Forty years ago, scientists started to describe the genetic cascade of events leading to cancer as “somatic evolution” (Cairns, 1975; Nowell, 1976). Even if the full relevance of these pioneer papers was not immediately perceived by the scientific community, they paved the way for one of the most stimulating and challenging research directions in the effort to predict cancer emergence, progression, and therapy outcomes. Evolutionary biology has indeed deeply transformed our understanding of cancer, gaining unprecedented international recognition among oncologists in the last decade (Ujvari, Roche & Thomas, 2017a). Nowadays, cancer is widely considered as a pathology that emerges due to clonal evolution and cell competition, Darwinian selection being the driver of cancer cells along selective landscapes, culminating in resistance to immune attack, malignant progression, resistance to therapies, metastasis, and even sometimes contagion between individuals and/or species (Ujvari et al., 2017b; Ujvari, Roche & Thomas,2017a). Thus, as recently proposed by Mel Greaves through paraphrasing Dobzhansky's famous dictum, “nothing in cancer makes sense except in the light of evolution” (Greaves, 2018). This interdisciplinary field of research remains at the moment extremely promising, but it is still in its infancy, and fundamental studies (both theoretical and experimental) are still needed to pursue our understanding of the evolutionary ecology of tumors and of host–tumor interactions. By assembling some of the latest, most exciting results, syntheses, and perspectives relating to the topic Ecology, Evolution and Cancer, our objective with this special issue is to reinforce the construction of a solid base for a balanced approach to cancer research, for oncologists and for ecologists.

Despite the great advancements in cancer research and treatment over the last 50 years, understanding cancer susceptibility, emergence, progression, resistance to therapies, and ultimately predicting treatment outcomes still largely remain challenging. Here, Brown and Gatenby (in press, This volume) put forward an alternative model of somatic evolution. They propose that mutations accumulated during the host lifetime become carcinogenic only when the cells which carry them have a real opportunity to evolve. Most of the time, this is not the case because cells in multicellular organisms are involved in the cooperative functioning that governs the host as the unit of natural selection. As a result, they remain under control by local tissue constraints. However, when for different reasons, these mutated cells become free from these host constraints, they have their own Darwinian dynamics. Mutations previously accumulated over the lifetime of the host serve as their “genetic heritage” in their malignant trajectory. Still on this topic, Solary and Laplane (2020, This volume) described the dynamics of somatic mutation accumulations in healthy tissues during the life and discussed the role of the host environment in tumor emergence and progression. They also explored how tumors in return remodel their close and distant environments. It appears that promising strategies against cancer consist in preserving, as long as possible, the tumor suppressive properties of healthy tissue landscapes.

Cancer cells are also under selection to evolve traits that generate heritable variation. The diversity of mechanisms yielding this evolvability is far from being fully understood at the moment. Pienta, Hammarlund, Axelrod, Brown, and Amend (2020, This volume) proposed that we have until now underestimated the role of poly‐aneuploid cancer cells. These cells would be an important source of heritable variation, allowing cancer cells to evolve rapidly, leading to therapy resistance and metastasis. On a related topic, Noble, Burley, Le Sueur, and Hochberg (2020, This volume) questioned the classical prediction that intratumor heterogeneity is a reliable prognostic biomarker for several cancer types. Employing a spatial computational model of tumor evolution, they highlight the need for considering both clonal diversity and genomic instability than each factor alone.

Birtwell, Luebeck, Carlo, and Maley (in press, This volume) also proposed that to understand the dynamics of cancer initiation and progression, it is crucial to acknowledge that epithelia are divided into subpopulations of tissue stem cells along with the transient amplifying cells and differentiated cells that they produce. Therefore, a fundamental question in cancers like those affecting the intestinal tract is to determine how the crypt‐level metapopulation dynamics affect the accumulation of somatic mutations during carcinogenesis. In addition to these malignant processes occurring during the host lifetime, Schenk, López, Kschischo, and McGranaham (n.d., This volume) also highlighted that, until now, little attention has been devoted to considering the potential influence of germline ancestry on cancer development and cancer evolution. This is unfortunate because emerging data suggest that germline ancestry can profoundly influence cancer disparities in cancer care and the subsequent disease course (e.g., Zhang, Edwards, Flemington, & Zhang, 2017, Akinyemiju, Sakhuja, Waterbor, Pisu, & Altekruse, 2018). Here, by comparing European Americans and African Americans, Schenk et al. (n.d., This volume) show that germline ancestry profoundly influences the somatic evolution of lung adenocarcinoma but not lung squamous cell carcinomas.

