The review, led by Julia Yescas and colleagues at Northwestern University Feinberg School of Medicine, together with collaborators at Yale, Case Western Reserve, and MD Anderson Cancer Center, examines how aggressive cutaneous T-cell lymphomas become addicted to dysregulated kinase signaling and how that addiction becomes both a therapeutic vulnerability and an escape route. The authors argue that understanding the molecular architecture of resistance is essential for designing next-generation inhibitors and rational combination strategies that could finally deliver durable remissions in these devastating diseases.

Primary cutaneous aggressive epidermotropic cytotoxic T-cell lymphoma, first recognized as a distinct entity in 1999, is characterized by epidermotropic CD8-positive cytotoxic T cells expressing granzyme B, perforin, and TIA-1. Despite its rarity, the disease carries a median overall survival of just 32 months and a five-year survival of only 31 percent. Recent high-throughput genomic studies have revealed that this lymphoma harbors recurrent and targetable kinase fusions at striking frequency. In one study, fusion genes involving JAK2 were detected in three of twelve patients, while another reported kinase gene fusions in six of six samples, with five harboring a JAK2 fusion and one carrying a novel ABL1 fusion. A separate report described a fusion joining SATB1 to FGFR1, a receptor tyrosine kinase for fibroblast growth factors. In all cases, the tyrosine kinase domains are conserved at the C-terminus and fused to a diverse set of partner genes including STAT3, KHDRBS1, PICALM, CAPRIN1, PCM1, and TFG. The biological basis for the recurrent involvement of JAK2, rather than the JAK1 and JAK3 family members typically utilized by CD8-positive T cells, remains unknown, though the authors speculate it may reflect lineage infidelity, with transformed cells deviating from canonical cytokine signaling to exploit JAK2-mediated proliferative pathways.

Primary cutaneous gamma delta T-cell lymphoma presents a different genomic landscape. This rare and highly aggressive subset, with a median overall survival of approximately 31 months and a five-year disease-specific survival of only 19.9 percent, is characterized by marked genomic instability, with a median of 166.5 somatic copy number variants per sample. Rather than kinase fusions, PCGDTL harbors recurrent point mutations in key oncogenic signaling pathways, including the MAPK pathway (KRAS, NRAS, MAPK1), the MYC pathway (MYC, MYCN, FBXW7), and the JAK/STAT pathway (STAT3, STAT5B, JAK3, SOCS1). Among these, KRAS mutations were most common, while approximately 21 percent of samples carried JAK/STAT point mutations. Notably, clinical and histopathologic features correlate with TCR delta-chain usage—epidermal and dermal cases typically express TRVδ1, while subcutaneous cases express TRδV2—yet next-generation sequencing has not identified major mutational differences between these subsets.

The clinical experience with targeted inhibitors in both subtypes tells a consistent story of initial sensitivity followed by adaptive escape. In the first reported clinical use of a tyrosine kinase inhibitor in PCAETL, a patient harboring the SATB1-FGFR1 fusion was treated with the FGFR inhibitor pemigatinib. The response was remarkable: approximately 90 percent regression of ulcerated lesions within two weeks, with partial remission maintained for around four months. However, adverse events including hyperphosphatemia, nail changes, and ocular irritation necessitated a dose reduction. The patient’s lesions relapsed within one month, and sequencing revealed secondary point mutations within the FGFR1 kinase domain. The patient expired two months later. In PCGDTL, a patient with SOCS1 loss treated with the JAK1/2 inhibitor ruxolitinib achieved near-complete regression after four weeks, but disease progression occurred after eight weeks, accompanied by newly acquired lesions. Sequencing of the relapse sample revealed a STAT5B p.N642H mutation, a well-characterized gain-of-function driver associated with T-cell neoplasms and drug-resistant leukemias. Another PCGDTL patient harboring a JAK3 p.A573V mutation was enrolled in a phase II trial of the dual SYK/JAK inhibitor cerdulatinib, achieving an 86 percent reduction in skin disease burden after seven weeks. But therapy was discontinued due to grade 3 adverse events, and shortly after, relapse occurred with sequencing revealing acquired JAK3 p.M511I, JAK1 p.L783F, and JAK1 p.T901A mutations in circulating tumor cells.

