防止手术引起肿瘤转移
史蒂芬Nemeroff ND在09/12/09 4:53 PM
癌症手术:你需要提前知道
绝大多数癌症治疗的基石,是原发肿瘤的手术切除。 这种做法的理由很简单:如果你可以通过简单地从它的身体摆脱癌症,治愈的可能可以实现。 不幸的是,这种方法不考虑癌症手术后会经常转移(扩散到不同的器官)。 经常转移复发是远远超过了原发肿瘤的严重。 事实上,在许多癌症的转移复发,而不是原发肿瘤,最终被证明是fatal.1
在一个令人震惊的讽刺,越来越多的科学证据显示癌症手术可增加的metastasis.2的风险,这将飞在面对传统医学思想,但事实是不可否认的。
以获得更好地了解如何能增加手术风险转移,让我们先来讨论癌症转移的实际过程。 一个复杂的事件序列必须为了在癌症的发生,蔓延到另一个隔离的body.2癌细胞脱离原发肿瘤的一部分,必须首先违反周围的结缔组织的癌症。 一旦癌细胞已打破周围的结缔组织,下一步就是进入血液或淋巴管。 这是说起来容易做起来难,作为进入血管的癌细胞分泌的酶降解基底膜进入血管血液vessel.3进入是非常重要的,有抱负的转移性肿瘤细胞,因为它使用了作为公路运送到人体的肝,脑,或肺部,它可以形成一个新的致命肿瘤等其他重要器官的血液。
现在,孤独的癌细胞终于进入了血液,它的问题只有刚刚开始。 血液内的旅行,可以是一个癌细胞的危险旅程。 从快速移动的血液湍流,可以损坏并摧毁癌细胞。 此外,肿瘤细胞必须避免从白血细胞在血液中循环的检测和销毁。
完成其航程,必须坚持流氓癌细胞血管衬里,它通过和退出的血管基底膜降解。 其最终任务是通过周围的结缔组织洞穴到达的器官,这是它的最终目的地。 现在癌细胞的繁殖和形成越来越多的殖民地,作为一个新的转移性肿瘤的基础。 时间正在对这些孤立的肿瘤细胞。 这一事件的整个序列必须很快发生,因为这些细胞有一个有限的生命span.1
我们现在看到的肿瘤转移是一个复杂而艰难的过程。 充满危险,很少有独立的癌细胞生存之本艰巨journey.2癌细胞的可能性尚存这次旅程,并形成新的转移可以通过增加任何服务,使这个过程更容易。
在外科医学杂志在2009年年报中公布了开创性的研究中,研究人员报告说,癌症手术本身可以创建一个在体内环境,大大减少了转移的障碍,癌症细胞必须正常face.2
仅仅是启示,癌症手术可产生转移的备用路由,绕过天然屏障有关。 在癌症手术,切除肿瘤几乎总是破坏肿瘤和/或喂养肿瘤的血管结构的完整性。 这可能会导致癌细胞的扩散到血液通畅,或直接到胸部或abdomen.4-7这种手术引起的“备用路由”这些癌细胞播种,可以大大简化转移的路径。
为了说明这一点,在“英国癌症杂志”上发表的一项研究在2001年相比有手术切除肿瘤,患有乳腺癌的妇女,谁没有接受手术的生存与乳腺癌妇女的生存。 正如所料,结果确定手术大大提高了早年的生存。
然而,进一步分析确定,谁动了手术的妇女有8年在穗死亡的风险,这不是明显在组谁没有在他们对结果的解释surgery.8数据,研究报告的作者指出:“一个合理的假说来解释观察到的模式的危害功能[癌症死亡的风险是假设...原发肿瘤切除,可能会导致突然加速转移过程中......”
另一组研究人员在研究结肠癌手术治疗的研究评论,大胆远在他们的结论:“这一发现有力地支持,手术改变疾病的自然过程在大部份的病人人口预期寿命拉长,但也同时缩短在一个较小的子集患者的生存。 因此,实验和临床证据支持手术,虽然大大降低了肿瘤的质量和潜在的治疗,矛盾也可以增加转移的发展。“
鉴于这些令人不安的调查结果,个人经历为他们的癌症手术可以做什么来保护自己,对转移的风险增加? 一个有价值的战略,将检查所有手术促进转移的机制,然后创建一个全面的计划,抵消每一个这些机制之一。
你需要知道:癌症手术
癌症手术切除,通常提供的无病生存的最佳机会。
•越来越多的证据表明,癌症手术本身可能通过许多机制,包括增加的风险转移(扩散到其他地区):增加粘附肿瘤细胞,抑制免疫功能,促进血管生成,并刺激炎症。
由于转移性疾病往往是致命的,比原发肿瘤,重要的是要利用预防战略,以防止癌细胞转移。
•有助于防止癌细胞转移的步骤包括:打击肿瘤细胞粘附,支持免疫系统的健康,加高免疫监视,抑制血管生成,减少炎症,选择医生和麻醉师,利用先进的技术,可降低转移风险。
某些营养物质,药品,麻醉的类型,和手术技巧与降低风险的转移。
手术增加癌症细胞粘附
