Mucin 1 (MUC1) is a diagnostic factor and therapy target in lung adenocarcinoma. MUC1 C-terminal intracellular domain (CD) interacts with estrogen receptor α (ERα) and increases gene transcription in breast cancer cells. Because lung adenocarcinoma cells express functional ERα and estrogen receptor β (ERβ) we examined MUC1 expression and MUC1-ER interaction. Since blocking MUC1 CD with an inhibitory peptide (PMIP) inhibited breast tumor growth, we tested whether PMIP would inhibit lung adenocarcinoma cell proliferation. We report that MUC1 interacts with ERα and ERβ within the nucleus of H1793 lung adenocarcinoma cells in accordance with MUC1 expression. PMIP was taken up by H23 and H1793 cells and inhibited the proliferation of H1793, but not H23 cells, concordant with higher MUC1 in H1793 cells. Lower MUC1 protein in H23 does not correspond to miR-125b and miR-145 that have been reported to reduce MUC1 expression. PMIP had no effect on the viability of normal human bronchial epithelial cells, which lack MUC1 expression. PMIP inhibited estradiol (E2) –activated reporter gene transcription and endogenous cyclin D1 and nuclear respiratory factor-1 (NRF-1) gene transcription in H1793 cells. These results indicate MUC1-ER functional interaction in lung adenocarcinoma cells and that inhibiting MUC1 inhibits lung adenocarcinoma cell viability.

Angioinvasive (type E) lymphomatoid papulosis (LyP) is a recently described subtype of LyP presenting with eschar-like lesions that can be mistaken for aggressive forms of angiocentric cutaneous T-cell lymphoma. None of the cases of angioinvasive LyP described thus far have been associated with mycosis fungoides (MF). Herein, we describe a case of angioinvasive LyP type E coexisting with MF. The patient presented with an eschar on his chest and over time developed new nodules and large plaques with eschar formation, all of which resolved spontaneously over a period of a few weeks without intentional therapy. Biopsy revealed a CD30+ atypical inflammatory cell infiltrate with marked angiocentricity. Later, he developed erythematous annular scaly patches histologically consistent with MF. Our patient's clinical course confirms the indolent behavior characteristic of LyP despite the aggressive clinical and histologic appearance of lesions. The co-occurrence of angioinvasive LyP and MF in our patient highlights the propensity for LyP type E to coexist with MF, as is characteristic of other LyP subtypes, and supports the theory that LyP and MF are related T-cell lymphoproliferative disorders. Patients with LyP can present with large lesions exhibiting eschar formation and an atypical angiocentric/angiodestructive lymphoid infiltrate and should be spared overtreatment.

dermis while minimizing irradiation of deeper tissue. Despite the potential benefit of symptom relief and improved quality of life, the use of ionizing radiation for ACH should be carefully balanced against the long-term risk of cancer at the site of administration, particularly in younger patients. 6 To our knowledge, this is the first case of ACH successfully treated with HDR brachytherapy. Further investigations using larger patient cohorts are needed to determine the reproducibility of our findings.

Trichosporon mycotoxinivorans was commonly used in various textile, agriculture, cosmetic, and pharmaceutical industries for its ability to detoxify mycotoxins such as ochratoxin A and zearalenone. In recent years, it has been isolated as a respiratory pathogen causing pneumonia in some cases of cystic fibrosis, but to our knowledge, a cutaneous manifestation has not been previously described. 6 We could not establish a route of exposure in our patient. Azoles have proven to be the most effective treatment options for other Trichosporon infections. 1-5 Our patient showed significant improvement of skin lesions with voriconazole.

Monoclonal antibodies against PD-1 are becoming increasingly important agents in the oncologist's armamentarium against a variety of cancers, including melanoma and squamous cell carcinoma. Most reported cutaneous reactions to these agents are mild and resolve with a conservative treatment approach. We present two cases of patients treated with anti-PD-1 agents who developed bullous pemphigoid shortly after initiation of therapy. We then review the literature of anti-PD-1-associated bullous pemphigoid, which is likely a bona fide side effect of anti-PD-1 therapy. Finally, we discuss management of these cases, where the risks of bullous pemphigoid must be weighed against the benefits of anti-PD-1 treatment. As the number of indications for PD-1 monoclonal antibodies expands, dermatologists will need to recognize their cutaneous adverse events and assist oncologists in the management of such complications.