therapy in cancer management was if host nutritional status could be maintained or improved, then host survival should also improve. Several clinical trials were designed to test this hypothesis and found that total parenteral nutrition (TPN) did not increase the survival of patients with various neoplastic diseases treated with systemic chemotherapy. The failure of aggressive nutritional therapy to improve patient survival may be attributed to the competition of host and tumor tissues for nutrients. While TPN can maintain or improve host nutritional status, tumor consumption of nutrients can result in progressive tumor growth, leading to early host demise as suggested by some investigators. Although TPN- induced tumor growth in man has not been observed, recent evidence suggests that TPN may stimulate tumor growth. Because polyamine biosynthesis is necessary for cell proliferation, our finding that increased erythrocyte polyamine levels appearing in cancer patients receiving TPN and not in noncancer patients treated similarly suggested enhanced tumor growth. Further studies are needed to provide direct evidence that TPN-induced increases of RBC polyamines are associated with measurable accelerated tumor growth. A preliminary study has shown that TPN stimulates tumor growth during the plateau phase of its Gompertzian curve. Controlled studies are necessary to determine if this increased tumor growth is associated with increased RBC polyamine levels. The polyamine biosynthetic pathways may be an important focus for designing therapeutic manuvers that selectively divert nutrients to host tissues and away from neoplastic cells. The hypothesis is that administration of polyamine inhibitors during TPN may inhibit tumor utilization of nutrients and improve host nutrition. Difluoromethylornithine (DFMO) is a specific irreversible inhibitor of ornithine decarboxylase and its effect on host-tumor competition for nutrients will be studied. The specific aims of this study are a) to determine if TPN will produce significant increases of RBC polyamine levels and tumor size during the nonexponential phase of growth, b) to determine if the administration of DFMO during TPN improves host utilization of nutrients while inhibiting tumor growth, and c) determine if DFMO in combination with cytotoxic chemotherapeutic agents will produce tumor regression further improving host utilization of exogenous nutrients.