利用附着力,以提高他们的能力,形成在远处器官转移手术,其中增加了风险转移的机制之一是通过提高肿瘤细胞adhesion.9癌症从原发肿瘤细胞。 这些癌细胞必须能够聚集在一起,形成菌落,可以扩大和发展。 这是不可能的,单一的癌细胞会形成转移性肿瘤,就像一个人是不可能形成一个繁荣的社区。 癌细胞使用粘附分子,如半乳糖凝集素3,以便他们能够聚集在一起。 目前对肿瘤细胞表面,galectin-3的表面粘附分子,这些分子的行为,允许独立的癌细胞坚持每个other.10癌症细胞的血液循环,如粘扣带使用含住血液衬vessels.11坚持循环肿瘤细胞(CTC)的血管壁为转移的过程中是必不可少的步骤。
滑下冰冷的山上,有一个人就像没有停止,如果他们不能抢上东西的希望,不能坚持到血管壁的癌细胞通过血液流无法形成转移只是将继续徘徊。 无法含住血管壁,这些循环肿瘤细胞变得像“没有一个港口的船舶无法停靠。 最终,白血细胞在血液中循环,将目标和破坏反恐委员会。 如果CTC成功绑定到血管壁挖洞他们的方式,并通过基底膜,然后他们将利用galectin-3的粘附分子,坚持机关形成一个新的转移性cancer.10
打击癌症细胞粘附
令人遗憾的是,研究表明,癌症手术提高肿瘤细胞的粘附。 在一项实验中,模拟手术的条件,科学家报告说,癌细胞血管壁的结合增加了250%,比不暴露手术conditions.12因此癌细胞,这是极为重要的接受癌症手术的人采取措施,可以帮助消除手术在癌症细胞粘附诱导增加。
改性柑橘果胶
幸运的是,一个自然的补充,被称为改良柑橘果胶(MCP)可以做到这一点。 柑橘果胶的膳食纤维不被吸收,从肠道。 然而,改良柑橘果胶已被改变,它可以吸收进入血液,并发挥其抗癌作用。 改性柑橘果胶的机制,抑制肿瘤细胞粘附galectin-3的癌细胞表面上粘附分子结合,从而阻止癌细胞粘在一起,形成1 cluster.13改性柑橘果胶还可以抑制肿瘤细胞从循环锁定到血管内壁。 这是由一个惊人的95%,其中改良柑橘果胶阻止血管内壁粘附galectin-3的实验证明。 改性柑橘果胶也大大降低乳腺癌细胞粘附血管walls.13
令人印象深刻的研究已经证明改性柑橘果胶的权力,直接抑制癌细胞的转移。 在全国癌症研究所杂志“发表的一项研究,改良柑橘果胶管理与前列腺癌细胞注入老鼠,而老鼠没有收到改性柑橘果胶作为对照组担任。 肺转移与会者指出,在对照组的93%,而只有50%的改性柑橘果胶组经验丰富的肺转移。 更值得注意的是发现,修改后的柑橘果胶组转移殖民地的大小减少89%,比控制在一个类似的实验group.14,饲喂改性柑橘果胶的黑色素瘤细胞注入老鼠经历在肺转移的减少大于90%相比,控制group.15
后,在动物研究这些激动人心的发现,改良柑橘果胶,然后把在男性前列腺癌的考验。 在这项试验中,10例复发性前列腺癌的男子接受改良柑橘果胶,每天(14.4克)。 一年后,在相当大的改善癌症进展注意到,所确定的前列腺特异抗原(PSA)水平increased.16这是研究中的削减率49不同,其罹患前列腺癌的男子类型改性柑橘果胶的四个星期的周期。 改性柑橘果胶的治疗周期后,22%的男性经历了他们的疾病或改善生活质量的稳定; 12%,有超过24周,病情稳定。 这项研究的作者得出结论:“(MCP改性柑橘果胶)似乎有积极影响,特别是关于远晚期实体瘤患者的临床受益和生活质量。”17
请记住,这些前列腺癌的研究对象已经从先进的疾病而痛苦。 它似乎更合乎逻辑的,如果这些患者手术前发起改性柑橘果胶的补充,以防止转移正在建立殖民地,是成功的实验室研究。
泰胃美(西咪替丁)和细胞粘附
在改性柑橘果胶,除了众所周知的过度的非处方药也可以减少肿瘤细胞粘附发挥了举足轻重的作用。 西咪替丁俗称为泰胃美®,是历史上用于缓解胃灼热的药物。 越来越多的科学证据表明,西咪替丁还具有强大的抗肿瘤活性。 西咪替丁抑制癌症细胞粘附阻断表达粘附分子所谓的E-选择排队血细胞表面上的vessels.15癌症细胞锁存E-选择上,为了防止血液vessels.18的衬坚持E-选择素的表达,西咪替丁大大限制了癌症细胞粘附到血管壁的能力。 这种效果是类似的清除血管壁,通常会启用循环肿瘤细胞绑定魔术贴。
2002年在“英国癌症杂志”上发表的一份报告中清楚地显示西咪替丁的强有力的抗癌作用。 在这项研究中,或不西咪替丁(每天800毫克)64结肠癌患者接受化疗一年。 西咪替丁组10年生存率近90%。 这是形成鲜明对比的对照组,其中有10年生存率仅为49.8%。 值得注意的是,对于那些更积极的形式与结肠癌患者,10年生存率为85%,与西咪替丁治疗者相比,一个令人沮丧的23%,在控制group.19这项研究的作者得出结论,“两者合计,这些结果,大概是通过阻断E-选择素的表达血管细胞和血管内皮抑制癌细胞粘附血管[衬里]建议西咪替丁对大肠癌患者的有益作用的机制。“这些研究结果支持由另一个研究大肠癌患者,其中20西咪替丁增加短短七天的手术时间定在3年生存率从59%到93%!
