本书目由九章各自的文献表合并去重后按西文字母序编次，共 426 条；方括号内标出该条在哪几章被引用。各章原文献表仍保留在相应章末。
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[H1] Kirkwood MK, Schenkel C, Hinshaw DC, et al. State of geographic access to cancer treatment trials in the United States: are studies located where patients live? JCO Oncol Pract. 2025;21(3):427-437. doi:10.1200/OP.24.00261. 《子宫癌》专著 · HOW 篇第二篇（H2） 有信号而无纠错 子宫癌如何在预警中继续推进 信息科学、免疫学与传播学揭示“回执越界”如何制造“失籍靶态” 陈晓艳 典范式学术论文 · 2026 年 8 月 摘要 子宫内膜癌通常被描述为一种“容易发出预警”的恶性肿瘤：异常阴道出血尤其是绝经后 出血，使相当一部分患者在疾病局限于子宫时即进入诊疗。但“信号可见”并不等于“病变已 被纠正”。现实中可以出现一类表面矛盾的过程：症状已经出现，患者已经叙述，医务人员已 经接收，检查已经启动，结果甚至已经形成；然而疾病所处的真实状态仍未被直接核验，后来 出现的同类信号又沿用上一轮解释，最终使诊断或治疗继续延后。既有研究分别把这种现象解 释为灵敏度不足、异常结果漏随访、过早结案、责任分散、就医障碍或肿瘤免疫逃逸，却较少 追问：为什么一个局部有效的回应会在新的时刻、针对新的对象，继续拥有并不属于它的证明 力？ 本文限定于子宫体恶性肿瘤中的子宫内膜癌，建立由信息科学、肿瘤免疫学与传播学共同 约束的发生机制。信息科学区分信号送达、意义理解、行动启动与靶状态核验；免疫学表明识 别并非对固定对象的被动读取，识别压力会改变克隆构成、抗原呈递及未来可识别性；传播学 则说明一次解释如何通过共同接受、叙事压缩和制度记录获得跨情境的持续效力。在此基础上， 本文区分机制与产物。机制是“回执越界”：一个在局部层级上真实、合法的回执——例如 “已收到”“已解释”“已安排”“一次取样未见恶性”——被跨越其证明对象或有效时段， 继承为“病灶状态已经改变或仍然不变”的证据，并改变后续信号的采样、显影、描述或升级。 其产物是“失籍靶态”：新信号已经使疾病状态重新成为当前未决问题，当前状态也尚未获得 相称核验，但这个未决对象既没有在可驱动行动的信息环境中被重新建立，也没有在医患共同 叙事中作为一个活问题存在；它的缺席可追溯到旧回执的继承。回执越界回答错误怎样发生， 失籍靶态则指出发生后多出了什么。后者不是不确定性、未办任务或过时诊断的别名，因为不 确定性可以被明确登记，任务可以全部完成，旧诊断甚至仍可正确；这里消失的是新事件所要 求的“待证对象”本身。 本文以公开队列作计算前锁定规则的检验。Visser 等对绝经后出血患者的长期随访显示， 在初始活检结果被认为较为 reassuring 的人群中，单纯性内膜增生无不典型者后来发生子宫 内膜癌的风险为 2/14，良性组织学者为 4/224，风险比为 8.00（95% CI 1.60—39.99； Fisher 双侧 P=0.042）；所有随访期癌症均以复发性绝经后出血再次出现。与此同时，初次 样本不足组在该队列随访中没有发生癌症；另一多中心队列还显示，复发性绝经后出血虽常见， 却并不等于更高恶性比例。两项逆风结果共同否定“检查不完整必然危险”与“复发必然意味 着癌症推进”，把经验命题压缩为：新信号是否重新生成一个可见、可核验的待证靶态，比 “有没有结果”或“是否复发”更关键。本文据此给出机制—产物双判据、二轴事件矩阵、事 件级数据字典、三臂反事实试验与撤回条件。关键干预不止是给旧结果附加“证明范围—有效 期—再开启触发器”，还要在触发器出现时重新实例化当前未决靶态。研究旨在解释预警为何 会在已回应状态下失去纠错力，不提供个体诊疗建议，也不把所有阴性结果、临床安慰或复发 症状视为错误或癌症。 关键词： 子宫内膜癌；异常子宫出血；信号；免疫编辑；临床传播；诊断安全；回执越界； 失籍靶态 Signal without Correction: How Uterine Cancer Can Progress amid Warning How Information Science, Tumor Immunology, and Communication Studies Explain the Production of a “De-registered Target State” CHEN Xiaoyan Abstract Endometrial cancer is commonly regarded as a malignancy that announces itself. Abnormal vaginal bleeding, particularly postmenopausal bleeding, often brings patients to care while disease remains confined to the uterus. Yet signal visibility is not equivalent to correction of the underlying lesion. A symptom may be reported, received, interpreted, investigated, and documented while the target disease state remains unverified. When a similar signal recurs, the prior response may be reused as evidence that the underlying state has already been settled. Existing accounts distribute this problem across low test sensitivity, failure to follow up abnormal results, premature closure, diffusion of responsibility, access barriers, or immune escape. They seldom identify the event through which a locally valid response acquires evidentiary authority beyond the object and time it can actually prove. This article develops a process account restricted primarily to endometrial carcinoma of the uterine corpus. Information science separates message delivery, interpretation, action initiation, and verification of target-state change. Tumor immunology demonstrates that recognition is not a passive reading of a stable source: immune pressure can reshape clonal composition, antigen presentation, and