The structural basis of these resistance mutations reveals elegant molecular logic. In the FGFR1 case, two secondary mutations were detected following pemigatinib treatment: E462V in the juxtamembrane region and V561L in the kinase domain. The E462V substitution, despite its location in a critical signaling hub, did not confer resistance—structural modeling showed no clashes or modulation of the drug-binding state. In contrast, V561L represents a canonical gatekeeper mutation that sterically impedes inhibitor binding and enhances ATP affinity, thereby reducing drug potency. Structural modeling of the analogous V561M substitution revealed that replacement with a bulky methionine side chain induces steric clashes within the inhibitor-binding pocket, accounting for observed resistance. This mutation has been previously described in FGFR1-driven myeloproliferative neoplasms, where it confers broad resistance to multiple FGFR inhibitors.

In the JAK pathway, the resistance architecture is equally instructive. The STAT5B p.N642H mutation occurs in the Src homology 2 domain and stabilizes STAT5B dimers, increases phosphorylation, and renders the protein constitutively active. Structural studies indicate that this substitution alters the hydrogen-bonding network within the phosphotyrosine pocket, favoring inter-protein interactions in the STAT5B dimer. The JAK3 mutations follow a different logic: M511 lies within the SH2-pseudokinase linker, which typically interacts with the kinase domain active site, and the M511I substitution destabilizes this linker, promoting kinase domain activation. A573 is located within the alphaC helix of the pseudokinase domain, a structural element that toggles between active and inactive conformations. Through structural modeling with cerdulatinib, the combination of M511I and A573V causes steric hindrance, suggesting these variants confer resistance through inter- or intramolecular interaction alterations. Remarkably, the JAK1 p.L783F mutation, which also causes steric hindrance with cerdulatinib, occurs in a different JAK family member than JAK3, raising important questions about how cross-kinase cooperation contributes to drug resistance. The combined presence of JAK3 p.A573V and JAK1 p.L783F conferred greater resistance to cerdulatinib compared to single mutants, indicating cooperative resistance across paralogous kinases.

Toxicity emerges as an indirect but powerful facilitator of resistance. Pemigatinib’s most common adverse events include hyperphosphatemia, nail toxicity, alopecia, diarrhea, anemia, dry eyes, and serous retinal detachment—manifestations that reflect the broad physiological role of FGFR signaling in the corneal epithelium, photoreceptors, iris, and hair follicles. Ruxolitinib, evaluated in a phase II trial of 53 patients with CTCL, produced anemia in 15 patients, diarrhea in 7, thrombocytopenia in 9, and neutropenia in 10, reflecting the critical role of JAK2 signaling in erythropoietin and thrombopoietin receptor function. Cerdulatinib, targeting both SYK and JAK families, produced frequent grade 3 or higher adverse events in a phase II trial of relapsed or refractory peripheral T-cell lymphoma and CTCL, including increased lipase in 29.2 percent, increased amylase in 43.1 percent, diarrhea in 43.1 percent, and anemia in 32.3 percent. Serious adverse events occurred in 64.6 percent of patients, and tragically, two deaths not related to disease progression were attributed to the drug. When dose reductions or discontinuations become necessary, resistant subclones may gain a selective advantage under reduced drug exposure.

The review argues that durable responses will require moving beyond single-agent therapy toward rational combination regimens. Preclinical and clinical evidence across malignancies supports combining kinase inhibitors with immune checkpoint blockade. In non-small cell lung cancer, the JAK1 inhibitor itacitinib combined with pembrolizumab achieved a 12-week overall response rate of 62 percent with a median progression-free survival of 23.8 months. In Hodgkin lymphoma, ruxolitinib combined with nivolumab yielded an overall response rate of 53 percent, with ruxolitinib appearing to rescue exhausted T cells and synergize with checkpoint blockade in reshaping the myeloid compartment. Although no clinical trials have yet evaluated such combinations in aggressive T-cell lymphomas, the authors suggest these approaches warrant investigation given the immune-evasive nature of these tumors. Topical application of inhibitors might also circumvent systemic toxicity and provide a window for prolonged therapeutic efficacy.

Aggressive cutaneous T-cell lymphoma thus presents both a challenge and an opportunity for precision dermato-oncology. The discovery of recurrent kinase alterations reveals that subsets of these lymphomas are mechanistically dependent on constitutive kinase activity for survival and proliferation, making them vulnerable to targeted inhibition. Yet the predictable emergence of adaptive resistance—through gatekeeper mutations, cooperative cross-kinase substitutions, and toxicity-driven dose reductions—underscores that single-agent approaches are insufficient. Future progress, the authors conclude, relies on molecular stratification based on kinase dependency, longitudinal genomic monitoring to detect resistance as it emerges, rational combination therapy, and the development of mutation-selective next-generation inhibitors capable of overcoming the adaptive mechanisms that currently limit treatment durability.