It is well known that most cancer‐related deaths are due to metastasis, but basic information is often missing concerning the evolutionary ecology of this dispersal process. An intriguing aspect concerns the fact that circulating malignant cells can be single or in clusters. Circulating tumor cells in clusters are generally associated with higher metastatic potential and worse prognosis. Campenni, May, Boddy, Harris, and Nedelcu (n.d., This Volume) proposed a mechanistic agent‐based model to investigate how clusters, depending on their sizes and densities, respond to different challenges. They also made predictions on the potential combination of factors and parameter values that could decrease the fitness and metastatic potential of malignant cells in these clusters.

Ecological and evolutionary approaches have already made great advances in explaining the origins and recrudescence of cancer cells, as well as elucidating the reasons of therapy failures, but would they be applicable to propose innovative novel directions in cancer treatment? The answer is yes. Following the theoretical advancement of the interface of Ecology, Evolution and Cancer a few years ago, the field is now moving into the experimental and clinical phases, and recent developments include the ability to predict which tumors will be harmful for patients (e.g., Campbell et al., 2020; Maley et al., 2017), as well as novel therapeutic approaches that are able to slow down tumor growth in invasive late‐stage cancers. Currently, the most emblematic and advanced evolutionary‐based cancer therapy is adaptive therapy, developed by Gatenby, Silva, Gillies, and Frieden (2009). A major conceptual breakthrough compared to traditional approaches has been the acceptance of when cancer eradication is no longer an option, treatment that focuses on containing the malignant progression is preferable. The latter approach aims to turn cancer into a chronic disease, by efficiently keeping the tumor burden below the level that threatens loss of life and/or quality. The majority of cancers are fatal due to the cancer cells' propensity of unlimited cell division, circumventing natural defenses, and ultimately resisting therapies. While the evolution of malignant cells represents a major hurdle in treatment development, it can actually be the Achilles heel of these fatal pathologies. Scientists could theoretically exploit the evolutionary pathways of cancer cells and strategically drive their evolution toward equilibria where they will no longer be detrimental to the host. To achieve this, evolutionary‐based therapies need to be adaptive and dynamic, and to continuously anticipate the evolutionary response of cancers and adjust treatments accordingly, ultimately thwarting evolutionary resilience. Some of these approaches are very similar to (and emerged from) the evolutionary double‐bind theories developed in pest management in applied ecology (Basanta, Gatenby, & Anderson, 2012). Similar to pest management, where the combination of chemical toxins, with introduction of predators, parasitoids, or pathogens, achieves more durable pest control, adaptive cancer therapy allows incurable tumors to persist but keeps them under control via various strategies (combination of chemo‐ and immune therapies, modulated dose schedule, competitive inhibitors (Enriquez‐Navas & Gatenby, 2017)). These latest approaches are the most innovative and promising directions so far proposed by ecological and evolutionary sciences to transform cancer from a lethal disease, into a chronic, manageable pathology. Oncologists may, however, sometimes face a dilemma between choosing treatments that can sometimes cure the patient and regimens that can delay progression but not cure the patient. In this special issue, Hansen and Read (2020, This volume) investigated this crucial question, discussing which aspects of the evolutionary ecology of tumor dynamics should determine whether it is better to attempt cure or to manage resistance. The authors also highlight that before the advent of evolutionary strategies aimed at resistance management, there was often no choice. Because this is not the case anymore, it is now important to also adapt the ways we communicate treatment options to patients.