这些数据提供了一个引人注目的情况下,为癌症病人,在手术前至少5天,每天摄取至少14克的改良柑橘果胶和西咪替丁800毫克。 这种组合方案,可随后一年或更长的时间,以减少转移风险。
防止手术诱发的免疫抑制
免疫系统在对抗癌症方面发挥的重要作用不能被夸大了。 虽然有许多方面,发挥抗癌免疫系统,自然杀伤细胞的作用占主导地位。 自然杀伤(NK)细胞是一种白血细胞,负责寻找和摧毁癌细胞。 有研究表明NK细胞可以自发地识别和杀死多种癌症cells.21
自然杀伤细胞(NK)活性和癌症
为了说明抗癌作用的NK细胞活性的重要性,一项研究发表在杂志乳腺癌研究和治疗研究乳腺癌手术后不久,女性NK细胞活性。 研究人员报告说,与死亡从乳房cancer.22增加风险水平较低的NK细胞活性,事实上,NK细胞活性降低是一个更好的生存预测比实际的癌症阶段。 在另一个令人震惊的研究中,NK细胞活性降低结肠癌手术前的个人有在以下31个月内增加350%的转移风险!23
手术诱导转移的可能性,需要免疫系统是非常活跃,在寻找和摧毁癌细胞在围术期(手术前和手术后的时间立即)叛徒警惕。 可悲的是,许多研究已经证明,在7,24,25 NK细胞activity.6的,在一个不祥的影响,乳腺癌手术的妇女NK细胞活性,减少50%以上的调查大幅减少癌症手术结果后surgery.24第一天,在这越来越多的证据表明,一组研究人员说:“因此,我们认为,手术后不久,甚至短暂的免疫功能紊乱,可能会允许肿瘤[癌症]进入下一阶段的发展,并最终形成可观转移。“
手术本身可降低NK细胞活性。 这NK细胞的损害作用,手术后立即发生,不可能发生在一个更坏的可能的时间。 NK细胞活性减慢,当它最需要的战斗转移。 手术诱导增加NK细胞活性降低转移风险相结合,可以接受癌症手术的人带来灾难性的后果。 随着中说,围术期提出了一个机会,积极加强免疫功能,增强NK细胞活性的窗口。 幸运的是,众多的保健品,制药,医疗干预措施,增强NK细胞活性的接受癌症手术的人。
PSK的提高NK细胞活性
一个突出的自然补充,可以提高NK细胞活性的PSK,(蛋白结合多糖K)特意准备了一个蘑菇云芝提取。 云芝已经证明,以加强在多个studies.26-29云芝的能力,增强NK细胞活性,NK细胞活性有助于解释为什么它已被证明大大提高癌症患者的生存。 例如,225例肺癌患者接受放射治疗或不PSK(每天3克)。 对于那些更先进的第三阶段癌症,超过3次服用云芝的许多个人活着,五年后(26%)相比,那些不服用PSK(8%)。 PSK的一倍以上五年在这些人的生存与欠发达阶段1或2疾病(39%vs.17%).30
A组的结肠癌患者随机接受单纯化疗或化疗加云芝,这是两年。 接收云芝组有特殊的10年生存率为82%。 可悲的是,组单独接受化疗的10年生存率只有51%,0.31在2004年的“英国癌症杂志”报道,在一个类似的试验,结肠癌患者接受化疗单独或结合云芝(每天3克)两年。 在一个更加危险的第三阶段结肠癌组,5年生存率为75%的PSK组。 这相比,到接收组化疗alone.32研究中只有46%的5年生存率已证实云芝也提高了乳房癌的生存,胃癌,食道癌,并uterus.33-36
保健品,中草药和药品,提高NK细胞活性
已被记录在案,以提高NK细胞活性的其他营养品大蒜,谷氨酰胺,IP6(肌醇六磷酸),AHCC(主动己糖相关化合物),lactoferrin.37-41发现与乳腺癌癌症的小鼠实验,在谷氨酰胺搭配40%的跌幅在肿瘤的生长在NK细胞activity.40增加2.5倍
德国科学家研究槲寄生提取物的影响,在62个接受结肠癌手术患者的NK细胞活性。 参加者立即随机接受静脉滴注槲寄生提取物,然后再给予全身麻醉,或单独给予全身麻醉。 NK细胞活性测定前和手术后24小时。 正如所料,没有收到槲寄生组手术后24小时内经历了在NK细胞活性降低44%。 有趣的是,科学家报告说,该集团接收槲寄生没有经历过手术后NK细胞活性显着下降。 他们去到结束,“槲寄生提取物的围术期输液可以预防癌症患者的NK细胞活性的抑制。”42
用于提高NK细胞活性的药品,包括α-干扰素和粒细胞 - 巨噬细胞集落刺激因子。 可能是这些药物被证明,以防止手术引起免疫抑制时给予perioperatively.43另一个考虑在围术期的免疫增强药物,44白细胞介素2.45
在手术前至少5天,就出现逻辑,以制定一个自然杀伤(NK)细胞增强计划涉及如PSK,乳铁蛋白,谷氨酰胺,和其他营养物质。 如白细胞介素-2和粒细胞 - 巨噬细胞集落刺激因子药物在美国批准,但医疗保险通常不包括他们的围术期的目的在这里建议。 要接收免费索取这些营养物质和药物剂量的最新建议,请致电1-800-841-5433或登录到我们的肿瘤外科的特别报告。
加高癌症疫苗的免疫监视
一个开明的治疗癌症的医疗方法,包括使用的癌症疫苗。 这个概念是使用传染病的疫苗,肿瘤疫苗的目标,而不是一个病毒的癌细胞,除外。 肿瘤疫苗的另一个显着特点是,创建从一个普通的病毒,而病毒疫苗,肿瘤疫苗是自体,也就是说,他们从自己一个人的癌症细胞在手术切除。 这是一个关键的区别,因为不可能有癌症之间的相当大的遗传差异。 这种高度个性化的癌症疫苗,极大地放大的识别和针对任何残留的癌细胞在体内的免疫系统能力。 癌症疫苗提供了具体的识别标记,然后可以被用来发动针对转移性肿瘤细胞的攻击成功的癌症的免疫系统。
自体肿瘤疫苗已被广泛研究,随机,对照临床试验,其中包括1300多名大肠癌患者在手术后的肿瘤疫苗中指出,最令人鼓舞的成果。 这些试验的报道,降低复发率和改善survival.46不同于化疗,这可能会导致严重的副作用和毒性,癌症疫苗是一个成熟的长短期safety.47温柔疗法
在2003年报道了里程碑式的研究,与结肠癌的567个人随机接受单纯手术治疗,或手术结合来自自己的癌细胞的疫苗。 癌症疫苗组的平均存活时间为7年以上,比接受单纯手术组的中位生存期为4.5年。 在癌症疫苗组的5年生存率为66.5%,其中所绘的45.6%,五年生存率为接受手术治疗五年生存率明显的差异alone.48这清楚地显示单独定制的癌症疫苗的力量组极大地关注人的自身免疫力,目标和攻击残余癌细胞转移。
肿瘤外科,血管生成和转移
癌症雇用聪明的策略在寻求增长和身体内蓬勃发展。 血管新生是从预先存在的血管形成新血管的过程。 新血管的形成,是为儿童的成长和发展正常的和必要的过程,以及伤口愈合。 不幸的是,癌症劫持这原本正常的过程,以提高对肿瘤的血液供应。 新的血液供应肿瘤的血管的形成是一个成功的转移,因为肿瘤不能生长超出了一个针头大小(即,为1-2mm)的绝对要求不扩大自己的鲜血supply.49,50
抗血管生成因子
这可能是令人惊讶的学习旨在抑制转移性肿瘤的生长,身体其他部位的原发肿瘤的存在。 原发肿瘤产生抗血管生成的因素限制增长metastases.51-54这些抗血管生成的因素,抑制新生血管形成的转移潜能的网站。 令人遗憾的是,手术切除原发癌,也导致在去除这些抗血管生成的因素,并转移的增长已不再是抑制。 随着这些限制的取消,现在是为转移癌的小网站更容易吸引新的血管,促进其growth.55事实上,这些问题的研究人员表示他宣布说:“......切除原发肿瘤可能消除对血管生成的保障从而唤醒休眠微[转移癌的小网站。“7
作为原发肿瘤的血管生成抑制的损失,如果没有足够的问题,事实证明手术导致另一种血管新生的困境。 手术后,血管生成又称血管内皮生长因子(VEGF)显着升高,增加的因素水平。 这可能会导致增加一个新的供血的血管转移癌领域形成。 一个科学家小组总结本研究相当好时,他们声称,“手术后,亲和血管生成抑制因子血管的平衡,有利于血管生成转移到促进伤口愈合。 特别是血管内皮生长因子(VEGF)的水平持续升高。 这不仅有利于肿瘤的复发和转移性疾病的形成,也导致激活处于休眠状态的微。“
养分,抑制血管内皮生长因子
鉴于转移性肿瘤的血液供应扩大的需要,抑制血管生成的肯定是一项全面战略,以打击手术,诱导转移的一个组成部分。 为此,各种营养成分已被证明能抑制血管内皮生长因子。 这些措施包括大豆异黄酮(染料木素),水飞蓟宾(水飞蓟的一个组成部分),白杨,从绿茶中的儿茶素酸酯(EGCG),和curcumin.56-62
In one experiment, EGCG—the active constituent of green tea —was administered to mice with stomach cancer. The results demonstrated that EGCG reduced the tumor mass by 60%, while also reducing the concentration of blood vessels feeding the tumor by 38%. Remarkably, EGCG decreased the expression of VEGF in cancer cells by an astounding 80%! The authors of the study concluded “EGCG inhibits the growth of gastric cancer by reducing VEGF production and angiogenesis, and is a promising candidate for anti-angiogenic treatment of gastric cancer.”56
