胶质瘤增殖活性和肿瘤基因蛋白表达及其意义

目的探讨胶质瘤增殖活性和肿瘤基因蛋白表达与分化和预后间的关系。方法应用免疫组化和图像分析技术对１２４例脑胶质瘤增殖细胞核抗原（ＰＣＮＡ）和几种肿瘤基因蛋白进行定性、定量研究。结果ＰＣＮＡ反应强度与级别和预后显著相关;ｃ－ｅｒｂＢ－２蛋白表达在分化程度高的胶质瘤强于分化程度低者,存活５年以上的病例阳性强于存活５年以下者。ＥＧＦ（４０．０％）、ＥＧＦＲ（９１．４％）和ｐ２１ｒａｓ（５３．３％）与分级和预后无显著关系。３种ｐ５３蛋白抗体阳性率均以Ⅱ～Ⅳ级胶质瘤为高;ｐ５３与ＰＣＮＡ反应强度平行。结论ｐ２１ｒａｓ、ｃ－ｅｒｂＢ－２、ＥＧＦ和ＥＧＦＲ改变在胶质瘤发生、发展过程中可能是早期事件,恶变后不再随级别增加而加重,而ｐ５３基因突变涉及胶质瘤发展各个阶段;ＰＣＮＡ能较好地反映胶质瘤的恶性程度。     

bcl-2、p53蛋白及PCNA表达与横纹肌肉瘤临床病理相关性研究

目的：研究横纹肌肉瘤（ＲＭＳ）中ｂｃｌ－２、ｐ５３、ＰＣＮＡ表达与其临床病理的相关性。方法：对５０例（随访４１例）横纹肌肉瘤进行免疫组化ＡＢＣ法标记。结果：ｂｃｌ－２、ｐ５３基因蛋白和ＰＣＮＡ，发现ｂｃｌ－２、ｐ５３、ＰＣＮＡ阳性表达率分别为２８％、７２％、７０％，其阳性表达与年龄、性别及不同组织类型的ＲＭＳ无关（Ｐ＞０．０５）。但与分化程度有关，ｐ５３、ＰＣＮＡ在低分化ＲＭＳ阳性率分别为８５％、９５％，显著高于高分化ＲＭＳ４２．８％和１４．３％（Ｐ＜０．０５），随访存活１年以内的ｐ５３、ＰＣＮＡ阳性率均为８６．７％，亦明显高于存活超过３年以上的阳性率３３．３％和４１．７％（Ｐ＜０．０５）。而ｂｃｌ－２在低分化ＲＭＳ阳性２０％显著低于高分化７１．４％（Ｐ＜０．０５），随访存活１年以内的阳性率１３．４％明显低于存活超过３年以上的４１．４％（Ｐ＜０．０５）。ｐ５３与ｂｃｌ－２阳性表达呈明显负相关，ｐ５３阳性率越高，而ｂｃｌ－２阳性率越低。结论：ＰＣＮＡ、ｐ５３、ｂｃｌ－２蛋白表达能比较准确地反映ＲＭＳ的生物学特性，ｐ５３、ｂｃｌ－２可作为肿瘤预后显著相关的有效指标。     

鼻咽癌中p53蛋白积聚的生物学特征和临床意义

收集３４７例鼻咽癌组织，全部或部分进行了ＣＭ－１、ｐＡｂ２４０、ｐＡｂ１８０１和ｐＡｂ４２１四种ｐ５３蛋白抗体以及ＰＣＮＡ和Ｋｉ６７抗体的染色。综合分析染色结果并结合组织学特征，临床分期以及预后等资料，得出以下结论：①鼻咽癌中ｐ５３蛋白的积聚率为４４．３％，积聚的ｐ５３蛋白其抗原性不完全一样；②ｐ５３积聚的癌细胞具有增殖活性较强和侵袭性较弱的特点；③ｐ５３蛋白积聚的百分率在无颈淋巴结转移的原发瘤中比有颈淋巴结转移者高；在早期原发瘤中比晚期原发瘤中高；在放疗后存活５年以上者中比放疗后１．５年内死亡者中高。     