On a related topic, it is also predicted that slowing down malignant progressions, rather than attempting to eradicate malignant cells, can be an efficient way to prevent tumor growth, prolong drug efficacy, and ultimately to prevent deaths. Using a strain of Saccharomyces cerevisiae as a model system, Merlo et al. (in press, This volume) investigated how the application of simultaneous selective pressures can be an efficient option to slow adaptation. Parallels with cancer cell populations are discussed in a therapeutic perspective. Finally, a novel evolutionary‐based strategy for cancer therapy is proposed by Girard et al. (2020, This volume). This innovative approach elegantly exploits the properties of the "smoke detector” principle (Nesse, 2001). By sending large amount of false alarms to malignant cells, the treatment induces a new “alarm down” state in the tumor cells which subsequently lower their ability to respond to high “danger” signal.

Cancer is not only a leading cause of human death worldwide but also a pathology that affects all multicellular organisms since the dawn of multicellularity more than 500 million years ago (Aktipis & Nesse, 2013). As a result, the field of comparative oncology has emerged and facilitated the comparison of cancer dynamics across taxa, leading to insights on how biological, genetic, and ecological factors drive individual and species variations in cancer diversity, incidence, and lethality. Disparities in natural history and life‐history strategies across species can exacerbate cancer risk and concomitantly drive the evolution of cancer defenses in organisms. Comparative oncology studies have so far mostly focused on the processes and patterns associated with “Peto's paradox” (lack of statistical relationships between cancer incidence and body size and longevity) that remain key to our understanding of cancer epidemiology, prevention, and improved therapies both in animal and in human populations. In this special issue, Nunney (in press, This volume) attempted to resolve this paradox, testing five hypotheses with a modeling approach, one due to intrinsic metabolic rate/body size scaling and four arising from adaptive evolution. This work supports the hypothesis that the incidence of cancer is regulated primarily through the recruitment of additional layers of genetic control whenever a cancer significantly reduces average fitness. On a related topic, Erten and Kokko (2020 This volume) introduced the concept of ‘ontogenetic management strategies’ to explore the rules of dividing, differentiating, and killing somatic cells depending on the mature body size targeted by organisms. With this approach, they also explored how well a strategy evolved in small‐bodied organisms performs if implemented in a large body and vice versa.

Rozhok and DeGregori (n.d., This volume) provided a complementary view, proposing that carcinogenesis is shaped by three major orthogonal processes: accumulation of somatic mutations over lifetimes, species‐specific evolution of cellular genetic machinery, and physiological aging‐induced shifts in selective microenvironments in tissues. Because these three processes are interconnected through the evolution of life‐history traits, they also vastly differ across species.

While large and long‐lived animals are often investigated for anti‐cancer defenses, Thomas et al. (2020, This Volume) argued that more attention should also be devoted to studying domesticated animals. For different reasons associated with the domestication process, domesticated species often display high rates of cancer, but artificial selection may have also favored the evolution of compensatory anti‐cancer defenses. Therefore, domesticated animals would constitute a group where seemingly rare anti‐cancer adaptations and novel cancer treatments could be found. Following the same idea that novel therapy strategies can emerge from the “secrets” used by wild and captive animals to fight this disease, Noble, Rohaj, Abegglen, and Schiffman (n.d., This volume) also provided a large synthesis on the most promising animal‐derived cancer therapeutic agents, notably derived from insects, arachnids, amphibians, and marine organism. For each compound, they present the history of their discovery, their mechanism of action, and their extent of clinical development.

A large proportion of cancers (app. 15%–20% across the globe) is initiated and caused by infectious agents, such as viruses, bacteria, and parasites (Dheilly, Ewald, Brindley, Fichorova, & Thomas, 2019; Plummer et al., 2016). These pathogens can disrupt signaling pathways that control cell proliferation, weaken the immune system, and/or cause chronic inflammation that can increase the risk of developing cancer (Ewald & Swain Ewald, 2014). As the pathogens can be passed from one individual to other, these cancers present fascinating topics to study for both evolutionary biologists, disease epidemiologists, and oncologists. Undoubtedly one of the major innovative direction of this field to emerge recently is understanding the reciprocal interactions between parasites, host microbiota, and cancer dynamics (Dheilly et al., 2019). Ewald & Ewald (in press, This volume) discussed the idea that symbionts may improve the effectiveness of immunological defenses against cancer, through a diversity of interactions between parasitic and mutualistic microbes. An original situation occurs when the host's ability to muster escalated attacks on tumor cells is influenced by symbionts, through the relaxation of immunological checkpoints.

