EvidenceHER2-positive breast cancer

NCCN is the source of the category grades on the triple-negative breast cancer page and the first major guideline to place an antibody-drug conjugate first line for the disease.

Platinum and immunotherapy are now consensus for early triple-negative disease; the open votes have moved to who can safely receive less.

This is the European standard the UK page for triple-negative breast cancer is compared against; NICE guidance covers the same ground with a narrower set of funded drugs.

AI can take over one reader's work in double-reading screening programmes while finding more cancers. Whether the extra cancers found are ones that would have harmed women, and whether interval cancers fall, is the question the trial's primary endpoint will answer.

St Gallen is where de-escalation questions in triple-negative disease (who needs the full KEYNOTE-522 regimen, who can skip adjuvant pembrolizumab) are first put to a vote; the 2023 panel framed intensity and duration as the central problem.

For HER2-positive metastatic breast cancer that has progressed after trastuzumab and a taxane, trastuzumab deruxtecan is now the standard second-line treatment and T-DM1 has moved later in the sequence. The benefit is large enough that ADC design, not just the target, is understood to be what matters. Patients need lung monitoring because of the risk of pneumonitis.

The external validation the 2017 paper asked for; it is why residual cancer burden is reported in UK and European pathology and used as a trial entry criterion rather than an MD Anderson curiosity.

The document that made immunotherapy, PARP inhibition and the first antibody-drug conjugate the European standard for metastatic triple-negative disease; every later first-line change is an amendment to it.

HER2-positive breast cancer is now routinely treated before surgery so that the pathology result can guide what comes after: patients with no residual cancer continue trastuzumab (with or without pertuzumab), while those with residual disease switch to T-DM1. This model of using the tumour's response as a test has since been copied in triple-negative and other cancers.

Turned residual disease from yes or no into a graded score; RCB II and III are now the entry criteria for post-neoadjuvant trials (ASCENT-05, TROPION-Breast03) and the population the ctDNA-guided idea targets.

Scalp cooling works, especially for taxane-based regimens, and is safe. The question moved from whether to how to make it available: device time in the chemotherapy chair, staff training, and who pays.

The basis of the US accelerated approval pathway on pathological complete response that KEYNOTE-522 and neoadjuvant trials since have used, together with the warning that a higher response rate in a trial is a promise, not a proof, of longer life.

The denominator for US triple-negative disparity statistics and the origin of the 10 to 15 percent figure quoted for the subtype's share of breast cancer.

This paper extended the cancer stem cell concept from leukaemia to a common solid tumour and started the search for tumour-initiating cells across cancers. It underpins research on why cancers relapse after treatments that shrink them and on therapies aimed at the cells that regrow disease.

The first evidence that the basal-like group is not just biologically distinct but clinically dangerous, the observation that triple-negative outcome studies of 2007 confirmed in the clinic.

This was the first proof that a monoclonal antibody against a growth receptor could extend life in a common solid tumour, and it created HER2-positive breast cancer as a disease treated differently from the rest. Its cardiac finding shaped every later HER2 regimen, which pair trastuzumab with taxanes rather than anthracyclines.

The origin of the intrinsic subtypes and of the word basal-like; triple-negative breast cancer is the clinical shadow of this molecular group, though the two overlap imperfectly.

This study confirmed HER2 as a prognostic marker and a therapeutic target, showed that immunohistochemistry could identify the patients, and extended the target to ovarian cancer. It set up the clinical development of trastuzumab and the HER2 testing that every breast cancer now receives.

Every HER2 test, every trastuzumab prescription and the whole HER2-positive breast cancer category trace back to this observation. It is the model for how a genomic marker of bad prognosis became a drug target and then the basis for one of the largest survival gains in solid tumour oncology.