肺癌中MTS1/p16和p53基因产物的表达与细胞增殖的关系

目的：研究肺癌中ＭＴＳ１／ｐ１６和ｐ５３基因产物的表达与细胞增殖的关系。方法：应用Ｓ－Ｐ免疫组织化学方法研究６２例肺癌组织中ｐ１６蛋白和ｐ５３蛋白的表达情况，并进行增殖细胞核抗原（ＰＣＮＡ）检测，计算细胞增殖指数（ｐｒｏｌｉｆｅｒａｔｉｏｎｉｎｄｅｘ，ＰＩ）。结果：６２例肺癌组织中ｐ１６蛋白和ｐ５３蛋白阳性率分别为５８．１％和５９．７％。腺癌ｐ１６蛋白的阳性率明显高于小细胞癌（Ｐ＜０．０５）；淋巴结转移阳性组ｐ１６蛋白的表达显著低于阴性组（Ｐ＜０．０５）；ＰＩ分级为Ⅱ级的ｐ１６蛋白表达显著高于Ⅳ级（Ｐ＜０．０５）。不同组织类型肺癌中ｐ５３蛋白的表达未见明显差异，淋巴结转移阳性组ｐ５３蛋白的表达高于阴性组（Ｐ＜０．０１）；不同ＰＩ分级中ｐ５３蛋白的表达，Ⅳ级明显高于Ⅰ级（Ｐ＜０．０５）和Ⅱ级（Ｐ＜０．０５），Ⅲ级明显高于Ⅰ级（Ｐ＜０．０５）和Ⅱ级（Ｐ＜０．０１）。ｐ１６蛋白低表达和ｐ５３蛋白过表达之间未见明显相关。结论：ｐ１６蛋白低表达和ｐ５３蛋白过表达均有促进肺癌细胞增殖的作用，ｐ１６蛋白的表达与肺癌的细胞分化有关，ｐ５３蛋白过表达对肺癌细胞的转移起重要作用。抑癌基因ｐ５３对ＭＴＳ１／ｐ１６基因无明显调控作     

骨肉瘤p53蛋白过度表达与预后的关系

目的；探讨ｐ５３蛋白过度表达与骨肉瘤临床病理，肿瘤细胞增殖活性及预后的关系。方法：用免疫组化方法检测５０例骨肉瘤标本中ｐ５３蛋白及增殖细胞核抗原（ＰＣＮＡ）的表达。结果５０例骨肉瘤中１６例ｐ５３蛋白阳性（３２％）；ｐ５３蛋白过度表达与骨肉瘤组织学类型，组织学分级及ＰＣＮＡ分级无关，１６例ｐ５３蛋白阳性病你中，１０例在２年内死亡（６２．５％）３４例阴性病例中，１１例在２年内死亡（３２．４％），结论；     

乳腺导管原位癌病理形态及c-erbB-2、p53和PCNA表达

目的：对乳腺导管原位癌进行病理形态分析，并行ｃ－ｅｒｂＢ－２、ｐ５３癌基因蛋白、增殖细胞核抗原（ＰＣＮＡ）表达以及相关性的研究，以期为临床判断潜在恶性程度及预后提供参考指标。方法：运用病理形态分析以及枸橼酸－微波－ＡＢＣ免疫组化法对２５例常规福尔马林固定、石蜡包埋乳腺导管原位癌组织进行回顾性研究。结果：（１）２５例乳腺原位导管癌ｃ－ｅｒｂＢ－２、ｐ５３、ＰＣＮＡ表达的阳性率分别为３６．０％，４０．０％和４０．０％；（２）粉刺型ｃ－ｅｒｂＢ－２、ｐ５３、ＰＣＮＡ表达的阳性率均高于非粉刺型，而且ｃ－ｅｒｂＢ－２阳性率相差有显著性（Ｐ＜０．０５）；（３）坏死、核异型性、核分裂数与ｃ－ｅｒｂＢ－２、ｐ５３、ＰＣＮＡ的表达有关，其中，坏死与ＰＣＮＡ阳性表达显著相关（Ｐ＜０．０５），核异型性与ｃ－ｅｒｂＢ－２蛋白表达显著相关（Ｐ＜０．０５）。结论：乳腺导管原位癌无论病理形态还是生物学行为都是异质性的，除了组织学亚型，某些形态指标以及ｃ－ｅｒｂＢ－２癌基因蛋白的表达也可作为恶性度指标。     