future detectability. Communication studies explain how a provisional interpretation becomes jointly accepted, compressed into a durable narrative, and inherited across encounters. Their joint implication has two levels. Receipt overreach is the generating mechanism: a locally truthful and procedurally legitimate receipt—“received,” “understood,” “ordered,” or “no malignancy in this sample”—is inherited across proof layers or validity intervals as if it demonstrated that the lesion itself had changed or remained unchanged. A de- registered target state is the resulting object: a new signal has made the disease state currently unresolved, yet no active representation of that unresolved state exists either in an action-capable information environment or in the shared clinical narrative, and this absence is causally traceable to the inherited prior receipt. The mechanism explains how the failure is produced; the object specifies what newly comes into existence. It is not synonymous with uncertainty, an unfinished task, or an outdated diagnosis: uncertainty may be explicitly represented, every task may be complete, and the old diagnosis may remain locally correct, while the target-state question demanded by the new event has disappeared. A calculation with decision rules locked before inspecting the published cell counts yielded a risk ratio of 8.00 (95% CI 1.60–39.99; two-sided Fisher P=0.042) for subsequent endometrial cancer after hyperplasia without atypia versus benign
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December 2019. https://www.fda.gov/regulatory-information/search-fda-guidance-documents/adaptive-design- clinical-trials-drugs-and-biologics-guidance-industry. 《子宫癌》专著 · WHY 篇第三篇（Y3） 风险不等于罪责 为何“得子宫癌”不能归结为个人生活方式 哲学、生态学与政治学如何分开病因、路径与责任 陈晓艳 学术论文 · 2026 年 8 月 摘要 肥胖、成人期体重增加及代谢异常与部分子宫内膜癌风险相关，应被准确告知并用于可获 得、非污名化的风险管理；但“增加风险”不能自动推出“患者因未管理好自己而患癌”。二 者之间至少横跨病因贡献、路径维持、控制能力、角色责任与道德责备五种关系。本文以子宫 体恶性肿瘤为对象，以子宫内膜癌为主轴、子宫肉瘤为边界，提出两个待检验概念。失权近因 不是体重等近端因素的新名称，而是一种事件关系：与拟议归责相匹配的个人选项已经关闭、 具名上游行为者的同路径选项仍然开放，身体近端状态却在这一“失权窗”内进入高代价区。 归责倒序则发生在事后评价仍把控制资格登记在患者名下，仅按身体近距回溯罪责之时。本文 的新对象因而不是一般意义上的“选择受限”，而是因果位置向身体靠近、可执行控制向上游 移位、归责记录却没有同步更新的三向错位事件。 本文以哲学的控制史、生态学的尺度反馈和政治学的权力配置建立三条不可互换的动力， 并与道德运气、充分—组分原因、受限选择、任务责任—责备责任、过度责任化、道德溃缩区、 多人之手、责任缺口、基本原因、生态社会理论、健康主义、结构性暴力、健康污名及商业健 康决定因素正面对照。最接近的“受限选择”已说明选择如何受限，道德溃缩区也已说明责任 为何会落到控制有限的近端人身上；本文仅在个人选项关闭与上游选项开放产生交互效应，而 非仅产生“个人受限”的主效应时具有独立解释力。 成文前冻结并运行了一项公开数据压力测试：以美国 50 州及哥伦比亚特区的 CDC 子宫 体及未特指子宫癌女性年龄标化发病率、女性肥胖率和公园可及性，检验州级肥胖率能否垄断 地理分布解释。2018—2022 年模型的肥胖系数为 −0.186，R²=0.061，10,000 次 bootstrap 的 R² 95%区间为 0.000—0.332；加入公园可及性仅增加 0.00012 的 R²，两项预注册判据均 未通过。结果既不否认肥胖的个体风险，也未证实环境机制；既往子宫切除率校正研究还提示 常规州级率存在分母偏差。现有资料缺少个人可行选项与上游权限字段，故不能确证失权近因。 本文将承重判断收紧为可证伪规则：讨论个案罪责前，必须回答风险路径首次进入高代价区时， 个人与各上游行为者各自还保有哪一个当时可执行的选项。 关键词： 子宫内膜癌；个人责任；失权近因；失权窗；归责倒序；政策反馈 Risk Is Not Blame: Why Developing Uterine Cancer Cannot Be Reduced to Personal Lifestyle How Philosophy, Ecology, and Political Science Separate Etiology, Pathway, and Responsibility CHEN Xiaoyan Abstract Obesity, adult weight gain, and metabolic conditions are associated with the risk of some endometrial cancers. These findings should inform accessible, non- stigmatizing prevention and survivorship care. They do not, however, establish that a patient developed cancer because she failed to manage herself. That inference collapses