Hair Loss Research Articles

Androgenetic alopecia (AGA) is the most common type of baldness, characterized by progressive miniaturization of the hair follicle and eventually atrophy. Both genetic and androgenic factors play definite roles in the pathophysiology of the disease, including androgens and growth factors, which induce a crosstalk between the dermal papilla and the hair follicle cells. The goal of AGA treatments is to prevent the hair miniaturization process; however, currently there are only two FDA-approved medications to treat AGA: topical Minoxidil (5% and 2%) for men and women, and oral Finasteride (1 mg tablets—Proscar and Propecia) for men. Nevertheless, these are costly, require lifelong treatment, and may have side effects. Thus, there have been many attempts to develop drugs that can harness the mechanisms controlling the pathogenesis of AGA. These pharmacological therapies might achieve more targeted and effective treatment for the disease. In this review, we present various treatments that have demonstrated their ability to induce hair growth by controlling the pathophysiological mechanisms involved in the development of AGA. Interestingly, treatment by a combination of some drugs has resulted in better outcomes than each of the drugs alone, hence demonstrating the advantage of activating different molecular mechanisms simultaneously.

A rare form of lymphoplasmacytic lymphoma, Waldenstrom’s Macroglobulinaemia (WM) progresses slowly and requires treatment only when the patient exhibits symptoms. Organomegaly, cytopenia, hyperviscosity syndrome, and constitutional symptoms are the most common presentations of WM. The main affliction of the tumour is with the bone marrow, which is made up of plasma cells, tiny lymphocytes, and plasmacytoid lymphocytes. An Immunoglobulin M (IgM) gammopathy is also present in the circulating blood. Here, we describe a 77-year-old man who complained of epistaxis, hair loss, elevated serum creatinine, hypercalcaemia, and a reversal of the albumin-to-globulin ratio. Additionally, the patient showed M band positive, which led to the diagnosis of WM rather than multiple myeloma, as was first believed. Our case report highlights the importance of considering WM in the differential diagnosis of patients presenting with symptoms such as epistaxis, fatigue, weakness, and Raynaud's phenomenon, particularly in elevated serum IgM levels. Prompt recognition and diagnosis of WM are essential for appropriate management and prognosis. In summary, our case underscores the importance of vigilance in recognising the clinical manifestations of WM and the necessity of a comprehensive approach to diagnosis, treatment, and follow-up care. Further research is warranted to elucidate the underlying pathogenesis of WM and to develop more effective and targeted therapeutic strategies for this rare haematological malignancy.

Emerging biomedical engineering strategies for hair follicle regeneration.

Sinapic acid and glabridin synergistically mitigate androgenetic alopecia by modulating ferroptosis through stabilization of β-catenin against ubiquitin-dependent degradation.

Self-assembling peptide inspired by insulin and type 1 insulin-like growth factor for the treatment of androgenetic alopecia.

Effects of GLP-1 Receptor Agonists on Hair Loss and Regrowth: A Systematic Review.

Alopecia areata (AA) is an autoimmune disease defined by hair loss and peribulbar infiltrate of CD8 and CD4 T cells. Prior studies have focused on the role of CD8 T cells in the development of AA. Multiple roles for CD4 T cell help have been demonstrated for support of CD8 T cell responses; however, the role of CD4 T cells in AA remains unclear. Here, we demonstrate that CD4 T cells from the skin-draining lymph nodes (SDLNs) of AA mice transferred disease to recipient mice. These cells exhibited a T helper type 1 (TH1) effector transcriptional and phenotypic profile, and their pathogenic activity required endogenous CD8 T cells and host IFN-γ responsiveness. Targeted deletion of CD4 T cell–mediated production of IFN-γ abrogated the ability of this cell population to transfer disease. Together, these data provide mechanistic insights into pathways driving AA development, strengthening our understanding of the disease and inviting studies into exploring alternative therapeutic strategies for human patients.

Tourniquet syndrome, also known as hair-thread tourniquet syndrome, is a rare but potentially serious condition. It is defined as the strangulation of a body part (toe, finger, penis, clitoris, nipple) by a thread-like object, most often a hair or textile thread. This phenomenon causes progressive circulatory obstruction, first venous and lymphatic, then arterial, which can progress to irreversible ischemia and tissue necrosis if diagnosis and treatment are delayed. First described by Quinn in 1971, this syndrome occurs primarily in infants and young children, a period when postpartum maternal hair loss is common and promotes the presence of loose hair in the child\'s environment. The most commonly reported locations are the toes (particularly the 2nd and 3rd), followed by the fingers and, more rarely, the genitals. In our paper, we describe two cases of this syndrome with an isolated and non-specific clinical presentation that could be the cause of a diagnostic delay.

