Yet the standard approach has a stubborn ceiling. Pathologic complete response rates with conventional neoadjuvant chemotherapy hover between roughly 6 and 16 percent, and long-term survival for patients with stage IIIA, IIIB, and IIIC disease remains only 30.5, 20.1, and 8.3 percent respectively. This gap has pushed oncologists to explore whether adding other therapeutic modalities before surgery can push more patients toward complete tumor eradication. A new systematic review and single-arm meta-analysis published in Frontiers in Oncology now offers the first quantitative synthesis of one such candidate: apatinib, an oral tyrosine kinase inhibitor of vascular endothelial growth factor receptor 2 developed in China, delivered as part of neoadjuvant regimens for resectable gastric and gastroesophageal junction adenocarcinoma.

The rationale for apatinib rests on a hallmark of cancer biology. Angiogenesis, the formation of new blood vessels, drives the growth and metastasis of aggressive tumors, with vascular endothelial growth factor and its receptors serving as key mediators. VEGFR2, one of three members of the VEGFR family, exerts a pivotal effect on VEGF-mediated tumor angiogenesis. Apatinib selectively targets this receptor and has already demonstrated efficacy in advanced disease: a phase III trial showed that apatinib improved progression-free survival from 1.8 to 2.6 months and overall survival from 4.7 to 6.5 months compared with placebo in patients with advanced gastric cancer refractory to two or more chemotherapy regimens. A phase I study also found that apatinib could enhance the efficacy of paclitaxel, oxaliplatin, and 5-FU/leucovorin in advanced gastric cancer, with objective response rates of 90 percent in the high-dose group versus 66.7 percent in the low-dose group.

To consolidate scattered preliminary clinical data, a team led by Kaiyi Xin and Zhilu Chen, with Yinghao Zhao as corresponding author, from Jilin University hospitals in Changchun, China, conducted a systematic search across PubMed, Embase, the Cochrane Library, Web of Science, and major oncology conference proceedings up to January 1, 2026. The review followed the PRISMA statement and was registered with PROSPERO under identifier CRD42023478481. The initial search identified 483 articles, from which 20 studies enrolling 1026 patients met the inclusion criteria. After excluding one potentially overlapping cohort from the same research group to avoid double-counting patients, the primary analysis rested on 19 studies with 975 patients. These comprised 11 single-arm cohort studies, 7 two-arm randomized controlled trials, and 1 three-arm randomized controlled trial, with study arms categorized as neoadjuvant apatinib combined with chemotherapy, apatinib combined with immunotherapy and chemotherapy, or apatinib combined with chemotherapy and radiotherapy. Each patient received at least two courses of neoadjuvant treatment, and most surgical resections were performed three to five weeks after the final preoperative cycle.

Because most included studies were single-arm trials reporting binary outcomes as proportions, the investigators applied a logit transformation to stabilize variance and used inverse-variance weighting to pool event rates with 95 percent confidence intervals, selecting random- or fixed-effects models based on between-study heterogeneity measured by the I-squared statistic. The headline efficacy numbers are striking. The pooled pathologic complete response rate was 21 percent (95 percent CI, 18 to 25 percent) with remarkably low heterogeneity of I-squared 19.4 percent. The pooled major pathologic response rate, a broader measure of deep tumor regression, reached 39 percent (95 percent CI, 34 to 45 percent). Complete resection with negative margins, the R0 resection rate, was achieved in 93 percent of patients (95 percent CI, 90 to 95 percent), while the pooled surgical resection rate was 92 percent. On imaging, the pooled objective response rate was 70 percent (95 percent CI, 66 to 74 percent) and the disease control rate was 95 percent (95 percent CI, 92 to 96 percent) with essentially no heterogeneity.

Safety outcomes were also quantified. The pooled incidence of grade 3 or higher treatment-related adverse events, graded according to NCI-CTCAE version 4.0, was 31 percent (95 percent CI, 21 to 43 percent), with substantial heterogeneity of I-squared 80.1 percent. Critically, no patients died as a result of these severe adverse events, and surgery was delayed in only one patient, for 93 days, because of treatment-associated pneumonia. The pooled postoperative complication rate was 27 percent (95 percent CI, 22 to 32 percent), and no patient died within 30 days of surgery from postoperative complications. Only one patient required a second operation, eventually recovering, due to bleeding from the gastrointestinal anastomosis. The most common complications, including pneumonia, hemorrhage, abdominal infection, anastomotic leakage, and pleural effusion, mostly belonged to Clavien-Dindo class II and did not dramatically affect survival prognosis.

In exploratory subgroup analyses, the pooled pathologic complete response rate was 12 percent in the apatinib plus chemotherapy group and 22 percent in the apatinib plus immunotherapy and chemotherapy group, with a descriptive estimate of 33 percent in the single apatinib plus chemoradiotherapy study. Similar directional differences appeared in major pathologic response, objective response, and R0 resection rates, which were 93.5 percent in the chemotherapy subgroup and 96.7 percent in the immunotherapy subgroup. The incidence of severe treatment-related adverse events was 23 percent in the immunotherapy subgroup versus 39 percent in the chemotherapy subgroup. The authors emphasize, however, that these are indirect, non-randomized comparisons derived from independent single-arm cohorts and are presented descriptively as hypothesis-generating, not as evidence of comparative efficacy.