Apart from malignancies with underlying pathogen infections (Ewald & Swain Ewald, 2013), cancer is generally not contagious. However, there are nine noticeable exceptions in the wild, where clonal cancer cell lines are able to transmit between individuals: one in dogs, two in Tasmanian devils, and six in six bivalve species (Ujvari et al., 2017a; Yonemitsu et al., 2019). Research into transmissible cancers has rapidly been gaining momentum, as these cancers are one of the most intriguing and unexplored host–pathogen systems. Although transmissible cancers are a rare type of life form, their ecological consequences can be major, as illustrated by the dramatic quasi eradication of a top predator, Tasmania devils (Sarcophilus harrisii). Despite the increasing interest in these malignancies, major questions still remain to be unanswered: Why do transmissible cancers emerge? How do they evolve? What are their ecological and evolutionary impacts and how to manage/mitigate them? Dujon et al. (2020, This volume) provided an interesting global meta‐analysis of over 50 years of multidisciplinary and international collaborations on transmissible cancers.

Oncogenic processes are inevitable phenomenon in metazoans. Despite their omnipresence in multicellular species, ecologists and evolutionary biologists have so far either neglected them, as well as their role in ecosystem functioning (Vittecoq et al., 2013), or considered them as “noise” on host phenotypic variations. Prior to becoming the direct cause of host death, oncogenic processes are likely to alter various fitness‐related traits in their hosts, like the vulnerability to predators or to pathogens, their competitive and dispersal abilities. There is also increasing evidence that malignant cells are involved in reciprocal interactions with symbiotic microbes and parasites, thereby indirectly leading to the possibility of triple reciprocal interactions (Thomas et al., 2017). Thus, the coming years bring exciting opportunities for ecologists and evolutionary biologists to finally consider and accept oncobiota as a key player of the holobiont, and thus initiate and conduct theoretical and empirical research that adopts a very innovative perspective on the ecological and evolutionary importance of malignant cells. Using Tasmania devils and DFTD as a model system, Hamede et al. (2020, This volume) discussed the relevance of cancer cells as selective agents and suggested a holistic framework to understand the interplay of ecological, epidemiological, and evolutionary dynamics of cancer in wildlife. Using a modeling approach, Perret, Gidoin, Ujvari, Thomas, and Roche (2020, This volume) explored, for the first time at the ecosystem level, the role of cancer in species interactions, notably host–predator interactions, and how in return, the outcome of alteredinterplay could affect the evolution of resistance mechanisms against cancer. A first conclusion is that cancer has a limited impact on prey populations compared to predator ones. Biotic interactions can also lead to a null or positive effect of cancer on host population densities and to vary resistance levels in predator populations. With anthropogenic impact (including pollution, climate change, urbanization) predicted to dramatically increase the coming decades, it is foreseeable that the risk of cancer, and the number of cancer incidences in the wild should also increase significantly in the near future (Giraudeau, Sepp, Ujvari, Ewald, & Thomas,2018). There is thus a need to explore, especially in long‐lived species, the evolution of protective mechanisms against neoplastic processes and natural cancer defense mechanisms in general. Meitern et al. (2020, This volume) proposed that seabirds are promising model given their longevity and their habitats that are currently often polluted. This study revealed that old gulls differ from young ones both from the aspect of cancer susceptibility and of tumor suppression at the genetic level.

More than ever the topic Ecology, Evolution and Cancer offer promising challenges not only to prevent and to cure cancer,but also to understand multiple aspects of the evolutionary ecology of multicellular organisms in our changing world. We hope that this special issue will present materials useful for a broad audience of scientists, from oncologists to ecologists and that it will stimulate novel discussions across the disciplines of evolutionary biology and oncology.