Purpose: To assess the association between hair loss in females and various biomarkers including hemoglobin, iron, ferritin, zinc, selenium, calcium, vitamin D, vitamin B12, folic acid, and thyroid hormones. Patients and methods: This study enrolled 100 women presenting with hair loss and 100 age-matched healthy controls. Venous blood samples were collected for analysis of hematological, hormonal and biochemical parameters. Results: The mean age of participants was comparable between groups (43.06 ± 10.76 vs. 41.39 ± 7.94 years; p = 0.88). Hair loss in females had significantly lower mean levels of Hb (11.45 ± 0.39 vs. 13.09 ± 0.46 g/dL; p < 0.001), iron (70.14 ± 7.85 vs. 94.42 ± 5.61 µg/dL; p < 0.001) and ferritin (39.34 ± 3.71 vs. 48.09 ± 5.31 ng/mL), all with p < 0.001. Serum levels of selenium (67.11 ± 5.53 vs. 71.45 ± 4.05 µg/L), zinc (86.07 ± 3.98 vs. 88.87 ± 2.03 µg/L), copper (90.71 ± 3.48 vs. 104.84 ± 5.38 µg/L), and calcium (8.61 ± 0.28 vs. 9.11 ± 0.27 mg/dL) were significantly reduced in women with hair loss (p < 0.001). Thyroid hormones were also significantly lower in the hair loss group, including TSH (1.74 ± 0.25 vs. 2.35 ± 0.39 µIU/mL) and FREE T4 (1.11 ± 0.11 vs. 1.32 ± 0.12 ng/dL), despite remaining within the normal reference ranges. Patients also showed lower serum folate (6.17 ± 0.63 vs. 6.96 ± 0.41 ng/mL), vitamin B12 (185.52 ± 35.27 vs. 258.30 ± 52.84 pg/mL), and vitamin D (26.32 ± 2.98 vs. 32.20 ± 3.76 ng/dL) levels (p < 0.001). Conclusions: Hair loss in females is significantly associated with reduced levels of circulating hemoglobin, iron, copper, selenium, vitamin D, vitamin B12, folate, thyroid-stimulating hormone and FREE T4 hormone.

Trichotillomania was recognized as a psychological disorder characterized by the compulsive urge to pull out one’s own hair, leading to noticeable hair loss. When ingested, this hair accumulated in the stomach and formed a trichobezoar — a rare and fascinating condition. Most cases of trichobezoar occurred in young female patients with underlying psychiatric disorders. We reported a case of an 18-year-old underweight female who presented with a two-month history of upper abdominal pain, intermittent vomiting, and epigastric discomfort. After two unsuccessful treatment attempts due to the size of the mass, surgical intervention was performed to remove the trichobezoar. Postoperatively, she was advised to receive intravenous antibiotics for one week due to the risk of infective endocarditis, which was justified by her history of congenital cardiac disease. Surgical removal remained the mainstay of treatment for trichobezoar. It was important to note that most patients had associated psychiatric or social issues. Therefore, a multidisciplinary approach was considered essential to prevent recurrence.

Hair loss is a global concern, driving substantial public interest in effective therapeutic solutions. Beyond its protective physiological functions, hair plays a pivotal role in social and non-verbal communication, which can be profoundly disrupted by hair loss. While conventional pharmacological treatments are commonly employed, their use is often limited by the risk of adverse effects. To address this limitation, we propose the exploration of phytochemicals derived from natural sources as safer and potentially effective alternatives for hair loss prevention. Many natural compounds have shown the capacity to activate key signaling pathways involved in hair growth, offering promising avenues for innovation in the hair industry. This study explores the biological mechanisms underlying hair development, morphogenesis, and regeneration, with a particular focus on the Wnt/β-catenin, Sonic hedgehog (Shh), and Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathways, which are critical to hair growth. Furthermore, we provide a comprehensive compilation of natural materials known to promote hair growth and their associated phytochemicals. This repository serves as a foundation for identifying and developing novel agents to enhance hair regeneration. Our review highlights the need for continued research into identifying and refining safe, naturally derived candidates for the prevention and treatment of hair loss, thereby addressing a pressing unmet medical and cosmetic need.

