Imiquimod in the Treatment of Breast Cancer Skin Metastasis

Imiquimod in dermatology: an overview

“…Although cutaneous metastases have a poor prognosis, its treatment may be beneficial for palliation. Several reports have described some benefit from the off‐label use of topical imiquimod as alternative to surgery and as adjunctive modality after surgical excision, alone or in combination with other systemic treatments, in the management of cutaneous metastases from different origins including melanoma and breast and renal cancer …”

“…Several reports have described some benefit from the off-label use of topical imiquimod as alternative to surgery and as adjunctive modality after surgical excision, alone or in combination with other systemic treatments, in the management of cutaneous metastases from different origins including melanoma and breast and renal cancer. [129][130][131][132][133][134] Other neoplastic entities Anecdotal reports have also described topical imiquimod's potential in the treatment of other cutaneous and mucosal precancerous and cancerous lesions such as solar cheilosis, 135,136 oral leukoplakia, 137 genital/vulval intraepithelial neoplasia, 138,139 and verrucous carcinoma. 140…”

An unexpected metastasis of breast cancer mimicking wheal rush

“…Many cases in the literature were pigmented metastases (melanoma) or damage -like "orange peel" (7). Skin metastases are a source of pain for the patient (intensity 8/10) and a cause of emotional depression (9). It is always required a skin biopsy for the diagnosis.…”

“…It is always required a skin biopsy for the diagnosis. The treatment includes cryotherapy, radiotherapy and chemotherapy, but the prognosis is usually poor (9,10).…”

Trial Watch: Immunotherapy plus radiation therapy for oncological indications

“…In addition, the safety and efficacy of EBRT combined with immunotherapy is being assessed in the context of (1) adoptive cell transfer, 87,212 in colorectal cancer patients receiving autologous DCs plus cytokine induced killer (CIK) cells along with FOLFOX (folinic acid plus 5-fluoruracil plus oxaliplatin) chemotherapy (NCT02202928), sarcoma patients treated with autologous CD8 C cytotoxic T lymphocytes (CTLs) genetically modified to recognize the TAA NY-ESO-1 (NCT02319824), and hepatocellular carcinoma patients receiving highly purified autologous CD8 C CTLs (NCT02678013); (2) TLR stimulation, 94 in soft tissue sarcoma patients receiving the experimental TLR4 agonist glucopyranosyl lipid adjuvant in stable emulsion (GLA-SE) 213,214 (NCT02180698), lymphoma patients concurrently administered with the experimental TLR9 agonist SD-101 215,216 (NCT02266147), and melanoma patients co-treated with the FDA-approved TLR7 agonist imiquimod [217][218][219][220][221] (NCT02394132); and (3) relatively unspecific immunostimulation with recombinant IL-2 or GM-CSF in patients with renal cell carcinoma (NCT02306954), glioblastoma (NCT02 663440), and NSCLC (NCT02735850), with thymalfasin (a recombinant version of the human T H 1-skewing peptide thymosin a1) 222 in colorectal cancer patients (NCT02535988), lung cancer patients (NCT02542137, NCT02542930), and esophageal cancer patients (NCT02545751), with TAM-targeting agents like trabectedin [223][224][225] or zoledronic acid 128,226 in subjects with soft tissue sarcoma (NCT02275286) or metastatic NSCLC (NCT02480634), with a chemical inhibitor of IDO1 (i.e., indoximod) 196,227 in children with brain tumors concurrently receiving temozolomidebased chemotherapy (NCT02502708), with chemical inhibitors of the TGFb1 receptor [228][229][230] in breast carcinoma patients (NCT025 38471) and rectal carcinoma patients concurrently treated with standard-of-care chemotherapy (NCT026887129), and with celecoxib, an inhibitor of the immunosuppressive enzyme prostaglandin-endoperoxide synthase 2 (PTGS2; best known as COX2), 231,232 in HNSCC patients (NCT02739204) ( Table 2).…”