P21,p53蛋白和增殖细胞核抗原在膀胱癌中的表达及意义

目的研究同一膀胱癌中癌基因蛋白产物和抗癌基因蛋白产物的表达。方法应用免疫组织化学ＡＢＣ方法检测５例正常膀胱组织和５８例膀胱癌组织中增殖细胞核抗原（ＰＣＮＡ）,Ｐ２１和ｐ５３蛋白的表达水平。结果５例正常膀胱组织中未发现Ｐ２１,ｐ５３和ＰＣＮＡ的表达,５８例膀胱癌组织中Ｐ２１,ｐ５３和ＰＣＮＡ阳性检出率分别为６２．１％、５５．２％和５８．６％。表达阳性的ＰＣＮＡ和ｐ５３均定位于肿瘤细胞核内,Ｐ２１蛋白定位于细胞膜上。Ｐ２１,ｐ５３和ＰＣＮＡ阳性表达率与膀胱癌的病理分级,临床分期和患者术后生存率关系密切。结论检测ｐ２１,ｐ５３和ＰＣＮＡ有助于评估膀胱癌的预后。     

bcl—2,p53蛋白及PCNA表达与横纹肌肉瘤临床病…

目的：研究横纹肌肉瘤（ＲＭＳ）中ｂｃｌ－２、ｐ５３、ＰＣＮＡ表达与其临床病理的相关性。方法：对５０例横纹肌肉瘤进行免疫组化ＡＢＣ法标记。结果：ｂｃｌ－２、ｐ５３基因蛋白和ＰＣＮＡ，发现ｂｃｌ－２、ｐ５３、ＰＣＮＡ阳性表达率分别为２８％、７２％、７０％，其阳性表达与年龄、性别及不同组织类型的ＲＭＳ无关。但民分化程度有关，Ｐ５３、ＰＣＮ在低分化ＲＭＳ阳性率分别为８５％、９５％，显著高于 化ＲＭＳ４２．     

nm23-H1、p53、PCNA表达与大肠癌浸润转移的关系

目的：研究大肠癌中ｎｍ２３－Ｈ１、ｐ５３、ＰＣＮＡ的表达与浸润转移的关系。方法：应用ＬＳＡＢ免疫组织化学方法检测７４例大肠癌中ｎｍ２３－Ｈ１、ｐ５３、ＰＣＮＡ和Ⅳ型原的表达。结果：大肠癌中ｎｍ２３－Ｈ１、ｐ５３和ＰＣＮＡ的阳性率分别为７１．６％、５２．７％和８１．１％。大肠癌中ｎｍ２３－Ｈ１低表达与淋巴结转移有关（Ｐ＜０．０２５），ｎｍ２３－Ｈ１的表达在Ⅳ型胶原表达不同的肠癌中无明显差异（Ｐ＞０．０５）；ｐ５３和ＰＣＮＡ过表达与浸润程度和淋巴结转移有关（Ｐ＜０．０５），ｐ５３和ＰＣＮＡ的表达在Ⅳ型胶原表达不同的肠癌中有非常显著的差异（Ｐ＜０．００５）；大肠癌中ｐ５３过表达与ｎｍ２３－Ｈ１低表达有关（Ｐ＜０．０１）。结论：实验结果揭示ｐ５３基因突变对于ｎｍ２３－Ｈ１基因的失活有一定影响，其作用机制有待深入研究。ｎｍ２３－Ｈ１低表达可能仅在大肠癌转移过程中发挥作用，ｐ５３过表达可在大肠癌浸润转移过程及细胞增殖中起重要作用。     

免疫组化和PCR—SSCP检测p53基因异常的一致性探讨

目的：探讨免疫组化检测ｐ５３蛋白表达和ＰＣＲ－ＳＳＣＰ检测ｐ５３基因突变的一致性。方法：单克隆抗体ＤＯ－７检测８５例非小细胞肺癌（ＮＳＣＬＣ）的ｐ５３蛋白表达，ＰＣＲ－ＳＳＣＰ检测其中３１例腺癌的ｐ５３基因突变。结果：８５例ＮＳＣＬＣ中ｐ５３蛋白表达阳性率为６８％（５８／８５），３１例腺癌中ｐ５３蛋白表达阳性率为６１％（１９／３１），１４例（４６％）出现ｐ５３基因５～８外显子突变，ｐ５３蛋白免疫组化和ＰＣＲ－ＳＳＣＰ检测ｐ５３基因突变无显著相关（χ２＝０．１，Ｐ＝０．７６），其一致率为５２％。结论：ｐ５３蛋白表达并不能很好地反映ｐ５３基因突变。     