Cancer is among the major causes of mortality, responsible for approximately 15% of all deaths worldwide. Despite remarkable progress in modern medicine, it remains a significant global health challenge. Nevertheless, conventional therapies such as chemotherapy and radiotherapy target healthy and malignant tissues, leading to adverse side effects, including hair loss, fatigue, and nausea, which significantly reduce patients' quality of life. Even more critically, the therapeutic response varies from patient to patient, which reduces the effectiveness of treatment. Therefore, cancer tissue engineering has evolved as a novel interdisciplinary field, aiming to develop structures that mimic the tumor microenvironment to elucidate cancer development mechanisms and devise effective treatment methods. However, producing a fully synthetic biosimilar matrix by assembling all individual ECM components remains unfeasible due to the heterogeneity and complex structure of tumor tissues, as well as the necessity of highly advanced micro- and nanoengineering techniques. Consequently, decellularization techniques have recently been applied to cancer tissues to produce biomimetic tumor models. In this review, we provided a comprehensive overview of the extracellular matrix (ECM) architecture and its role in tumor progression. We also discussed the structural differences between normal and malignant tissues. We briefly reviewed decellularization techniques and analytical approaches for ECM characterization. Emphasizing the cutting-edge research, we categorized developments into three groups: decellularized tumor-derived extracellular matrix (dT-ECM), hydrogels, and bioinks. Subsequently, we critically assessed the benefits, limitations, and potential future developments of dT-ECM-based strategies. Finally, we envision that tumor tissue engineering will provide preventive treatment approaches by developing patient-specific predictive and personalized cancer models through integrating advanced biomaterials with artificial intelligence and machine learning.

Background: This clinical study was undertaken to assess the safety, efficacy of an Ayurvedic leave-on treatment for hair loss in healthy Indian adults (both male and female). The study also aimed to elucidate the product’s mechanism of action through in vitro analyses. Methods: Healthy male and female volunteers experiencing hair loss and hair thinning were enrolled for clinical study. Subjects were screened based on predefined criteria, including specific hair density and thinning parameters, and the absence of underlying medical conditions that could contribute to hair loss. The study design included a washout period prior to treatment initiation. The treatment phase lasted for three months, during which participants applied the product regularly and visited the study center at scheduled intervals for follow-up assessments and measurements. An in vitro study was conducted using human dermal papilla cells to investigate the mechanism of action (MoA) of the Ayurvedic leave-on treatment. Results: The Ayurvedic leave-on treatment demonstrated significant efficacy in reducing hair fall and improving hair density in both male and female subjects compared to baseline measurements. Noticeable improvements observed in increase in hair density, reduction in hair fall and over all hair and scalp health from the second week of application and continued throughout the treatment period. Conclusion: The Ayurvedic leave-on formulation demonstrated a clinically significant increase in hair density and improvement in the anagen: telogen ratio, indicating reduced hair fall and normalization of the hair cycle. This is mechanistically supported by the upregulation of vascular endothelial growth factor (VEGF) in dermal papilla cells, promoting follicular angiogenesis.