Subject of Research: Kinase inhibitor resistance in cutaneous T-cell lymphomas

Article Title: Mechanisms of kinase inhibitor resistance in subtypes of cutaneous T-cell lymphomas

Article References: Yescas, J. A., Bunick, C. G., Grada, A., Guitart, J., Torres-Cabala, C. A., Le Poole, I. C., & Zhou, X. A. (2026). Mechanisms of kinase inhibitor resistance in subtypes of cutaneous T-cell lymphomas. Frontiers in Hematology, 5, Article 1812908. https://doi.org/10.3389/frhem.2026.1812908

Image Credits: AI Generated

DOI: 10.3389/frhem.2026.1812908

Keywords: cutaneous T-cell lymphoma, kinase inhibitors, drug resistance, JAK/STAT pathway, FGFR1, precision oncology, hematology, Mechanisms, kinase, inhibitor, resistance, subtypes

The review, led by Katarzyna Bilińska and Magdalena Pasińska of Nicolaus Copernicus University in Poland together with Fernando de Castro of the Cajal Institute in Madrid, systematically combed through publicly available genomic databases and the scientific literature to identify CNVs reported in individuals with anosmia, hyposmia, or structural abnormalities of the olfactory system. Rather than treating all reported associations as equally reliable, the authors stratified the strength of evidence linking each CNV to olfactory dysfunction using a four-tier framework: established, probable, possible, and speculative. This approach allows well-supported loci with documented human olfactory phenotypes and mechanistic evidence to be distinguished from hypothesis-generating observations based primarily on isolated cases or biological plausibility alone.

Copy number variants are submicroscopic chromosomal abnormalities involving the loss or gain of DNA segments, typically ranging from a few kilobases to several megabases. While often undetectable by conventional cytogenetic methods, they can be readily identified using high-resolution genomic approaches such as array comparative genomic hybridization and next-generation sequencing. The molecular mechanisms by which CNVs exert their effects are diverse and often locus-dependent. In the context of olfactory dysfunction, CNVs may contribute to the phenotype through gene dosage effects, where altered copy number of dosage-sensitive genes disrupts the delicate balance of molecular pathways required for olfactory system development; gene interruption, where partial deletion or duplication truncates coding sequences; gene fusion, where CNVs juxtapose exons from two different genes; position effects, where structural changes relocate genes relative to regulatory elements; unmasking of recessive alleles, where deletion of one allele exposes pathogenic variants in the remaining allele; and regulatory disruption, where noncoding CNVs affect long-range regulatory elements or allele-allele communication.

Among the strongest associations identified in the review are deletions involving the SEMA3A gene at locus 7q21.11. In an extensive study involving a cohort of 120 patients diagnosed with Kallmann syndrome, a condition characterized by the coexistence of anosmia and hypogonadotropic hypogonadism, SEMA3A was identified as contributing to the molecular pathogenesis of the disorder. Comparative genomic hybridization identified a heterozygous 213 kb deletion at 7q21.11 in a male patient with Kallmann syndrome and complete anosmia, encompassing 11 of the 17 exons of SEMA3A. A similar finding was reported in another male patient carrying a heterozygous deletion encompassing the entire SEMA3A locus. SEMA3A is a well-established member of the secreted semaphorin family that signals primarily through neuropilin-containing receptor complexes and plays an important role in cell migration and axonal guidance during central nervous system development, including the formation of the lateral olfactory tract. Additional supporting evidence comes from mutant mouse models lacking a functional semaphorin-binding domain in neuropilin-1, which show abnormal olfactory system development and defective embryonic migration of gonadotropin-releasing hormone neurons.

Deletions involving the 8p11.22 region represent another well-supported association, with FGFR1 as the principal candidate gene for the olfactory and neuroendocrine phenotype. FGFR1 encodes a fibroblast growth factor receptor essential for embryonic development, including skeletal formation and the establishment of the olfactory and neuroendocrine systems. It plays a key role in the development of the olfactory placode and in shaping the migratory environment guiding GnRH neurons toward the hypothalamus. Disruption of FGFR1 signaling impairs olfactory bulb development and indirectly affects GnRH neuronal migration, leading to congenital anosmia or hyposmia in the context of Kallmann syndrome. However, the frequently multigenic nature of these rearrangements complicates interpretation, as larger deletions encompassing FGFR1 have been associated with a broad phenotypic spectrum including spherocytosis, growth delay, micrognathia, and bilateral crumpled ears.