Opportunities and challenges in the prevention and control of cancer and other chronic diseases: children's diet and nutrition and weight and physical activity

OBJECTIVE: The purpose of this article is to review the role of behavioral research in disease prevention and control, with a particular emphasis on lifestyle- and behavior-related cancer and chronic disease risk factors--specifically, relationships among diet and nutrition and weight and physical activity with adult cancer, and tracking developmental origins of these health-promoting and health-compromising behaviors from childhood into adulthood. METHOD: After reviewing the background of the field of cancer prevention and control and establishing plausibility for the role of child health behavior in adult cancer risk, studies selected from the pediatric published literature are reviewed. Articles were retrieved, selected, and summarized to illustrate that results from separate but related fields of study are combinable to yield insights into the prevention and control of cancer and other chronic diseases in adulthood through the conduct of nonintervention and intervention research with children in clinical, public health, and other contexts. RESULTS: As illustrated by the evidence presented in this review, there are numerous reasons (biological, psychological, and social), opportunities (school and community, health care, and family settings), and approaches (nonintervention and intervention) to understand and impact behavior change in children's diet and nutrition and weight and physical activity. CONCLUSIONS: Further development and evaluation of behavioral science intervention protocols conducted with children are necessary to understand the efficacy of these approaches and their public health impact on proximal and distal cancer, cancer-related, and chronic disease outcomes before diffusion. It is clear that more attention should be paid to early life and early developmental phases in cancer prevention.     

Beta-endorphin and drug-induced reward and reinforcement

Although drugs of abuse have different acute mechanisms of action, their brain pathways of reward exhibit common functional effects upon both acute and chronic administration. Long known for its analgesic effect, the opioid beta-endorphin is now shown to induce euphoria, and to have rewarding and reinforcing properties. In this review, we will summarize the present neurobiological and behavioral evidences that support involvement of beta-endorphin in drug-induced reward and reinforcement. Currently, evidence supports a prominent role for beta-endorphin in the reward pathways of cocaine and alcohol. The existing information indicating the importance of beta-endorphin neurotransmission in mediating the reward pathways of nicotine and THC, is thus far circumstantial. The studies described herein employed diverse techniques, such as biochemical measurements of beta-endorphin in various brain sites and plasma, and behavioral measurements, conducted following elimination (via administration of anti-beta-endorphin antibodies or using mutant mice) or augmentation (by intracerebral administration) of beta-endorphin. We suggest that the reward pathways for different addictive drugs converge to a common pathway in which beta-endorphin is a modulating element. beta-Endorphin is involved also with distress. However, reviewing the data collected so far implies a discrete role, beyond that of a stress response, for beta-endorphin in mediating the substance of abuse reward pathway. This may occur via interacting with the mesolimbic dopaminergic system and also by its interesting effects on learning and memory. The functional meaning of beta-endorphin in the process of drug-seeking behavior is discussed.     

PTEN与信号转导及肿瘤

ＴＥＮ[1] (ｐｈｏｓｐｈａｔａｓｅａｎｄｔｅｎｓｉｎｈｏｍｏｌｏｇｙｄｅｌｅｔｅｄｏｎｃｈｒｏｍｏｓｏｍｅｔｅｎ)又名ＭＭＡＣ1 [2 ] (ｍｕｔａｔｅｄｉｎｍｕｔｉｐｌｙａｄａｎｃｅｄｃａｎｃｅｒ 1 )和ＴＥＰ1 [3 ] (ＴＧＦ -βｒｅｇｕｌａｔｅｄａｎｄｅｐｉｔｈｅｌｉａｌｃｅｌｌ -ｒｉｃｈｅｄｐｈｏｓｐｈａｔａｓｅ 1 ) (以下均称为ＰＴＥＮ) ,是 1 997年由 3个研究小组先后发现的一个具有双特异磷酸酶活性的抑癌基因。ＰＴＥＮ基因异常广泛存在于人类多种恶性肿瘤 ,如恶性神经胶质瘤、前列腺癌、子宫内膜癌、黑色素瘤等…     