To investigate the impact of removal surgery in women with breast implant illness (BII) on the improvement of symptoms, as well as on the current quality of life of women. This is an observational study of a cohort of women undergoing definitive implant removal for BII-related symptomatology between 2016 and 2022 in Cali, Colombia. All data were collected from medical records and through a telephone survey. The severity of 10 clinical manifestations before and after removal surgery was evaluated with a five-point Likert scale. Quality of life was assessed with the BREAST-Q scale. A total of 125 women who underwent breast removal surgery were included; mean age was 48.8 ±9.7 years. The three most frequent reported symptoms at baseline were sore/aching joint (48.0%), fatigue (32.0%), and hair loss (25.6%). At a median follow-up of 18 months after implant removal, significant improvement was observed in all symptoms (p value<0.05) with a mean reduction in the percentage of women with symptomatology of 55.8% ±6.4%. At least half of the women reported a BREAST-Q of 100 points on the dimensions of satisfaction with breasts, physical well-being, and satisfaction with surgical outcome. This study provides evidence in favor of breast removal surgery as a treatment option in women with BII symptomatology. Highlights Nowadays, the evidence on breast implant illness is not conclusive. However, due to media interest and growing concern among patients and decision-makers, it is necessary to increase knowledge about BII, especially in low- and middle-income countries where evidence is poor. Consistent with the results of other studies, implant removal surgery significantly reduced the severity of symptoms at a median follow-up of 18 months after explantation in 125 women included in this study. Women after explantation reported a good quality of life and satisfaction with their breast appearance, physical well-being and surgical outcome with the BREAST-Q score. This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Abstract Disclosure: K. Feng: None. S. Ozair: None. J. Perkins: None. Panhypopituitarism is the deficiency of all anterior pituitary hormones. Two of these hormones, thyroid-stimulating hormone (TSH) and adrenocorticotropic hormone (ACTH), play integral roles on the heart [1]. A 36-year-old female with history of craniopharyngioma status-post radiotherapy and radiosurgery, panhypopituitarism, and diabetes insipidus presented to the hospital with several days of weakness, shortness of breath, nausea and vomiting. At home, the patient was prescribed levothyroxine, calcitriol, hydrocortisone, and desmopressin. Initial lab findings were significant for sodium 125 mEq/L, calcium 7.4 mg/dL, magnesium 2.7 mg/dL, potassium 3.6 mEQ/L, TSH 0.060 UIU/mL with reflex T4 &amp;lt;0.04 ng/dL, and cortisol 1.8 mcg/dL.Cardiac monitoring demonstrated ventricular tachycardia (VT) with a prolonged QT interval of 456 ms. She was treated with IV levothyroxine, IV hydrocortisone, electrolyte replacement, and IV fluid resuscitation. TTE revealed normal heart function without concern for new ischemic changes. Cardiology was consulted and recommended continued correction of hormonal abnormalities and electrolytes. With continued correction of her abnormalities she became hemodynamically stable with no further episodes of VT. She was discharged with levothyroxine and hydrocortisone. Several weeks after discharge, her ECG demonstrated a corrected QT interval of 371 ms. Commonly, adrenal insufficiency causes fatigue, weight loss, abdominal pain, hypotension and hypoglycemia [2]. Hypothyroidism results in fatigue, weight gain, constipation, hair loss, cold intolerance, and sinus bradycardia. Additionally deficiency of these hormones contribute to electrolyte imbalances that result in QT interval prolongation leading to unstable cardiac electrical activity and VT. This patient had severe adrenal insufficiency and thyroid hormone deficiency, which caused the electrolyte imbalance leading to QT interval prolongation and VT. When evaluating patients with ventricular arrhythmias it is essential to not only measure electrolyte levels but also to measure hormone levels, such as TSH and ACTH. It is critical to consider underlying endocrine pathology when evaluating cardiac dysfunction and arrhythmias. Presentation: Sunday, July 13, 2025

Abstract Disclosure: H.K. Boparai: None. A. Randhawa: None. M. Sattar: None. Hypothyroidism and hyperthyroidism are both known to be associated with alterations in cardiac output and vascular resistance. Additionally, decreased vascular endothelial growth factor is noted with hypothyroidism. Immunocomplexes may also be deposited in the basement membrane of glomeruli in autoimmune thyroid disorders. All these mechanisms have previously been known to contribute to renal function derangements. Our case is about a 21-year-old female who went for a pre-employment checkup and was incidentally found to have a TSH of 368 with a free T4 &amp;lt;0.25. She was referred to an endocrinology clinic for further evaluation and management of hypothyroidism. During the interview, she reported some hair thinning, cold intolerance, fatigue, and irregular periods in the past few months. Her family history revealed that her maternal grandmother and aunt had thyroid disease. Concurrently, her labs also revealed an elevated creatinine of 1.8, along with albuminuria, prompting a referral to a nephrology clinic. Renal Doppler and urinalysis were unremarkable. A repeat set of TSH and T4, along with Thyroid peroxidase (TPO) antibody confirmed the diagnosis of hypothyroidism (elevated TSH, severely suppressed T4, and a positive TPO antibody) and she was started on a weight-based dose of levothyroxine 75 mcg daily. On follow-up visits, the patient’s thyroid hormone levels improved significantly and returned to normal, and her creatinine level also improved, coinciding with the initiation of thyroid hormone supplementation. The patient’s fatigue, cold intolerance, hair loss, and menstrual periods returned to normal with Levothyroxine administration. Since the patient’s kidney function returned to normal, a decision was made not to pursue a kidney biopsy or any further investigations, so the cause of the initial kidney disease remains uncertain. While thyroid hormone supplementation has been previously shown to delay the progression of chronic kidney disease, our case highlights an unusual complete resolution of significant kidney disease in a young, otherwise healthy individual after thyroid hormone supplementation. Literature suggests that hypothyroidism can cause renal dysfunction but also that renal dysfunction itself, in particular, nephrotic syndrome can cause hypothyroidism. In this patient, it is uncertain if protein losses from kidney disease contributed to her significant hypothyroidism or if the thyroid disease contributed to the kidney disease. This case not only highlights the importance of diagnosing and treating hypothyroidism with a subtle clinical presentation, but also explores the association between renal dysfunction and thyroid disease, and the need to investigate secondary causes of these disorders. Presentation: Saturday, July 12, 2025

