Contents — Breast Cancer

Part I · Foundations and the global landscape

Two centuries of being confidently wrong about where breast cancer goes and why. Each idea is read for the error it corrected and the one it introduced.

Part II · Normal biology, carcinogenesis, and inherited susceptibility

What the normal breast does, and how much of it a tumor keeps. Precursor states come before any malignant biology, because that is the order the tissue works in.

Part III · Pathology and classification

Every taxonomy in this field was built for a purpose. The useful question is not whether a classification is true but what it was built to decide.

Part IV · Molecular biology and therapeutic vulnerabilities

Organized by pathway rather than by drug. Each chapter closes on the resistance mechanisms that the metastatic chapters will have to act on.

Part V · Immunology and the tumor microenvironment

Compartments first, then function, then spatial arrangement, then the host. Checkpoints arrive late here on purpose.

Part VI · Heterogeneity, evolution, and metastatic biology

The core of the book. It sits before the treatment chapters so that all of them can assume it, and every chapter in it separates what is biology from what is measurement.

Part VII · Detection, diagnosis, and biomarker assessment

Every assay here is a sampling procedure. What it measures, what it stands in for, and how far apart those two can drift.

Part VIII · Therapeutic foundations

Modality and drug class, carried once and in full. The disease chapters cite this part instead of repeating it, which is what keeps them short.

Part IX · Early-stage disease: in situ, locally advanced, residual, and the neoadjuvant platform

Setting-level chapters. What to do about a lesion that may not need treating, about disease that presents late, about a blood test that finds disease no scan can, and about the neoadjuvant window as an experiment rather than a schedule.

Part X · Metastatic disease: principles and cross-cutting management

What holds across every subtype once the disease is incurable. Goals, burden, and the organ-specific problems that do not sort by receptor.

Part XI · Hormone receptor-positive, HER2-negative disease

The commonest subtype, read end to end rather than twice. Endocrine dependence is the thread the whole part pulls on: what establishes it, what sustains it, how it fails, and what is left when it has. The synopsis states the spine; the chapters argue it.

Part XII · HER2-positive disease

One target and two decades of drugs against it. This is the subtype whose neoadjuvant platform taught the rest of the field how to de-escalate, and the only one where a second receptor changes the question rather than the dose. Triple-positive disease sits here.

Part XIII · Triple-negative disease

A subtype named for what it lacks, which is why its treatment history is the history of finding something to aim at. Chemotherapy, then the immune microenvironment, then the antigens a conjugate can reach.

Part XIV · Special populations and uncommon presentations

The patients trials enroll least and clinics see often enough. Extrapolation is the default here, so each chapter says how far it is being stretched.

Part XV · Supportive care, survivorship, and patient experience

A full part rather than an appendix. Most of what a patient actually lives with sits here.

Part XVI · Disparities, access, and health systems

Biology and access are separated at every step, and race is not allowed to stand in for either.

Part XVII · Research methods, evidence, and emerging therapy

The part that will age fastest. Organized by mechanism rather than by agent, so that a new drug does not require a new chapter.