Tobacco and alcohol and the risk of head and neck cancer

Summary We carried out two case-control studies on the relative risk of head and neck cancer in association with tobacco and alcohol consumption. The first study carried out at the ENT Department of the University hospitals of Heidelberg and Giessen (FRG) comprised 200 male patients with squamous cell cancer of the head and neck and 800 control subjects matched for sex, age, and residential area (1:4 matching design). Of the tumour patients, 4.5% had never smoked, in contrast to 29.5% of the control group. The average tobacco and alcohol consumption of the patients was approximately twice as high as in the control subjects. The highest alcohol and tobacco consumption was observed in patients suffering from oropharyngeal cancer. Tobacco and alcohol increased the risk of head and neck cancer in a dose-dependent fashion and acted as independent risk factors. In heavy smokers (> 60 pack-years) a relative risk of 23.4 (alcohol adjusted) was calculated. Combined alcohol and tobacco consumption showed a synergistic effect. The risk ratio increased more in a multiplicative than in an additive manner. Oral and laryngeal cancer were associated with the highest tobacco-associated risk values. The highest ethanol-associated risk values were associated with oropharyngeal and laryngeal cancer. The second study was carried out at the ENT Department of the University of Heidelberg on 164 males with squamous cell carcinoma of the larynx and 656 control subjects matched for sex, age and residential area (1:4 matching design). Of the cases, 4.2% had never smoked, compared with 28.5% of the control subjects. The risk of laryngeal cancer by tobacco consumption was dose dependent, reaching a maximum value of 9.1 (adjusted for alcohol) for a consumption of more than 50 tobacco-years (TY). The relative risk of laryngeal cancer associated with alcohol intake was also dose dependent, reaching a value of 9.0 (adjusted for tobacco) for a mean daily consumption of more than 75 g alcohol. An analysis of subsite specific risks showed that heavy smokers (> 50 TY) carried a nearly ten times higher risk of supraglottic cancer than of glottic cancer. The risk of supraglottic cancer from alcohol consumption was also higher than that of glottic cancer.     

Postinfectious immunodeficiency and autoimmunity: pathogenic and clinical values and implications

Autoimmunity is still a mystery of clinical immunology and medicine as a whole. The etiology and pathogenesis of autoimmune disorders remain unclear and, thus, are assessed as a balance between hereditary predisposition, triggering factors and the appearance of autoantibodies and/or self-reactive T cells. Among the immunological armamentarium, molecular mimicry, based on self-reactive T- and B-cell activation by cross-reactive epitopes of infectious agents, is of special value. Hypotheses regarding the possible involvement of molecular mimicry in the development of postinfectious autoimmunity are currently very intriguing. They provide new approaches for identifying etiological agents that are associated with postinfectious autoimmunity, paired microbial- and tissue-linked epitopes targeted for autoimmune reaction determination, postinfectious autoimmunity pathogenesis recognition and specific prevention, and therapy for autoimmune disorder development.     

Pain and Effusion and Quadriceps Activation and Strength

Context:

Quadriceps dysfunction is a common consequence of knee joint injury and disease, yet its causes remain elusive.

Objective:

To determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion affect the magnitude of quadriceps dysfunction.

Design:

Crossover study.

Setting:

University research laboratory.

Patients or Other Participants:

Fourteen (8 men, 6 women; age = 23.6 ± 4.8 years, height = 170.3 ± 9.16 cm, mass = 72.9 ± 11.84 kg) healthy volunteers.

Intervention(s):

All participants were tested under 4 randomized conditions: normal knee, effused knee, painful knee, and effused and painful knee.

Main Outcome Measure(s):

Quadriceps strength (Nm/kg) and activation (central activation ratio) were assessed after each condition was induced.

Results:

Quadriceps strength and activation were highest under the normal knee condition and differed from the 3 experimental knee conditions (P < .05). No differences were noted among the 3 experimental knee conditions for either variable (P > .05).

Conclusions:

Both pain and effusion led to quadriceps dysfunction, but the interaction of the 2 stimuli did not increase the magnitude of the strength or activation deficits. Therefore, pain and effusion can be considered equally potent in eliciting quadriceps inhibition. Given that pain and effusion accompany numerous knee conditions, the prevalence of quadriceps dysfunction is likely high.Key Words: arthrogenic muscle inhibition, central activation failure, voluntary activation, muscles

Key Points

• Knee pain and effusion resulted in arthrogenic muscle inhibition and weakness of the quadriceps.
• The simultaneous presence of pain and effusion did not increase the magnitude of quadriceps dysfunction.
• To reduce arthrogenic muscle inhibition and improve muscle strength, clinicians should employ interventions that target removing both pain and effusion.