四十年前，科学家开始将导致癌症的事件的遗传级联描述为“体细胞进化”（Cairns，  1975； Nowell，  1976）。即使科学界没有立即意识到这些开创性论文的全部相关性，他们也为预测癌症的发生，进展和治疗结果的努力中最刺激和最具挑战性的研究方向之一铺平了道路。进化生物学确实已经深刻地改变了我们对癌症的理解，在过去十年中获得了肿瘤学家前所未有的国际认可（Ujvari，Roche＆Thomas，2017a）。如今，癌症被广泛认为是由于克隆进化和细胞竞争而出现的一种病理学，达尔文选择是沿着选择性区域发展癌细胞的驱动力，最终导致对免疫攻击，恶性进展，对疗法，转移，甚至有时的抵抗力个体和/或物种之间的传染（Ujvari et al。，2017b ; Ujvari，Roche＆Thomas，2017a）。因此，正如梅尔·格雷夫斯（Mel Greaves）最近通过解释多布赞斯基的著名格言所提出的那样，“除了进化论，癌症中没有任何意义”（Greaves，  2018年））。目前，这一跨学科的研究领域仍然非常有前途，但是它仍处于起步阶段，仍然需要基础研究（理论和实验）来追求我们对肿瘤的进化生态学以及宿主-肿瘤相互作用的理解。通过汇总与生态，进化和癌症有关的一些最新，最令人兴奋的结果，综合研究和观点，我们针对这一特殊问题的目标是为肿瘤学家加强癌症研究平衡方法的坚实基础对于生态学家。

尽管在过去的50年中癌症研究和治疗取得了巨大的进步，但了解癌症的易感性，出现，进展，对治疗的抵抗力以及最终预测治疗结果仍然在很大程度上具有挑战性。在这里，布朗和盖特比（印刷中，本卷）提出了一种体细胞进化的替代模型。他们提出，只有当携带它们的细胞真正有机会进化时，在宿主生命中积累的突变才具有致癌性。在大多数情况下，情况并非如此，因为多细胞生物中的细胞参与了将宿主作为自然选择单位的宿主的协同功能。结果，它们仍然受到局部组织约束的控制。但是，当由于各种原因这些突变的细胞摆脱宿主约束时，它们便具有自己的达尔文动力学。先前在宿主一生中积累的突变在其恶性轨迹中充当其“遗传遗产”。仍然在这个主题上，Solary and Laplane（2020，本卷）描述了生命过程中健康组织中体细胞突变积累的动态，并讨论了宿主环境在肿瘤发生和发展中的作用。他们还探索了肿瘤如何在近距离和远距离环境中重塑。似乎有希望的抗癌策略在于尽可能长地保存健康组织景观的抑癌特性。

癌细胞也在选择中，以进化产生可遗传变异的特征。目前尚不能完全理解产生这种发展性的机制的多样性。Pienta，Hammarlund，Axelrod，Brown和Amend（2020年，本册）提出，到目前为止，我们仍低估了多异倍体癌细胞的作用。这些细胞将是遗传变异的重要来源，可使癌细胞迅速进化，导致治疗耐药性和转移。在相关主题上，诺布尔，白肋烟，勒苏尔和霍赫伯格（2020，此卷）质疑经典预测，即肿瘤内异质性是几种癌症类型的可靠预后生物标志物。他们利用肿瘤进化的空间计算模型，强调了需要同时考虑克隆多样性和基因组不稳定性，而不是单独考虑每个因素。

Birtwell，Luebeck，Carlo和Maley（印刷中，本卷）还提出，要了解癌症发生和发展的动态，至关重要的是要认识到上皮细胞被分为组织干细胞亚群，以及它们产生的瞬时扩增细胞和分化细胞。因此，像影响肠道的癌症一样，癌症中的一个基本问题是确定隐窝水平的代谢动力学如何影响致癌过程中体细胞突变的积累。除了在寄主一生中发生的这些恶性过程外，Schenk，López，Kschischo和McGranaham（本卷）还强调指出，到目前为止，很少有人关注种系祖先对癌症发展和发展的潜在影响。癌症演变。 2017，Akinyemiju，Sakhuja，Waterbor，Pisu和Altekruse，  2018年）。在这里，通过比较欧洲裔美国人和非裔美国人，Schenk等人。（第，本卷）显示种系祖先对肺腺癌的体细胞进化有深远影响，但对肺鳞状细胞癌没有影响。