In the evaluation of the research pertaining to curcumin’s anti-angiogenic effects, researchers at Emory University School of Medicine noted that “Curcumin is a direct inhibitor of angiogenesis and also downregulates various proangiogenic proteins like vascular endothelial growth factor…” Additionally, the scientists remarked, “Cell adhesion molecules are upregulated in active angiogenesis and curcumin can block this effect, adding further dimensions to curcumin's antiangiogenic effect.” In conclusion, they commented that “Curcumin's effect on the overall process of angiogenesis compounds its enormous potential as an antiangiogenic drug.”44
Five days prior to surgery, the patient may consider supplementing with standardized green tea extract, curcumin, soy genistein extract and other nutrients that suppress VEGF and thus may help protect against angiogenesis. To receive a free copy of the latest dosing recommendations for these nutrients, call 1-800-841-5433 or log on to the Life Extension Foundation's Cancer Surgery Special Report: http://www.lef.org/featured-articles/Cancer-Surgery-Special-Report.htm
The Choice of Surgical Anesthesia Can Influence Metastasis
The conventional medical approach to surgical anesthesia has been the use of general anesthesia during surgery, followed by intravenous morphine after surgery for pain control. The conventional approach, however, may not be the optimal approach for preventing surgery-induced metastasis. The use of morphine directly after surgery poses significant problems. At a time when immune function is already suppressed, morphine further weakens the immune system by diminishing NK cell activity.63
Surgical anesthesia has also been shown to weaken NK cell activity.64 One study found that morphine increased angiogenesis and stimulated the growth of breast cancer in mice. The researchers concluded: “These results indicate that clinical use of morphine could potentially be harmful in patients with angiogenesis-dependent cancers.”65
Regional Anesthesia and Pain Control
Given the inherent problems associated with the use of morphine and anesthesia, researchers have explored other approaches to surgical anesthesia and pain control. One novel approach is the use of conventional general anesthesia combined with regional anesthesia, which refers to anesthesia that only affects a specific part of the body. The benefits achieved with this approach are two-fold: the use of regional anesthesia reduces the amount of general anesthesia required during surgery, as well as decreasing the amount of morphine needed after surgery for pain control.55
This elegant approach to surgical anesthesia and pain control has been validated in scientific studies. In one experiment, cancerous mice received surgery with general anesthesia alone or combined with regional anesthesia. The scientists reported that the addition of regional anesthesia to general anesthesia “markedly attenuates the promotion of metastasis by surgery.” Regional anesthesia reduced 70% of the metastasis-promoting effects of surgery caused by general anesthesia alone.66
美国宾夕法尼亚州立大学医学院的医生在接受全身或局部麻醉腹部手术的患者相比,NK细胞活性。 NK细胞活性大幅下降,在全身麻醉组,而NK细胞活性的保存组收到区域anesthesia.67大厦后,这些令人鼓舞的结果在手术前的水平,然后,研究人员探索区域麻醉会影响手术的妇女的转移乳腺癌。 在一个开创性的研究,50名妇女乳房癌手术全身麻醉与局部麻醉相结合吗啡控制疼痛的乳腺癌手术全身麻醉期间收到的79名妇女进行了比较。 区域用于麻醉的类型被称为椎旁阻滞,其中包括脊柱椎体骨骼之间的脊神经周围注射局部麻醉。 经过近三年的随访期间,戏剧性的差异,指出两组之间。 只有6%的患者接受局部麻醉经历了复发,到24%的风险转移复发组中未接受局部麻醉。 换句话说,区域和全身麻醉的妇女有75%为转移性癌的风险降低。 这些发现使研究人员宣布为乳腺癌手术,局部麻醉,在手术后的最初几年中显着降低复发或转移的风险。“55