Quadriceps weakness is a common consequence of traumatic knee joint injury^1,2 and chronic degenerative knee joint conditions.^3,4 Arthrogenic muscle inhibition (AMI), a neurologic decline in muscle activation, results in quadriceps weakness and hinders rehabilitation by preventing gains in strength.⁵ The inability to reverse AMI and restore muscle function can lead to decreased physical abilities,⁶ biomechanical deficits,⁷ and possibly reinjury.⁵ Furthermore, researchers^8,9 have suggested that quadriceps weakness resulting from AMI may place patients at risk for developing osteoarthritis in the knee. In light of the substantial influence of quadriceps AMI on these clinically relevant outcomes, we need to improve our understanding of the factors that contribute to this neurologic decline in muscle activity so efforts to target and reverse it can be implemented and gains in strength can be achieved more easily.Joint injury and disease are accompanied by numerous sequelae (ie, pain, swelling, tissue damage, inflammation), so ascertaining which one ultimately leads to neurologic muscle dysfunction is difficult. Whereas a joint effusion can result in AMI,^10–12 the effects of pain are less understood despite many clinicians attributing AMI to pain. Using techniques that introduce knee pain without accompanying injury may provide insights into the role of pain in eliciting AMI.The degree of knee joint damage may play a role in the quantity of AMI that manifests. Hurley et al^13,14 demonstrated that quadriceps AMI, measured using an interpolated-twitch technique, was greater in patients with extensive traumatic knee injury (eg, fractured tibial plateau, ruptured medial collateral ligament, and medial meniscectomy) than patients with isolated joint trauma (ie, isolated anterior cruciate ligament [ACL] rupture). Similarly, patients with more knee joint symptoms (ie, greater number of symptoms and increased severity of symptoms) may present with greater magnitudes of quadriceps inhibition. Recently, investigators¹⁵ have suggested that patients with more pain display less quadriceps strength, supporting this tenet. Given that effusion and pain often present simultaneously with joint injuries and diseases, such as ACL injury and osteoarthritis, examining both the isolated and cumulative effects of these sequelae appears warranted to determine if they influence the magnitude of muscle inhibition.Experimental joint-effusion and pain models are safe and effective experimental methods that allow for the isolated examination of their effects on muscle function. The effusion model, whereby sterile saline is injected directly into the knee joint capsule,⁷ produces a clinically relevant magnitude of the joint effusion that may be present with traumatic injury. Effusion is thought to activate group II afferents responding to stretch or pressure,^16–18 which in turn may facilitate group Ib interneurons and result in quadriceps AMI.⁵ The pain model involves injecting hypertonic saline into the infrapatellar fat pad to produce anteromedial knee pain similar to that described in patients with patellofemoral pain syndrome.¹⁹ Pain is considered to initiate AMI through activation of group III and IV afferents that act as nocioceptors to signal damage or potential damage to joint structures.^16–18 The firing of these afferents then may lead to facilitation of group Ib interneurons, the flexion reflex, or the gamma loop, ultimately resulting in quadriceps inhibition.²⁰ Thus, these models allow us to create symptoms that are associated with knee injury and have the added benefit of providing a way to examine their effects in isolation.Therefore, the purpose of our study was to determine the effects of pain on quadriceps strength and activation and to learn if simultaneous pain and knee joint effusion would affect the magnitude of quadriceps dysfunction. We hypothesized that pain alone would result in quadriceps inhibition and that the magnitude of inhibition would be greater when effusion and pain were present simultaneously.     

类赖氨酰氧化酶2与肿瘤转移和发生

类赖氨酰氧化酶2(lysyl oxidase-like 2,LOXL2)是赖氨酰氧化酶(lysyl oxidase,LOX)基因家族的成员之一,其表达产物能促进胶原沉积.LOXL2的过表达能促进纤维化,并与肿瘤侵袭、转移及不良预后有关.目前大部分学者认为LOXL2是一种转移促进基因,也有实验支持其是一种肿瘤抑制基因.研究发现LOXL2可以通过激活Snail/Ecadherin通路或Src/FAK通路促进转移.LOXL2有望作为肿瘤生物标志物,用于预后判断,成为一个新的治疗靶点.