众所周知，大多数与癌症相关的死亡是由于转移引起的，但是关于这种扩散过程的进化生态学，通常缺少基本信息。一个有趣的方面是循环的恶性细胞可以是单个或成簇的事实。簇中循环的肿瘤细胞通常与较高的转移潜力和较差的预后相关。Campenni，May，Boddy，Harris和Nedelcu（第二册）提出了一种基于机制代理的模型，以研究集群如何根据其大小和密度来应对不同的挑战。他们还对可能降低这些簇中恶性细胞的适应性和转移潜力的因素和参数值的潜在组合进行了预测。

生态学和进化论方法在解释癌细胞的起源和复发以及阐明治疗失败的原因方面已经取得了长足的进步，但是它们是否可用于提出创新的癌症治疗方向？答案是肯定的。随着几年前生态学，进化论和癌症之间的相互作用的理论发展，该领域现在正进入实验和临床阶段，最近的发展包括能够预测哪些肿瘤对患者有害（例如，Campbell等）。等人，  2020年；马利等人，  2017年），以及能够减慢浸润性晚期癌症中肿瘤生长的新型治疗方法。目前，最有代表性和最先进的基于进化的癌症疗法是适应性疗法，由Gatenby，Silva，Gillies和Frieden（2009）。与传统方法相比，一个重大的概念突破是可以接受以下观点：当不再需要根除癌症时，以抑制恶性进展为重点的治疗是可取的。后一种方法旨在通过有效地将肿瘤负担保持在威胁生命和/或质量丧失的水平以下，将癌症转变为慢性疾病。大多数癌症都是致命的，这是由于癌细胞倾向于无限的细胞分裂，绕过自然防御系统并最终抵抗疗法。尽管恶性细胞的进化是治疗发展的主要障碍，但实际上它可能是这些致命病理的致命弱点。从理论上讲，科学家可以利用癌细胞的进化途径，从战略上推动癌细胞向平衡的方向发展，使它们不再对宿主有害。为了实现这一目标，基于进化的疗法需要具有适应性和动态性，并不断地预测癌症的进化反应并相应地调整治疗方法，最终阻碍了进化的适应力。其中一些方法与应用生态学中虫害管理中发展的进化双绑定理论非常相似（并从中衍生）（Basanta，Gatenby和Anderson，最终阻碍了进化的弹性。其中一些方法与应用生态学中虫害管理中发展的进化双绑定理论非常相似（并从中衍生）（Basanta，Gatenby和Anderson，最终阻碍了进化的弹性。其中一些方法与应用生态学中虫害管理中发展的进化双绑定理论非常相似（并从中衍生）（Basanta，Gatenby和Anderson， 2012）。与有害生物管理类似，通过结合化学毒素，引入掠食性动物，寄生虫或病原体，可以实现更持久的有害生物控制，适应性癌症治疗可以治愈无法治愈的肿瘤，但可以通过各种策略（化学疗法和化学疗法相结合）来控制它们。免疫疗法，调整剂量方案，竞争性抑制剂（Enriquez‐Navas＆Gatenby，2017））。这些最新方法是生态学和进化科学迄今为止提出的将癌症从致死性疾病转变为慢性，可控制的病理学方法以来最具创新性和前途的方向。然而，肿瘤学家有时可能会在选择有时可以治愈患者的治疗方法和可能延缓病情但不能治愈患者的治疗方案之间面临两难选择。在本期特刊《 Hansen and Read（2020，本卷）研究了这个至关重要的问题，讨论了肿瘤动力学进化生态学的哪些方面应该确定尝试治愈还是控制耐药性更好。作者还强调指出，在针对抗性管理的进化策略出现之前，通常没有选择。由于情况不再如此，因此现在也必须调整我们向患者传达治疗方案的方式，这一点很重要。