The 22q11.2 deletion, typically spanning approximately 1.5 to 2.54 megabases, underlies the classical 22q11.2 deletion syndrome, also known as DiGeorge syndrome or velocardiofacial syndrome, which occurs in approximately 1 in 4,000 to 5,000 live births. Assessment using the University of Pennsylvania Smell Identification Test has shown that up to 68 percent of children with 22q11.2 deletion syndrome exhibit olfactory deficits, compared with 13 percent of their unaffected siblings. These impairments are not attributable to general intellectual disability, although they may be influenced by velopharyngeal insufficiency and altered nasal airflow. The deleted region encompasses multiple dosage-sensitive genes implicated in central nervous system development and olfactory processing, including COMT, PRODH, DGCR8, and CRKL, providing a plausible genetic basis for the high prevalence of olfactory dysfunction in this population.

Deletions in the Xp22.3 region encompassing the ANOS1 gene, formerly known as KAL1, represent perhaps the most well-established molecular basis for congenital anosmia. ANOS1 encodes anosmin-1, a protein essential for the proper development and interconnection of olfactory structures and migration of GnRH neurons during embryonic development. Anosmin-1 exerts its function through protein-protein interactions within the extracellular matrix, notably modulating FGF signaling via interaction with FGFR1. Classic studies documented intragenic deletions of ANOS1 in families with X-linked Kallmann syndrome, with affected males typically showing anosmia or severe hyposmia, delayed puberty, and hypogonadism, while carrier mothers were unaffected. More recent studies have expanded the spectrum of ANOS1 defects, demonstrating that both point mutations and CNVs, including exon-level and whole-gene deletions, contribute substantially to Kallmann syndrome and normosmic isolated hypogonadotropic hypogonadism, with ANOS1 defects accounting for approximately 14 percent of cases in one cohort.

Among the probable associations, large terminal deletions of the distal long arm of chromosome 6 at 6q27 have been linked to olfactory bulb aplasia and anosmia. In two unrelated individuals, high-resolution MRI revealed hydrocephalus, midline brain anomalies, and bilateral aplasia of the olfactory bulbs. While the adult patient had clinically confirmed anosmia, anosmia was strongly suspected based on neuroimaging findings in the 3-year-old child. Olfactory bulb aplasia and anosmia had not been widely recognized features of 6q27 microdeletion before this report, and the authors proposed these as part of the expanded phenotype. Over two dozen patients with terminal 6q27 deletions of similar size have been described in the literature and the DECIPHER database, and while there is a consistent association with brain malformations and intellectual disability, the prevalence of anosmia remains uncertain and may be underreported.

The review also highlights several possible and speculative associations that warrant further investigation. Haploinsufficiency of ARID1B at 6q25, a member of the SWI/SNF chromatin-remodeling complex, has been associated with Coffin-Siris syndrome, and some patients exhibit absent olfactory bulbs and anosmia. Structural variants involving the CHD7 gene at 8q12.2, which encodes a chromatin remodeler playing critical roles in neural crest development and olfactory system development, have been reported in patients with CHARGE syndrome, in which anosmia or hyposmia is frequently observed. Experimental evidence indicates that CHD7 regulates neural progenitor proliferation in the olfactory placode and influences the expression of key developmental genes including FGFR1, BMP4, and OTX2. A de novo 2.38 megabase deletion at 9q31.2 encompassing six protein-coding genes has been reported in a patient with congenital hypogonadotropic hypogonadism and anosmia, while a de novo heterozygous microduplication of approximately 178 kilobases at 9q34.3 including the NSMF gene has been identified in a male patient with Kallmann syndrome.

The authors emphasize that the interpretation of CNVs in olfactory disorders raises several challenges. Distinguishing pathogenic from benign CNVs is difficult due to incomplete penetrance, variable expression, and the frequent occurrence of CNVs in the general population. Phenotypic variability among individuals carrying the same CNV complicates genotype-phenotype correlations, suggesting the presence of genetic modifiers, epigenetic influences, or environmental interactions. Many candidate genes within olfactory-related CNVs remain poorly characterized in humans, and much of the knowledge derives from animal models, which may not fully reflect human biology. Another major limitation is the heterogeneity of olfactory phenotyping, as standardized psychophysical testing was available only for a subset of reported cases, whereas other observations relied on clinical history, self-report, or structural abnormalities detected by neuroimaging. The absence of reported olfactory dysfunction cannot be interpreted as evidence of normal olfactory function when smell was not specifically assessed. More systematic use of validated olfactory tests, together with dedicated assessment of olfactory bulb and tract morphology, would substantially improve genotype-phenotype correlations and may ultimately inform diagnostics and guide the development of targeted therapies for individuals affected by congenital or syndromic loss of smell.

