Leukemia Cutis at an Excision Site

> Research explainer: This briefing examines verified primary research published 61 days before the briefing date. It is not a same-day research update and does not provide medical advice.

Evidence

The report describes a 69-year-old man with a history of keratinocyte carcinomas who had a 7-mm keratotic papule on the inner left thigh excised. Histopathology identified keratoacanthoma with clear margins. Approximately two months later, he returned with two progressively enlarging lesions at the excision site. They had enlarged over the preceding two to three weeks. Examination documented two red, indurated plaques measuring 5 cm and 3 cm; the biopsy scar crossed the larger plaque. The patient denied systemic symptoms reported in the case, including fever, chills, fatigue, night sweats, weight change, and shortness of breath. [pmid:42368379]

Punch-biopsy histopathology showed cutaneous involvement by acute myeloid leukemia (AML) with monocytic differentiation, consistent with leukemia cutis. Subsequent work-up showed systemic AML. The report states that peripheral blood and marrow assessments confirmed AML with an NPM1 mutation and monocytic differentiation. It also describes a white blood cell count of 31.8 K/μL with 17% blasts and a monocytic population comprising approximately 30% of peripheral-blood flow-cytometry events. These laboratory details belong to this individual case and do not describe a broader patient population. [pmid:42368379]

The authors report that the patient received AML-directed induction chemotherapy followed by bone marrow transplantation. The skin lesions resolved with treatment. A post-transplant marrow biopsy showed complete remission with undetectable NPM1 measurable residual disease. At day 139 after transplantation, the patient was clinically well and had no evidence of relapse. These outcomes document the course reported for this patient; they do not establish expected outcomes for other people with AML or leukemia cutis. [pmid:42368379]

Analysis — Interpreting a Koebner-Like Pattern

The notable research question is localization: leukemia cutis appeared where a keratoacanthoma had been excised. The authors characterize that distribution as consistent with a Koebner-like response, a term used here for disease localization at prior cutaneous trauma. Their discussion presents trauma- or stress-related increases in chemokine receptors and adhesion molecules as a possible route by which leukemic cells could home to and accumulate at an affected site. It also raises the possibility that the prior tumor and excision created a localized immunocompromised cutaneous district, sometimes termed a locus minoris resistentiae. [pmid:42368379]

Those mechanisms should be read as hypotheses, not as demonstrated causes in this case. The report explicitly says that it is uncertain whether subclinical leukemic cells were already present at the original excision site. That uncertainty prevents a definitive causal conclusion that trauma produced leukemic infiltration. Likewise, discussion of impaired antigen presentation, T-cell exhaustion, and altered extramedullary immune conditions provides a biologic framework but does not show that any one mechanism caused these plaques in this person. [pmid:42368379]

The case has an additional diagnostic framing. It occurred in a person without an established leukemia diagnosis, and the skin finding led to systemic AML staging. The authors describe this as the first reported case, to their knowledge, of leukemia cutis arising at a prior biopsy site as the initial manifestation of AML. That statement is an authorial assessment of the published literature, rather than evidence of how often this presentation occurs. The article also notes that prior reported trauma-site cases involved patients already diagnosed with leukemia. [pmid:42368379]

For a dermatology research audience, the report illustrates why lesion location alone is not a diagnosis. The plaques developed at a scar after an excision that had been pathologically cleared as keratoacanthoma, yet biopsy identified a distinct hematologic process. The source frames histopathological evaluation of new infiltrative plaques at prior trauma or biopsy sites as a clinical consideration, including when hematologic malignancy is not known. This is a description of the authors’ conclusion, not a patient-specific instruction or a basis for inferring leukemia from any scar-associated lesion. [pmid:42368379]

Limitations

This source is a single case report. It cannot estimate the frequency of leukemia cutis at trauma or biopsy sites, quantify risk, establish causation, or support general population conclusions. The patient’s AML had monocytic differentiation and an NPM1 mutation, but one case cannot determine whether those features explain the skin distribution or predict similar presentations. [pmid:42368379]

The temporal sequence—excision followed by plaques about two months later—supports the observation of co-localization, not proof that the excision caused infiltration. The authors specifically identify the unresolved possibility of pre-existing subclinical leukemic cells at the site. Proposed contributions from trauma-induced signaling, local immune dysregulation, impaired antigen presentation, and T-cell exhaustion therefore remain possible explanations. [pmid:42368379]

Finally, lesion resolution, remission, and no relapse at day 139 are short, case-specific follow-up observations. They should not be treated as a prediction of treatment response, prognosis, recurrence, or management for other cases. [pmid:42368379]