在一个相关的主题上，还可以预测，减慢恶性肿瘤的进展而不是试图根除恶性细胞，可以是预防肿瘤生长，延长药物疗效并最终预防死亡的有效方法。Merlo等人使用酿酒酵母菌株作为模型系统。（在印刷中，该卷）研究了同时选择压力的应用如何成为减缓适应的有效选择。从治疗角度讨论了与癌细胞群体平行的问题。最后，Girard等人提出了一种基于进化论的新型癌症治疗策略。（2020年，本卷）。这种创新方法巧妙地利用了“烟雾探测器”原理的特性（内塞 2001）。通过向恶性细胞发送大量错误警报，该疗法在肿瘤细胞中诱导了新的“警报下降”状态，随后降低了它们对高“危险”信号做出响应的能力。

自5亿多年前多细胞性诞生以来，癌症不仅是全球人类死亡的主要原因，而且是一种影响所有多细胞生物的病理学（Aktipis和Nesse，  2013年））。结果，出现了比较肿瘤学领域，并促进了整个分类单元中癌症动态的比较，从而使人们对生物学，遗传和生态因素如何驱动癌症多样性，发病率和致死率中个体和物种变异的见解。物种间自然历史和生活史策略的差异会加剧癌症风险，并随之带动生物体中癌症防御系统的发展。迄今为止，比较肿瘤学研究主要集中在与“ Peto悖论”相关的过程和模式（癌症发病率与体型和寿命之间缺乏统计关系），这些仍然是我们对癌症流行病学，预防和改进疗法的理解的关键。动物和人类。在本期特刊中，Nunney（在印刷中，本册试图解决这一悖论，用一种建模方法测试了五个假设，一个是由于内在的代谢率/体重比例变化而来的，而四个是由于适应性进化而产生的。这项工作支持以下假设：只要癌症显着降低平均适应度，就主要通过募集额外的遗传控制层来调节癌症的发生率。关于相关主题，Erten和Kokko（2020本册介绍了“本体遗传学管理策略”的概念，以探索根据生物体靶向的成熟身体大小划分，分化和杀死体细胞的规则。通过这种方法，他们还探讨了如果在大型机体中实施，则在小型生物体中发展的策略的执行效果如何，反之亦然。

Rozhok和DeGregori（第二卷，本卷）提供了一个补充性的观点，认为致癌作用是由三个主要的正交过程决定的：一生中体细胞突变的积累，细胞遗传机器的物种特异性进化以及选择性微环境中生理老化引起的转变。在组织中。由于这三个过程是通过生命历史特征的演变相互联系的，因此它们在物种之间也存在很大差异。

尽管经常对大型长寿动物进行抗癌防御研究，但Thomas等人。（2020年，本卷）认为，还应该更多地关注驯养动物的研究。由于与驯化过程相关的不同原因，被驯化的物种通常显示出很高的癌症发生率，但是人工选择可能也有利于代偿性抗癌防御的发展。因此，驯养的动物将组成一个群体，在这些群体中可能会发现看似罕见的抗癌适应性和新颖的癌症治疗方法。遵循同样的想法，即新的治疗策略可以从野生和圈养动物用来对抗这种疾病的“秘密”中出现，Noble，Rohaj，Abegglen和Schiffman（第二册，本册）也为最有前途的动物提供了广泛的综合方法。源自癌症的治疗剂，特别是来源于昆虫，蜘蛛，两栖动物和海洋生物。对于每种化合物，

很大一部分癌症（全球范围内约15％至20％）是由诸如病毒，细菌和寄生虫之类的传染原引发和引起的（Dheilly，Ewald，Brindley，Fichorova和Thomas），2019年; Plummer等。，  2016）。这些病原体可以破坏控制细胞增殖，削弱免疫系统和/或引起慢性炎症的信号传导途径，从而增加罹患癌症的风险（Ewald＆Swain Ewald，2014）。由于病原体可以从一个人传播到另一个人，因此这些癌症提出了引人入胜的主题，供进化生物学家，疾病流行病学家和肿瘤学家研究。毫无疑问，该领域最近出现的主要创新方向之一是了解寄生虫，宿主微生物群和癌症动力学之间的相互作用（Dheilly et al。，  2019）。埃瓦尔德＆埃瓦尔德（印刷中，本卷）讨论了共生体可能通过寄生微生物和共生微生物之间的多种相互作用来提高针对癌症的免疫防御效力的想法。当宿主通过放松免疫学检查点而受到共生体影响时，宿主对肿瘤细胞发起逐步升级攻击的能力就会发生。