Subject of Research: Genetics

Article Title: Olfactory dysfunction and submicroscopic abnormalities: unveiling hidden pathologies

Article References: Bilińska, K., Pasińska, M., & de Castro, F. (2026). Olfactory dysfunction and submicroscopic abnormalities: unveiling hidden pathologies. Frontiers in Molecular Neuroscience, 19, Article 1861373. https://doi.org/10.3389/fnmol.2026.1861373

Image Credits: AI Generated

DOI: 10.3389/fnmol.2026.1861373

Keywords: copy number variants, CNVs, anosmia, olfactory dysfunction, Kallmann syndrome, microdeletion, microduplication, SEMA3A, FGFR1, ANOS1, 22q11.2 deletion syndrome, genetics

The biology underlying peripheral nerve repair is intricate. After a nerve is transected, the segment downstream of the cut undergoes Wallerian degeneration, a process in which the axoplasm and axolemma break down and myelin debris accumulates in the injured stump. This debris must be cleared before new axons can grow. Schwann cells, the glial cells of the peripheral nervous system, respond by rapidly de-differentiating into repair-mode cells that secrete pro-regenerative factors, digest myelin through autophagy, recruit macrophages, and form regeneration tracks, known as bands of Büngner, that guide growing axons from the proximal stump back toward their original targets. Macrophages, meanwhile, perform the dual tasks of removing debris and supporting axon elongation. Coordinating all of these players takes time; axons may need up to ten months to reach their target tissues, which is why clinicians have long sought drugs that can safely speed the process.

Neurotrophic factors, the signaling proteins that nurture neuronal survival and growth, have been an obvious place to look. Molecules such as nerve growth factor, brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor, VEGF and IGF-1 have all shown promise in experimental settings. Yet their clinical translation has been hampered by poor pharmacokinetics, high costs and significant side effects. Basic fibroblast growth factor, or bFGF, is one of the most powerful of these agents, secreted by Schwann cells and neuronal populations, and it stimulates the proliferation of neurons, Schwann cells and fibroblasts while playing a pivotal role in nerve and spinal cord repair. But native bFGF has a troubled clinical record. A trial in acute stroke patients failed to demonstrate efficacy and revealed fever, lowered blood pressure, elevated leukocyte counts and potential carcinogenic effects, largely because the growth factor also drives cell proliferation.

SUN11602 was designed to sidestep that problem. It is a small aniline-derivative molecule that mimics the neuroprotective effects of bFGF by engaging the same receptor, FGFR1, a transmembrane tyrosine kinase receptor to which bFGF binds with high affinity. Crucially, SUN11602 activates FGFR1 to induce expression of calbindin-D28k, a calcium-binding protein that helps maintain intracellular calcium homeostasis, without triggering the proliferative activity that makes native bFGF risky. The compound also boasts pharmacokinetics that make it a plausible drug candidate: oral bioavailability above 65 percent in rodents and dogs. Previous studies have suggested neuroprotective effects in models of Alzheimer’s disease, depression, Parkinson’s disease and traumatic spinal cord injury, but its role in peripheral nerve regeneration had not been tested.

To fill that gap, the Messina team used sixteen female Wistar rats and a surgically precise injury model. Under an operative microscope, the median nerve of the left upper limb was exposed at the middle third of the brachium and transected, then repaired with an end-to-end suture using two to three epineurial stitches of 9-0 monofilament nylon, replicating the standard clinical repair technique. Beginning 24 hours after surgery, one group of injured rats received SUN11602 at 2.5 milligrams per kilogram by oral gavage once daily for seven consecutive days, while injured controls received only saline. A sham group underwent incision without nerve section. The dose and route were grounded in earlier in vivo work by the same laboratory, and the study was conducted under Italian and European animal research regulations with approval from the Ministry of Health.

