Prevention and Early Detection Take Center Stage at NP/PA Connect Cutaneous Oncology Workshop

Prevention and early detection opened the educational programming at the inaugural Dermatology Times Cutaneous Oncology Workshop: Empowering Advanced Practice Providers in Cutaneous Oncology, held September 12 in Tampa, Florida.

Across sessions on photoprotection, actinic keratoses (AKs), hereditary skin cancer syndromes, and dermoscopy, faculty emphasized practical strategies advanced practice providers (APPs) can use to identify risk earlier, counsel patients more effectively, and determine when further evaluation or biopsy is warranted. The morning program featured Amit Om, MD, FACMS; Tristan Hasbargen, PA-C; and Amy Spizuoco, DO, FAOCD.

What Works and What Remains Uncertain in Photoprotection

Om, a board-certified dermatologist and fellowship-trained Mohs surgeon with Dermatology Group of the Carolinas, opened with an examination of established and emerging approaches to photoprotection.

Among the most significant recent developments is the addition of bemotrizinol, also known as BEMT or Tinosorb, to the US sunscreen landscape. In June 2026, the FDA permitted bemotrizinol at concentrations of up to 6%, marking the first expansion of permitted sunscreen active ingredients in approximately 2 decades.

Om noted that the ingredient has been available internationally for years and reviewed data supporting its efficacy and low systemic absorption under maximal-use conditions. Studies presented during the session showed SPF benefits across formulations, while the geometric mean maximum concentration of BEMT remained below the FDA's 0.5-ng/mL threshold.

For clinicians fielding patient concerns about sunscreen absorption, however, Om emphasized keeping the larger clinical picture in perspective.

“Sunscreen is good. Period. We know that it prevents skin cancer,” Om said.

Patients who remain concerned about chemical sunscreen ingredients can be directed toward mineral formulations containing zinc oxide or titanium dioxide, he added.

The discussion also explored products and technologies increasingly marketed as supplemental photoprotection. Studies of sunscreens containing DNA-repairing enzymes have demonstrated reductions in UV-associated damage markers, but Om cautioned that evidence demonstrating a corresponding reduction in skin cancer remains limited.

A similar distinction emerged with oral Polypodium leucotomos. Clinical studies presented during the session demonstrated increases in minimal erythema dose and reductions in UV-induced erythema, but Om stressed that supplements should not be viewed as substitutes for sunscreen.

Photobiomodulation, including red-light therapy, also has emerging evidence showing effects on UV-induced cellular damage and photodamage markers. However, much of the evidence remains preclinical, and the available data do not establish red light as a skin cancer prevention strategy.

Om also addressed sunless tanners, noting that although they can provide cosmetic color without intentional UV exposure, they should not be mistaken for meaningful sun protection.

Ultimately, he returned to familiar interventions: adequate sunscreen application, protective clothing, shade, and avoiding peak UV exposure. Om said he often favors UPF clothing because it removes 2 common barriers to sunscreen efficacy, inadequate application and failure to reapply.

For sunscreen, he recommended at least SPF 30 and reminded attendees that approximately a shot glass–sized amount is needed to cover the entire body.

Treating the Field, Not Just the Visible AK

Om then shifted from primary prevention to AKs, emphasizing that the lesions clinicians see represent only part of the damage produced by chronic UV exposure.

AKs commonly develop after years of cumulative sun exposure and occur most frequently on areas including the face, scalp, ears, lips, forearms, and dorsal hands. Although the probability that any individual lesion will progress to invasive squamous cell carcinoma (SCC) varies considerably, the slides highlighted that adjacent AKs have been identified histologically in more than 60% of SCC cases.

That risk underpins the concept of field cancerization.

Chronic UV exposure produces genetic and epigenetic alterations throughout an area of sun-damaged skin, meaning a visible AK may be surrounded by subclinical abnormal keratinocytes. Treating only what can be seen can therefore leave the broader cancerized field unaddressed.

Treatment selection should account for lesion burden, efficacy, tolerability, cost, treatment burden, and patient preference. Lesion-directed approaches such as cryosurgery may be appropriate for isolated AKs, whereas field-directed options include topical 5-fluorouracil, imiquimod, diclofenac, photodynamic therapy, and chemical peels.

The effectiveness of those therapies, Om emphasized, also depends heavily on counseling and adherence.

Patients should understand what erythema, crusting, and other expected local reactions may look like before treatment begins. The session recommended using photographs to establish expectations, simplifying regimens when possible, and explaining why treatment matters rather than providing instructions alone.

In particular, clinicians were encouraged to frame field therapy as cancer prevention rather than cosmetic treatment and connect AK management with the patient's future SCC risk.

Recognizing the Patient Who May Have Hereditary Risk

Hasbargen, of Dermatology Associates of Tallahassee, next challenged attendees to consider when an unusual skin cancer presentation may be signaling something beyond cumulative UV exposure.

Most skin cancers are sporadic. However, several characteristics should raise suspicion for a hereditary predisposition, including disease arising in childhood or early adulthood, multiple primary tumors, cancers developing on non–sun-exposed skin, a tumor burden disproportionate to UV exposure, or clustering of cutaneous and noncutaneous cancers within a family.