five distinct relations: etiologic contribution, maintenance of a risk pathway, control capacity, role responsibility, and moral blame. Focusing on malignancies of the uterine corpus, with endometrial carcinoma as the main case and uterine sarcoma as a boundary condition, this article proposes two falsifiable concepts. A disempowered proximate cause is not a new label for obesity or another bodily factor. It is an event relation in which the patient’s feasible option over a specified pathway has closed, a named upstream actor’s functionally equivalent option over that pathway remains open, and the etiologically relevant bodily state enters a high-cost region during this disempowerment window. Reversed attribution occurs when later evaluation continues to register control with the patient and assigns blame by bodily proximity while omitting the chronology of option control. The proposed object is therefore a three-way misalignment: causation moves bodily downstream, executable control is located upstream, and attribution fails to update. Three dynamics are developed. Philosophically, tension between an outcome and an attribution path changes the responsibility framework, which feeds back into what evidence is recorded and what action is demanded. Ecologically, tension between an exposure pathway and organism–environment conditions changes disease distributions and subsequent exposures. Politically, tension between disease distributions and prevention arrangements reallocates resources and responsibility, thereby reshaping individual options. The proposal is tested against moral luck, sufficient-component causation, constrained choice, task versus blame responsibility, over-responsibilization, moral crumple zones, the problem of many hands, responsibility gaps, fundamental-cause theory, ecosocial theory, social- ecological models, healthism, structural violence, stigma frameworks, and commercial determinants of health. The proposal remains distinct only if a factorial test finds an interaction between closure of the patient’s option and retention of an upstream option: a main effect of constraint alone would leave constrained-choice theory sufficient. A preregistered public-data stress test examined whether state-level female obesity prevalence could monopolize the explanation of geographic variation in US uterine corpus cancer incidence. Across 50 states and the District of Columbia, the model for mean 2018–2022 age-adjusted incidence yielded an obesity coefficient of −0.186 and R²=0.061; the bootstrap 95% interval for R² was 0.000–0.332. Adding park proximity increased R² by only 0.00012. Neither preregistered criterion passed. These ecological results neither negate individual-level obesity risk nor confirm an environmental mechanism. Prior work on hysterectomy correction instead highlights denominator bias in conventional state rates. Because existing registries lack event-level fields for feasible options and upstream authority, the central mechanism remains unconfirmed. The resulting evidentiary rule is deliberately narrow: before attributing blame in an individual case, identify which executable option remained with the person and with each upstream actor when the pathway first entered a high-cost state.
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