除了具有潜在病原体感染的恶性肿瘤外（Ewald＆Swain Ewald，2013年），癌症通常不会传染。但是，在野生环境中有九种明显的例外情况，其中克隆癌细胞系能够在个体之间传播：一种在狗中，两种在塔斯马尼亚恶魔中，六种在双壳类中（Ujvari等人，2017a ; Yonemitsu等人。 ，  2019）。可传播性癌症的研究已迅速获得发展，因为这些癌症是最引人入胜且未开发的宿主-病原体系统之一。尽管可传播的癌症是一种罕见的生命形式，但其生态后果可能是严重的，如顶级捕食者塔斯马尼亚恶魔（Sarcophilus harrisii）的戏剧性准根除所说明的那样。）。尽管人们对这些恶性肿瘤的兴趣日益浓厚，但仍需回答以下主要问题：为什么会出现可传播的癌症？它们如何演变？它们对生态和进化有何影响，以及如何对其进行管理/缓解？Dujon等。（2020年，本卷）提供了有趣的全球荟萃分析，涉及超过50年的关于可传播性癌症的多学科和国际合作。

在后生动物中，致癌过程是不可避免的现象。尽管它们在多细胞物种中无所不在，但迄今为止，生态学家和进化生物学家还是忽略了它们，以及它们在生态系统功能中的作用（Vittecoq等，  2013），或将它们视为宿主表型变异的“噪音”。在成为宿主死亡的直接原因之前，致癌过程可能会改变宿主的各种适应性相关特征，例如对天敌或病原体的脆弱性，其竞争能力和传播能力。越来越多的证据表明，恶性细胞参与与共生微生物和寄生虫的相互作用，从而间接导致三重相互作用的可能性（Thomas等人，  2017）。因此，未来的几年为生态学家和进化生物学家带来了令人兴奋的机会，他们最终考虑并接受了癌菌群作为全生命周期的关键参与者，从而发起并进行了理论和实证研究，这些研究对恶性肿瘤的生态和进化重要性采用了非常创新的观点。细胞。Hamede等人使用塔斯马尼亚恶魔和DFTD作为模型系统。（2020年，本卷）讨论了癌细胞作为选择因子的相关性，并提出了一个整体框架来理解野生生物中癌症的生态，流行病学和进化动力学之间的相互作用。使用建模方法，Perret，Gidoin，Ujvari，Thomas和Roche（2020，本卷）首次在生态系统层面探讨了癌症在物种相互作用中的作用，尤其是宿主与捕食者之间的相互作用，以及相互作用改变的结果如何反过来会影响抗癌机制的演变。第一个结论是，与捕食者相比，癌症对猎物种群的影响有限。生物相互作用也可能导致癌症对寄主种群密度的无效影响或积极影响，并改变捕食者种群的抵抗水平。预计人为影响（包括污染，气候变化，城市化）将在未来几十年急剧增加，因此可以预见，在不久的将来，癌症的风险以及在野外的癌症发病率也将显着增加（Giraudeau，Sepp ，Ujvari，Ewald和Thomas，2018）。因此，有必要特别是在长寿物种中探索针对肿瘤形成过程的保护机制和自然癌症防御机制的演变。Meitern等。（2020年，本卷）提出，鉴于海鸟的寿命和目前经常受到污染的栖息地，它们是有前途的模型。这项研究表明，从癌症易感性和在基因水平上抑制肿瘤的角度来看，老海鸥与年轻海鸥不同。

生态，进化和癌症这一主题比以往任何时候都面临着充满希望的挑战，不仅要预防和治疗癌症，而且要了解我们不断变化的世界中多细胞生物进化生态学的各个方面。我们希望本期专刊将提供对从肿瘤学家到生态学家的广大科学家有用的材料，并希望它能激发有关进化生物学和肿瘤学各个学科的新颖讨论。