在杜克大学医学中心的医生相比,仅局部麻醉在乳腺癌手术的妇女的全身麻醉。 外科医生,而39%的恶心,呕吐,全身麻醉组所需的药物,局部麻醉组只有20%需要这种药物。 麻醉药物,手术后疼痛控制需要在全身麻醉组的98%相比,只有25%的区域麻醉组。 和96%的妇女接受局部麻醉,回国后在一天内手术相比,有76%的妇女接受全身麻醉。 外科医生的结论是,可用于减少恶心,呕吐,手术疼痛,椎旁阻滞[局部麻醉局部麻醉“执行的主要业务为乳腺癌并发症少......最重要的是,显着提高了患者术后恢复质量谁治疗乳腺癌,因此提供了选择的病人,手术后回家早需要返回。“68
这些研究的结果有极大的影响,为那些接受癌症手术,一组研究人员热情地宣布:“由于[麻醉]区域技术很容易实现,价格低廉,不构成威胁大于全身麻醉,将很容易麻醉师实施,从而减少疾病的复发和转移的风险。“55
最后,那些手术后疼痛控制的要求吗啡可以考虑要求他们的医生,一个叫曲马多,而不是药物。 Unlike morphine, tramadol does not suppress immune function.69 On the contrary, tramadol has been shown to stimulate NK cell activity. In one experiment, tramadol blocked the formation of lung metastasis induced by surgery in rats. Tramadol also prevented the surgery-induced suppression of NK cell activity.70
Less Invasive Surgery Reduces Risk of Metastasis
Surgery places an enormous physical stress upon the body. There is considerable scientific evidence supporting that surgeries that are less invasive—and therefore less traumatic—pose less risk of metastasis, compared to more invasive and traumatic surgery. Laparoscopic surgery is one type of minimally invasive surgery, in which operations in the abdomen, pelvis, and other regions are performed through small incisions, as compared to the much larger incisions needed in traditional “open” surgeries.
A study published in the prestigious medical journal The Lancet compared laparoscopic to open surgery to remove part of the colon (colectomy) in patients with colon cancer. In contrast to the group receiving traditional open surgery, the laparoscopic surgery group had a 61% decreased risk of cancer recurrence coupled with a 62% decreased risk of death from colon cancer. The surgeons concluded that laparoscopic colectomy is more effective than open colectomy for treatment of colon cancer as assessed by tumor recurrence and cancer-related survival.71 A long-term follow-up of these patients (median time 95 months) reported a 56% decreased risk of death from colon cancer for laparoscopic surgery as compared to traditional open surgery.72 Another comparison of laparoscopic surgery to open surgery for colon cancer reported a five-year survival rate of 64.1% for the laparoscopic group, and a five-year survival rate of 58.5% for the group receiving open surgery.73
Minimally invasive surgery has produced substantial improvements in survival for those with lung cancer. Video-assisted thoracoscopic surgery (VATS), a minimally invasive surgery, was compared to traditional open surgery for removing lung tumors (lobectomy). The five-year survival from lung cancer was 97% in the VATS group. This greatly contrasts the 79% five-year survival in the open surgery group.74
Commenting on the use of minimally invasive surgery for lung cancer, surgeons at Cedars-Sinai Medical Center stated that minimally invasive surgery for lung cancer “… can be performed safely with proven advantages over conventional thoracotomy [chest surgery] for lobectomy: smaller incisions, decreased postoperative pain,…decreased blood loss, better preservation of pulmonary function, and earlier return to normal activities… the evidence in the literature is mounting that VATS may offer reduced rates of complications and better survival.”75
管理术前化疗和放射疗法
在北卡罗莱纳州大学医学院的医生研究使用联合放疗和化疗手术前个人与食管癌。 第二十六条患者接受单纯手术,而30名患者接受放疗和化疗手术。 接受联合治疗组有39%的5年生存率,而单纯手术治疗组经历了5年生存率只有16%,0.99
一项研究发表在新英格兰医学杂志在2006年与手术治疗的治疗与直接前和手术后在胃或食道癌患者化疗。 接受了手术和化疗组的5年生存率为36%,而23%的五年组的生存接受手术alone.100的
研究还支持使用在关键的围手术期化疗和放射治疗。 在一项研究中,544例胃癌患者接受手术后不久,联合化疗和放射治疗。 生存进行了比较类似的446名胃癌患者的手术治疗组。 术后化疗和放疗在生存的显着改善。 单独手术治疗组的中位生存期仅为62.6个月,比在接受术后放疗和chemotherapy.101组的平均存活了95.3个月与术后放疗和化疗相比,使用了类似的研究还表明改善生存手术alone.102
炎症和转移
Cancer surgery causes an increased production of inflammatory chemicals, such as interleukin-1 and interleukin-6.76-78 These chemicals are known to increase the activity of cyclooxygenase-2 (COX-2). A highly potent inflammatory enzyme, COX-2 plays a pivotal role in promoting cancer growth and metastasis.