Seven days after suture, the differences between groups were visible under the microscope. Haematoxylin and eosin staining revealed that the injured, untreated nerves had the expected hallmarks of acute Wallerian degeneration: structural disorganization, oedema, vacuolization and early myelin and axonal degeneration. Nerves from the SUN11602-treated animals, by contrast, showed comparatively preserved architecture, with reduced vacuolization and less tissue disarray. In other words, the drug appeared to blunt the secondary damage that typically accompanies the degenerative phase, without abolishing degeneration itself, which the authors emphasize is a physiologically required step for successful regeneration.

The anti-inflammatory effects were equally striking. Toluidine blue staining, which highlights mast cells, showed that injured control nerves accumulated large numbers of these cells in the connective tissue and along axon fibres with irregular morphology and degenerating myelin sheaths. Mast cells congregate near peripheral nerves and are considered key orchestrators of neurogenic inflammation and neuropathic pain. In the SUN11602-treated group, mast cell accumulation was suppressed and axon fibre density was higher. Immunostaining for IBA-1, a marker of activated resident macrophages, and CD68, a marker of pro-inflammatory M1 macrophages that infiltrate the injury site and release cytokines, both showed intense upregulation after nerve transection. SUN11602 treatment significantly attenuated both, suggesting the drug restrains the inflammatory response that can otherwise impede repair in the critical first days after injury.

The compound also appeared to support the rebuilding side of the ledger. Immunofluorescence labeling for S100, a Schwann cell marker, showed more consistent and interconnected stained areas in treated nerves, indicating enhanced Schwann cell proliferation and myelinization. Quantification of myelin basic protein by ELISA confirmed the histological picture: concentrations of MBP were significantly higher in the SUN11602 group than in injured controls, evidence of increased myelin production at the molecular level. MCOLL staining, a histochemical method that distinguishes myelin in blue from collagen fibers in red, allowed the researchers to visualize the nodes of Ranvier and the organization of connective tissue around nerve fibers. Injured control nerves showed marked demyelination and disorganized collagen deposition consistent with fibrosis, whereas treated nerves displayed axonal remyelination and reorganized collagen architecture.

The authors are careful about what these findings do and do not mean. All evaluations were performed at a single early time point, seven days after suture, when axonal regeneration and remyelination are only beginning. The observed attenuation of myelin degradation, they write, should not be read as a global inhibition of Wallerian degeneration; rather, they hypothesize that SUN11602 may selectively reduce secondary or excessive demyelination in spared fibers, a distinction that will require ultrastructural analysis and time-course studies of myelin clearance to confirm. The histological improvements also remain unlinked to functional recovery, since no electrophysiological or behavioral testing was included. Future work, the team notes, should incorporate extended follow-up periods, functional and electrophysiological assessments, and combination strategies such as nerve conduits and biomaterials to better mimic complex clinical conditions.

Even with those caveats, the study adds SUN11602 to a short list of candidates that could reshape how peripheral nerve injuries are treated. Because it is orally bioavailable and lacks the proliferative liabilities of native bFGF, the compound addresses the two biggest obstacles that have kept neurotrophic therapies out of the clinic: delivery and safety. If the early histological benefits observed here translate into sustained axonal regrowth, remyelination and functional recovery in longer studies, an oral pill taken in the days and weeks after nerve repair surgery could become a genuine adjunct to the operating microscope. For now, the message from Messina is a proof of principle: the molecular machinery of nerve regeneration can be pharmacologically tuned, and the earliest, most inflammatory phase of repair may be the best place to intervene.

Subject of Research: Pharmacological enhancement of early peripheral nerve regeneration using the oral FGFR1 agonist SUN11602 in a rat median nerve transection model

Article Title: SUN11602 Accelerates Early Peripheral Nerve Regeneration in an Experimental Median Nerve Transection Model

Article References: Casili, G., Papalia, I., Ardizzone, A., Basilotta, R., Costa, A. L., Titolo, P., Esposito, E., Colonna, M. R., & Galeano, M. (2026). SUN 11602 Accelerates Early Peripheral Nerve Regeneration in an Experimental Median Nerve Transection Model. Journal of Cellular and Molecular Medicine, 30(19), Article e71375. https://doi.org/10.1111/jcmm.71375

Image Credits: AI Generated

DOI: 10.1111/jcmm.71375

Keywords: peripheral nerve injury, SUN11602, FGFR1, bFGF, Schwann cells, Wallerian degeneration, mast cells, macrophages, myelination, median nerve transection, neuroprotection, rat model