Hasbargen reviewed several syndromes in which dermatologic findings may provide an early clue to broader systemic risk.

In familial atypical multiple mole melanoma (FAMMM) syndrome, numerous and often atypical nevi and a family history of melanoma can signal an underlying CDKN2A mutation. The mutation is also associated with increased pancreatic cancer risk, making recognition relevant well beyond dermatologic surveillance.

Hasbargen described using photography and longitudinal monitoring in patients with extensive atypical nevi to help identify evolving lesions while also limiting unnecessary procedures in patients experiencing biopsy or surgical fatigue.

He also discussed Gorlin syndrome, or nevoid basal cell carcinoma syndrome, in which patients can develop numerous basal cell carcinomas at unusually young ages. Other clues include palmoplantar pits and jaw keratocysts. The condition is most commonly associated with PTCH1 mutations and follows an autosomal dominant inheritance pattern.

Additional conditions reviewed included epidermodysplasia verruciformis, xeroderma pigmentosum, BAP1 tumor predisposition syndrome, and Muir-Torre syndrome. Their manifestations vary, but the overarching message remained consistent: the skin can be the first visible indication of cancer susceptibility elsewhere in the body.

The session's key takeaways emphasized age, tumor count, and tumor location as important triggers for suspicion. Once a hereditary syndrome is identified, dermatology remains involved through risk-based surveillance, photoprotection counseling, and coordination with specialties including gastroenterology, ophthalmology, neurology, urology, oncology, and genetics.

Dermoscopy Should Support, Not Override, Clinical Judgment

Spizuoco, a board-certified dermatologist and dermatopathologist at True Dermatology, closed the block with a practical approach to differentiating benign and malignant lesions using dermoscopy.

Her first message was particularly straightforward: dermoscopy can strengthen clinical decision-making, but it should not persuade a clinician against biopsy when a lesion is already concerning.

“It’s never meant to talk you out of a biopsy,” Spizuoco said.

She recommended beginning with a 3-point checklist evaluating asymmetry of color and structure, an atypical pigment network, and blue-white structures before examining disease-specific vascular, pigment, and keratin patterns.

For basal cell carcinoma (BCC), important dermoscopic clues include arborizing vessels, blue ovoid nests, maple-leaf and spoke-wheel structures, blue-gray dots and globules, ulceration, and shiny white streaks. A particularly useful discriminator in pigmented BCC is the absence of a true pigment network.

Spizuoco contrasted these findings with benign mimickers. Sebaceous hyperplasia, for example, typically demonstrates crown vessels that radiate around rather than cross the center of a lesion, whereas dermatofibromas commonly demonstrate a central white scar-like area and delicate peripheral pigment network.

For SCC, she highlighted glomerular or coiled vessels, white and brown circles, rosettes, yellow scale, and a strawberry pattern. Increasing architectural disorder, keratinization, suspicious vascular morphology, rapid growth, tenderness, or ulceration should progressively lower the threshold for biopsy as lesions move along the AK–SCC in situ–invasive SCC spectrum.

The session ultimately reinforced a theme that connected all 4 morning presentations: prevention and early detection depend not on a single tool, but on recognizing risk in context. From counseling patients on what actually constitutes effective photoprotection to identifying a hereditary cancer syndrome or recognizing a subtle malignant pattern under dermoscopy, APPs are positioned to intervene well before advanced disease develops.

References

1. U.S. Food and Drug Administration. (2026, June 9). FDA expands sunscreen options for first time in 20 years. https://www.fda.gov/news-events/press-announcements/fda-expands-sunscreen-options-first-time-20-years
2. Nestor, M. S., Berman, B., & Swenson, N. (2015). Safety and efficacy of oral Polypodium leucotomos extract in healthy adult subjects. Journal of Clinical and Aesthetic Dermatology, 8(2), 19–23. https://pubmed.ncbi.nlm.nih.gov/25741399/
3. Eisen, D. B., et al. (2021). Guidelines of care for the management of actinic keratosis. Journal of the American Academy of Dermatology, 85(4), e209–e233. https://pubmed.ncbi.nlm.nih.gov/35439607/
4. Soura, E., Eliades, P. J., Shannon, K., Stratigos, A. J., & Tsao, H. (2016). Hereditary melanoma: Update on syndromes and management—Genetics of familial atypical multiple mole melanoma syndrome. Journal of the American Academy of Dermatology, 74(3), 395–407. https://pubmed.ncbi.nlm.nih.gov/26892650/
5. Onodera, S., Nakamura, Y., & Azuma, T. (2020). Gorlin syndrome: Recent advances in genetic testing and molecular and cellular biological research. International Journal of Molecular Sciences, 21(20), 7559. https://pubmed.ncbi.nlm.nih.gov/33066274/
6. Lallas, A., Apalla, Z., Argenziano, G., et al. (2014). The dermatoscopic universe of basal cell carcinoma. Dermatology Practical & Conceptual, 4(3), 11–24. https://pubmed.ncbi.nlm.nih.gov/25126452/
7. Rosendahl, C., Cameron, A., Argenziano, G., et al. (2012). Dermoscopy of squamous cell carcinoma and keratoacanthoma. Archives of Dermatology, 148(12), 1386–1392. https://pubmed.ncbi.nlm.nih.gov/22986634/