This was evident in an article appearing in the journal Cancer Research that found levels of COX-2 in pancreatic cancer cells to be 60 times greater than in normal pancreatic cells.79 Levels of COX-2 were 150 times higher in cancer cells from individuals with head and neck cancers compared to normal tissue from healthy volunteers.80 COX-2 fuels cancer growth by stimulating the formation of new blood vessels feeding the tumor.81,82 COX-2 increases cancer cell adhesion to the blood vessel walls,83 and also enhances the ability of cancer cells to metastasize. Experiments in mice revealed that colon cancer cells expressing high levels of COX-2 metastasized freely to the liver, while colon cancer cells expressing low levels of COX-2 did not metastasize to the liver.83
The adverse influence of COX-2 on the growth and progression of cancer was clearly revealed in a study published in the journal Clinical Cancer Research in 2004. Two hundred eighty-eight individuals undergoing surgery for colon cancer had their tumors examined for the presence of COX-2. The findings were alarming—when other factors were controlled for, the group whose cancers tested positive for the presence of COX-2 had a 311% greater risk of death compared to the group whose cancers did not express COX-2.84 A subsequent study in lung cancer patients found that those with high tumor levels of COX-2 had a median survival of only 15 months, whereas those with low tumor levels of COX-2 had a median survival of 40 months.85
Given these findings, researchers began investigating the anti-cancer effects of COX-2 inhibitor drugs. Although initially used for inflammatory conditions, such as arthritis, COX-2 inhibitor drugs have been shown to possess powerful anti-cancer activity. For example, 134 patients with advanced lung cancer were treated with chemotherapy alone or combined with Celebrex® (a COX-2 inhibitor). For those individuals with cancers expressing higher amounts of COX-2, treatment with Celebrex® dramatically prolonged survival.86 Treatment with Celebrex® also slowed cancer progression in men with recurrent prostate cancer.87
Perhaps the most impressive display of the anti-metastatic effects of COX-2 inhibitor drugs was presented at the annual conference of the American Society of Clinical Oncology in 2008. In this study, the incidence of bone metastases in breast cancer patients who had taken a COX-2 inhibitor for at least six months following the diagnosis of breast cancer was compared to the incidence of bone metastases in breast cancer patients who had not taken a COX-2 inhibitor. Remarkably, those who were treated with a COX-2 inhibitor were almost 80% less likely to develop bone metastases than those who were not treated with a COX-2 inhibitor drug.88
Non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen, are COX inhibitors. The widespread use of NSAIDs for pain and arthritis has created an ideal environment in which to examine if these drugs can prevent cancer. Large-scale studies have documented a substantial reduction in cancer risk with the use of NSAIDs. A comprehensive review of the scientific literature (91 published studies) reported that the long-term use of NSAIDs (primarily aspirin) produced risk reductions of 63% for colon cancer, 39% for breast cancer, 36% for lung cancer, 39% for prostate cancer, 73% for esophageal cancer, 62% for stomach cancer, and 47% for ovarian cancer. “This review provides compelling… evidence that regular intake of NSAIDs that… block COX-2 protects against the development of many types of cancer,” the authors concluded.89
A number of nutritional and herbal supplements are known to inhibit COX-2. These include curcumin, resveratrol, vitamin E, soy isoflavones (genistein), green tea (EGCG), quercetin, fish oil, garlic, feverfew, and silymarin (milk thistle).58,90-97
Scientists at Memorial Sloan-Kettering Cancer Center in New York created an experimentally-induced increase in COX-2 activity in human breast cells, which was completely prevented by resveratrol. Resveratol blocked the production of COX-2 within the cell, as well as blocking COX-2 enzyme activity.98
结论
A group of noted experts in the field of surgery-induced metastasis stated that cancer treatment “…necessitates the surgical excision of the primary tumor in order to relieve the patient of the major tumor burden, which is the main source of mutating and metastasizing cells. However, along with its obvious benefits, the surgical procedure has been suggested to involve serious hazards as it releases tumor cells into the circulation or lymphatics, promotes the secretion of angiogenic and growth factors, and induces suppression of CMI [immune function]. These consequences synergistically facilitate the establishment of new metastases and the development of preexisting micrometastases. As cancer-related death is most commonly the result of metastatic disease, it is crucial to minimize this facilitation.”55
Remarking further, they commented that “Taken together, it is evident that the perioperative period harbors many risks; however, it is also the ideal time for battling MRD [small numbers of cancer cells remaining after surgery] to reduce recurrence and future metastases.” Thus, these scientists believe “…it is essential to employ preventative interventions during this critical time.” Additionally, they urge that, “Ideally, each problematic aspect of surgery should be treated when oncological patients undergo resection [surgery] in order to minimize recurrence and metastatic spread.”55
Armed with the knowledge discussed in this article, the person with cancer can reap all the benefits that cancer surgery offers, while simultaneously avoiding the metastatic perils imposed by this procedure.
As this article was going to press, a dedicated team of clinical oncologists and researchers are preparing a meticulous report on the optimal doses of nutrients and drugs that a cancer patient should consider during the pre- and post-operative period. You can obtain a free copy of this report by logging on to our Cancer Surgery Special Report — http://www.lef.org/featured-articles/Cancer-Surgery-Special-Report.htm — or calling 1-800-841-5433.
If you have any question on the scientific content of this article, please call a Life Extension® Health Advisor at 1-866-864-3027.
参考文献
1。 J Surg Oncol. 2006 Jul 1;94(1):68-80.
2。 安例。 2009 May;249(5):727-34.
3。 Cancer Metastasis Rev. 2004 Jan;23(1-2):119-35.
4。 Brain Behav Immun. 2003 Feb;17 Suppl 1S27-S36.