Disclosure: W. Akhter: None. R. Akhter: None. A.J. Zaidi: None. J.L. Gilden: Novartis Pharmaceuticals.IntroductionThyroid disorders are common, affecting more than 10% of people in the US. Apart from understanding normal physiology, it is important to be familiar with possible pitfalls and caveats in the use of thyroid function tests (TFT) tests, so that they can be interpreted accurately. When results are discordant, it is important to consider possible assay interferences and/or the effect of medications. In addition, thyroid function may appear abnormal in the absence of actual dysfunction in pregnancy and in critical illness. Therefore, it is important to consider the clinical context when interpreting TFT.Case PresentationWe present the case of a 41-year-old female who presented to the Endocrine clinic for evaluation and management of abnormal TFT. Patient endorsed symptoms of 25 lb. weight gain, severe fatigue, feeling foggy, joint pains, hair loss and constipation, which started after childbirth. Thyroid exam was normal. Thyroid ultrasound was normal. Both father and sister have Hashimoto’s thyroiditis. As a nurse, she self-diagnosed herself with postpartum thyroiditis with low TSH 0.058 uIU/mL (Normal = 0.550-4.780 uIU/mL), low Free T4 0.8 ng/dL (Normal= 0.89-1.76 ng/dL) and normal Free T3 3.65 pg/mL (Normal = 2.30-4.20 pg/mL). She convinced her primary care provider to prescribe levothyroxine 50 mcg daily but had little improvement in symptoms. Laboratory values 3 months later, when the patient presented to the endocrine clinic: TSH =0.137 uIU/mL, normal Free T4 =1.26 ng/dL and Free T3 2.98 pg/mL. with positive thyroid peroxidase antibodies, >2000. Repeat labs two months later showed normal TSH 0.880 uIU/mL, Free T4 1.17 ng/dL and Free T3 3.28 pg/mL Peroxidase antibodies >1500 while still taking the same dose of Levothyroxine 50 mcg daily, with symptomatic improvement. ConclusionNormal changes in thyroid physiology during pregnancy and the postpartum period make TFT interpretation very challenging. Owing to the structural similarity between Hcg and TSH, high Hcg levels during pregnancy stimulate TSH receptors, resulting in thyroid gland enlargement, increased thyroid hormone production and decreased TSH levels. After pregnancy when Hcg levels fall, free thyroid hormones decrease and TSH increases. Women who have a history of autoimmune thyroid disease or other forms of autoimmunity may develop postpartum thyroiditis, the incidence of which is approximately 5.4%. Postpartum thyroiditis follows a triphasic pattern and usually starts with transient hyperthyroidism followed by transient hypothyroidism and eventually a euthyroid state. Most cases of postpartum thyroiditis do not require treatment. However, some patients do not follow this classical pattern. Therefore, it is important to recognize that changes of TFT can occur in the postpartum state. In addition, not all symptoms of fatigue and weight gain can be attributed to hypothyroidism.Presentation: Monday, July 14, 2025