5。 安例。 2000 Jul;232(1):58-65.
6。 Surgery. 1998 Sep;124(3):516-25.
7。 Ann Surg Oncol. 2003 Oct;10(8):972-92.
8。 Br J Cancer. 2001 Aug 17;85(4):490-2.
9。 J Surg Res. 2002 Sep;107(1):1-6.
10。 Cancer Metastasis Rev. 1987;6(3):433-52.
11。 J Biol Chem. 2007 Jan 5;282(1):773-81.
12。 Int J Cancer. 2004 Dec 20;112(6):943-50.
13。 J Natl Cancer Inst. 2002 Dec 18;94(24):1854-62.
14。 J Natl Cancer Inst. 1995 Mar 1;87(5):348-53.
15。 J Natl Cancer Inst. 1992 Mar 18;84(6):438-42.
16。 Prostate Cancer Prostatic Dis. 2003;6(4):301-4.
17。 Clin Med Oncol. 2007;1:73–80.
18。 癌症水库。 2008 Jul 1;68(13):5167-76.
19。 Br J Cancer. 2002 Jan 21;86(2):161-7.
20。 Lancet. 1994 Dec 24;344(8939-8940):1768-9.
21。 科学。 1981 Oct 2;214(4516):24-30.
22。 Breast Cancer Res Treat. 2000 Apr;60(3):227-34.
23。 Int Surg. 1997 Apr;82(2):190-3.
24。 Br J Surg. 1993 Aug;80(8):1005-7.
25。 Brain Behav Immun. 2007 May;21(4):395-408.
26。 Oncol Rep. 2006 Apr;15(4):861-8.
27。 Anticancer Res. 2002 May;22(3):1737-54.
28。 Cancer Immunol Immunother. 2001 Jun;50(4):191-8.
29。 Int J Clin Lab Res. 1999;29(4):135-40.
30。 Cancer Detect Prev. 1997;21(1):71-7.
31。 Cancer Biother Radiopharm. 2008 Aug;23(4):461-7.
32。 Br J Cancer. 2004 Mar 8;90(5):1003-10.
33。 Gan No Rinsho. 1986 Feb;32(2):181-5.
34。 Lancet. 1994 May 7;343(8906):1122-6.
35。 Gan To Kagaku Ryoho. 1988 Nov;15(11):3143-51.
36。 Cancer. 1992 Nov 15;70(10):2475-83.
37。 J Nutr. 2006 Mar;136(3 Suppl):816S-820S.
38。 癌变。 1989 Sep;10(9):1595-8.
39。 J Interferon Cytokine Res. 2006 Jul;26(7):489-99.
40。 J Surg Res. 1996 Jun;63(1):293-7.
41。 J Hepatol. 2002 Jul;37(1):78-86.
42。 Forsch Komplementmed. 2007 Feb;14(1):9-17.
43。 Br J Surg. 2001 Apr;88(4):539-44.
44。 Adv Exp Med Biol. 2007;595:185-95.
45。 Hepatogastroenterology. 2002 Mar-Apr;49(44):385-7.
46。 Ann Oncol. 2005 Jun;16(6):847-62.
47。 Adv Cancer Res. 2006;95:147-202.
48。 World J Gastroenterol. 2003 Mar;9(3):495-8.
49。 Ribatti D. History of Research on Tumor Angiogenesis. Springer;2009:9.
50。 Neuro Oncol. 2005 Apr;7(2):106-21.
51。 Eur J Cancer. 2005 Mar;41(4):508-15.
52。 Curr Mol Med. 2003 Nov;3(7):643-51.
53。 Ann Chir Plast Esthet. 2000 Aug;45(4):485-93.
54。 Presse Med. 1998 Jul 4-11;27(24):1221-4.
55。 Breast Dis. 2006;26:99-114.
56。 World J Gastroenterol. 2007 Feb 28;13(8):1162-9.
57。 Clin Hemorheol Microcirc. 2006;34(1-2):109-15.
58。 Gut. 2008 Nov;57(11):1509-17.
59。 J Nutr Biochem. 2007 Jun;18(6):408-17.
60。 Cancer. 2004 Jan 1;100(1):201-10.
61。 Planta Med. 2006 Jun;72(8):708-14.
62。 J Surg Res. 2003 Jul;113(1):133-8.
63。 Am J Ther. 2004 Sep;11(5):354-65.
64。 Anesth Analg. 2003 Nov;97(5):1331-9.
65。 癌症水库。 2002 Aug 1;62(15):4491-8.
66。 Anesthesiology. 2001 Jun;94(6):1066-73.
67。 Am J Surg. 1996 Jan;171(1):68-72.
68。 安例。 1998 Apr;227(4):496-501.
69。 J Huazhong Univ Sci Technolog Med Sci. 2006;26(4):478-81.
70。 J Neuroimmunol. 2002 Aug;129(1-2):18-24.
71。 Lancet. 2002 Jun 29;359(9325):2224-9.
72。 安例。 2008 Jul;248(1):1-7.
73。 Arch Surg. 2008 Sep;143(9):832-9.
74。 中华胸心血管外科杂志。 2000 Nov;70(5):1644-6.
75。 Thorac Surg Clin. 2007 May;17(2):223-31.
76。 Br J Surg. 1992 Aug;79(8):757-60.
77。 Dis Colon Rectum. 2003 Feb;46(2):147-55.
78。 Cytokine. 2003 Dec 21;24(6):237-43.
79。 癌症水库。 1999 Mar 1;59(5):987-90.
80。 癌症水库。 1999 Mar 1;59(5):991-4.
81。 Cell. 1998 May 29;93(5):705-16.
82。 Mol Cancer Ther. 2003 Jan;2(1):1-7.
83。 癌症水库。 2002 Mar 1;62(5):1567-72.
84。 Clin Cancer Res. 2004 Dec 15;10(24):8465-71.
85。 Int J Cancer. 2005 Jul 1;115(4):545-55.
86。 J Clin Oncol. 2008 Feb 20;26(6):848-55.
87。 Clin Cancer Res. 2006 Apr 1;12(7 Pt 1):2172-7.
88。 http://www.asco.org/ASCOv2/Meetings/Abstracts?&vmview=abst_detail_view&confID=55&abstractID=31561.
89。 Oncol Rep. 2005 Apr;13(4):559-83.
90。 Mol Carcinog. 2006 May;45(5):309-19.
91。 Ann NY Acad Sci. 1999;889:214-23.
92。 J Biol Chem. 1998 Aug 21;273(34):21875-82.
93。 癌变。 2007 Apr;28(4):809-15.
94。 Mutat Res. 2004 Jul 13;551(1-2):245-54.
95。 Biochem Biophys Res Commun. 1996 Sep 24;226(3):810-8.
96。 Prostaglandins Leukot Essent Fatty Acids. 1995 Dec;53(6):397-400.
97。 Mol Cell Biochem. 2008 Jun;313(1-2):53-61.
98。 J Biol Chem. 1998 Aug 21;273(34):21875-82.
99。 J Clin Oncol. 2008 Mar 1;26(7):1086-92.
100。 N Engl J Med. 2006 Jul 6;355(1):11-20.
101。 Int J Radiat Oncol Biol Phys. 2005 Dec 1;63(5):1279-85.
102。 N Engl J Med. 2001 Sep 6;345(10):725-30.
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Jacqui Salazar
Oct 31st, 2010
I was interested in the posting from Peter McLellan, but disappointed that he mentioned that it would be less financially beneficial for the doctor and the hospital if regional anesthesia was used as opposed to general anesthesia (much more common and more accepted). Why not actually inform patients about the differences and allow them to make the decision without having the added pressure of having to think about how much “dosh” they were goiing to make out of any operation. This is obviously how most Dr's think and why we dont have a much better outcome after surgery in general.
Jacqui
丹尼斯
Dec 16th, 2009
This was all very interesting but now I am left trying to establish how the use of low dose naltrexone might factor into some of these curative measures; it certainly seems to have some significant anti-cancer properties! Any comment on this would be much appreciated particularly as my wife is now established on her maintenace dose of ldn as a preventative supplement because she is genetically predisposed to increased risk of cancer.
Peter MacLellan
Dec 15th, 2009
这篇文章是非常有趣和令人兴奋的。 Work on the impact of anesthesia on the immune system has been done, in my direct knowledge, since the 1980′s, and necessarily depended on new details on how the immune system functions. As an anesthesiologist, my role has been one of enabling, but it is now apparent that it can also be therapeutic. There is increasing evidence that the choice of anesthetic can affect long term outcome for the patient receiving the anesthetic, because of the effect of anesthetic agents on the immune system.
It may be reassuring for patients to know that this information is not only in the anesthesia literature, some of which is documented in the article, but also in Continuing Medical Education material from the American Society of Anesthesiologists. However given the long-time perception of anesthesia in the eyes of both the public and the profession as merely a means to enable surgery to take place with no or minimal pain and suffering, and also given the “production pressures” in operating rooms, there may be considerable resistance to increasing the use of regional anesthesia. Regional anesthesia tends to take longer than general anesthesia and will therefore decrease the number of cases that can be done, therefore reducing income for both the anesthesia practitioner and the institution. This is a significant barrier to overcome.
There are also 2 significant references missing from the article which describe the possible beneficial effects on outcome of epidural anesthesia for prostate cancer surgery, and of paravertebral block for major breast cancer surgery:
Biki B, Mascha E, Moriarity DC, et al. Anesthetic technique for radical prostatectomy surgery affects cancer recurrence: A retrospective analysis. Anesthesiology. 2008; 109:180-187.
Exadaktylos AK, Buggy DJ, Moriarty DC, Mascha E, Sessler DI: Can anesthetic technique for primary breast cancer surgery affect recurrence or metastasis? Anesthesiology 2006; 4:660-4
Both of these papers are retrospective, and therefore should be viewed as not definitive, but the information is very dramatic.
Epidural anesthesia is fairly widely accepted as a modality for post-operative pain relief after radical prostatectomy, so request for it is more likely to be entertained. Paravertebral block for mastectomy is less likely to be available since most anesthesiologists do not know this technique (myself included.)
Other factors to consider are the use of propofol infusion instead of a volatile agent (gas), since volatile agents seem to have anti-analgesic properties and lead to more post-operative narcotic use, and narcotics have immune suppression effects, inhibiting both cellular and humoral immune function in humans. There is also a small study from Mount Sinai Hospital in Toronto which showed that eating a ground flax containing muffin for several weeks before breast surgery reduced tumor size (no risk – possible benefit). And of course Vitamin D3 deficiency is widespread, is easily avoided and/or corrected (10,000 units per day clearly safe over a 6 months period, therefore could easily and safely be done pre-operatively) and its correction in the wider community will prevent breast cancer occurence in some patients, which in the final analysis is the best way to avoid recurrence – prevent the disease completely.
德博拉
Dec 13th, 2009
Thank you for this article. I had surgery for breast cancer 1 1/2 years ago. I wish my doctor had given me this kind of information. I did know some of the things you mentioned from the reading that I do and i took Modified Citrus Pectin before and after my surgery.
I also take curcumin, vitamin E, green tea (EGCG), quercetin, fish oil, garlic, Maitake D, and Avemar.
How long do you recommend taking Modified Citrus Pectin after surgery?
谢谢你,
德博拉
Catherine L. Pearson
Dec 12th, 2009
Thank you so much for this new info. Both my mother and sister have had breast cancer. My sister twice. They both were in their mid 40′s. I am 64, so far cancer free. I have used natural progesterone cream since menopause, try to eat healthy foods, plus use the important supplements.
I will bookmark this study, and also share info with my family and friends.
-Cathie