Disclosure: E. Krishnaraju: None. S. Samarasinghe: None.Introduction: Ovarian hyperthecosis (OH) is a rare cause of hyperandrogenism typically seen in postmenopausal women. Severe hyperandrogenism with testosterone levels over 150 ng/dL but slowly progressive clinical signs of virtualization and metabolic complications characterize this disease. Clinical Case: A 62-year-old woman was being followed in the clinic for diabetes mellitus, atrial flutter, obstructive sleep apnea, hypertriglyceridemia, kidney stones, proteinuria, obesity, coronary artery disease, and a partial hysterectomy for uterine fibroids. She presented with symptoms of gradual but worsening hair loss in an androgenic pattern and hirsutism for 1-2 years. On exam, she had facial plethora, a dorsal hump, central obesity, thin yet muscled extremities, and male-pattern balding. She was also noted to have coarse facial hair and normal external genitalia. Lab work was remarkable for a high serum testosterone of 238 ng/dl, free testosterone of 24.2 pg/ml, FSH of 57.6 miu/ml, and LH of 51.6 miu/ml. She had a normal TSH, prolactin, estradiol DHEA-S, and SHBG level. Several late-night salivary cortisol levels were normal and a 1 mg DST showed a suppressed cortisol of 1.6 ug/dl. A CT adrenal demonstrated normal appearing adrenal glands while an MRI pelvis showed an absent uterus but noted an enlarged 2.7 cm right ovarian cyst. The right ovary measured 3.0 x 2.6 x 3.6 cm and the left ovary measured 2.4 x 1.7 x 1.9 cm with both glands exhibiting homogeneous enhancement and a normal T2 signal without solid lesions. Given the markedly elevated testosterone levels and the findings of an ovarian cyst, the patient underwent an exploratory laparotomy with bilateral salpingo-oophorectomy. The final histopathology revealed ovarian stromal hyperthecosis of both ovaries with positive immunohistochemical stains for inhibin and calretinin. Her postoperative testing confirmed normalization of testosterone at 21 ng/dl at four weeks and 29 ng/dl at one year after surgery. Her symptoms of hirsutism and hair loss gradually improved after surgery but her body weight and overall appearance remain unchanged. Conclusion: OH must be considered in the differential of severe hyperandrogenism. Other etiologies include hormonally active ovarian and adrenal tumors. OH classically causes ovarian enlargement, but should be suspected even with normal-sized ovaries on imaging. Prompt referral for oophorectomy and histopathologic diagnosis is the gold standard for management.Presentation: Sunday, July 13, 2025

To evaluate treatment results of a neoadjuvant regimen consisting of Docetaxel + Cisplatin + S-1 (DCS) in patients with locoregionally advanced unresectable gastric adenocarcinoma characterized by tumors with bulky regional lymph nodes (T1-4a, N-bulky, M0) or T4b tumors (any N, M0)). This study included 78 patients with locoregionally advanced gastric adenocarcinoma treated at a university hospital in Vietnam, comprising 47 retrospective and 31 prospective cases. Patients received 2 - 4 cycles of DCS chemotherapy, with each cycle comprising intravenous docetaxel (35mg/m2) and cisplatin (35mg/m2) on days 1 and 15, and oral S-1 (40mg/m2/twice daily) from days 1 to 14, repeated every 4 weeks. Clinical treatment response was assessed after every three cycles and re-staging evaluation by using the RECIST criteria and contrast-enhanced CT scans after 2 - 4 cycles, depending on patient response and tolerability. Patients with a good response and down-staging were referred for gastrectomy. The median age was 58 years, and 64.1% were male. Following neoadjuvant chemotherapy, the proportion of T4b tumors decreased from 78.2% to 52.6%, while T4a tumors increased from 20.5% to 43.6%. The rate of N-bulky decreased from 23.1% to 11.5%. Anemia and neutropenia were the most common hematological toxicities, predominantly grade 1-2. Gastrointestinal toxicity and hair loss were the most frequent clinical adverse events, mostly grade 1-2. Among 65 patients (83.3%) achieving an objective response to neoadjuvant chemotherapy, 42 (53.8%) underwent gastrectomy, with R0 resection achieved in 92.9%. Neoadjuvant chemotherapy using the DCS regimen every 4 weeks demonstrated high effectiveness and safety in patients with locoregionally advanced unresectable gastric adenocarcinoma characterized by extensive regional metastases, and increased their eligibility for successful gastrectomy (R0 resection). Not applicable. This study is a retrospective and prospective cohort study, not a clinical trial.

Chinese herbal prescription JZ-1 enhances host resistance to herpes simplex virus type 2 through regulating the MRN-ATM-CHK2 DNA damage response.