The biological plausibility of combining apatinib with immune checkpoint inhibitors adds technical depth to these findings. Beyond directly suppressing tumor angiogenesis, apatinib targets components of the tumor microenvironment outside tumor cells and promotes the infiltration and activation of CD8-positive T lymphocytes. Immune checkpoint inhibitors targeting PD-1 have demonstrated antitumor activity in gastric and gastroesophageal junction adenocarcinoma, and apatinib-based regimens combined with PD-1 inhibition have shown activity in advanced disease and other solid tumors. In a three-arm randomized controlled study by Xiong and Li, the apatinib plus immunotherapy and chemotherapy group showed improved one-, two-, and three-year disease-free survival and overall survival compared with the other groups, though it caused a higher incidence of peripheral neuropathy, while the apatinib plus chemotherapy group increased the incidence of hypertension. Possible explanations include PD-1 inhibitor-induced autoreactive antibodies, cytotoxic T cells, and inflammatory cytokines affecting neural integrity, as well as apatinib-induced endothelin-1 activation and oxidative stress.

The authors also confront important limitations. The evidence base is predominantly non-comparative and heterogeneous, drawn mostly from single-arm phase II trials and retrospective cohort studies, some of which are conference abstracts without full-text peer review. Most trials have not yet reached predefined long-term endpoints, so the impact on overall and disease-free survival remains unconfirmed. Substantial clinical heterogeneity existed across studies in apatinib dose, combination regimens, number of neoadjuvant cycles, tumor stage, histology, and patient selection. Notably, the included studies generally did not stratify outcomes by histologic type or differentiation grade, and whether apatinib can overcome the relative resistance of poorly differentiated diffuse-type tumors to conventional neoadjuvant chemotherapy remains unclear. Age-related tolerability also warrants attention: a phase II study in elderly patients reported high incidences of fatigue and hypertension, and the NMPA-approved drug label in China advises caution in patients over 70 years, with individualized management including regular blood-pressure monitoring, routine urinalysis for proteinuria, and possible dose reduction to 250 mg/day for patients with poor tolerability.

Sensitivity analyses, including leave-one-out calculations and re-inclusion of the excluded overlapping cohort, confirmed that the pooled estimates remained essentially unchanged, and Egger’s regression test revealed no statistically significant publication bias for any outcome. The overall picture is one of feasibility rather than proof: apatinib-containing neoadjuvant therapy appears deliverable with an acceptable safety profile in selected patients, achieving pathologic response rates that may inform future hypothesis-driven research. The authors conclude that these descriptive estimates provide a basis for the design of future large multicenter randomized controlled trials to validate the role of apatinib in the neoadjuvant setting, while cautioning that no conclusion regarding comparative efficacy or safety superiority over conventional therapy can yet be drawn. For a cancer whose standard of care has plateaued, that call for rigorous randomized evidence may prove the most consequential finding of all.

Subject of Research: Apatinib-containing neoadjuvant therapy for resectable gastric and gastroesophageal junction adenocarcinoma

Article Title: Efficacy and safety of apatinib-containing neoadjuvant regimens for resectable gastric and gastroesophageal junction adenocarcinoma: a systematic review and single-arm meta-analysis

Article References: Xin, K., Chen, Z., Yang, L., Qin, L., Chen, S., Xiao, T., & Zhao, Y. (2026). Efficacy and safety of apatinib-containing neoadjuvant regimens for resectable gastric and gastroesophageal junction adenocarcinoma: a systematic review and single-arm meta-analysis. Frontiers in Oncology, 16, Article 1910490. https://doi.org/10.3389/fonc.2026.1910490

Image Credits: AI Generated

DOI: 10.3389/fonc.2026.1910490

Keywords: apatinib, gastric cancer, gastroesophageal junction adenocarcinoma, neoadjuvant therapy, pathologic complete response, meta-analysis, VEGFR2 inhibitor, immunotherapy, R0 resection, surgical oncology, Frontiers in Oncology, Efficacy

The rationale behind the trial rests on a growing understanding of how tumors interact with the immune system. Camrelizumab is a humanized monoclonal antibody that blocks PD-1, a receptor on T cells that, when engaged by its ligand PD-L1, acts as a molecular brake on immune attack. Blocking PD-1 releases that brake, allowing T cells to recognize and destroy cancer cells. Apatinib, by contrast, is an oral small-molecule inhibitor of vascular endothelial growth factor receptor 2, or VEGFR2, which disrupts the signaling that tumors use to grow new blood vessels. Anti-angiogenic therapy does more than starve tumors of nutrients; at appropriately low doses it can normalize the chaotic vasculature inside tumors, improve oxygen delivery, and reverse an immunosuppressive microenvironment, making the tissue more permeable to infiltrating immune cells. Preclinical work has shown that low-dose anti-angiogenic therapy can sensitize breast tumors to PD-1 blockade, and the combination of camrelizumab and apatinib had already demonstrated activity in advanced triple-negative breast cancer in an earlier phase II trial.

The design of the new study was deliberately selective. Between December 2022 and March 2024, the researchers screened 25 patients with stage II to III triple-negative breast cancer and enrolled 14, all of whom had baseline tumor-infiltrating lymphocytes exceeding 10 percent. Tumor-infiltrating lymphocytes, or TILs, are immune cells that have already penetrated the tumor bed, and their abundance is a recognized marker of an inflamed, immunologically active tumor microenvironment. By restricting enrollment to TIL-high patients, the investigators aimed to treat those most likely to benefit from immunotherapy alone, without the immune-priming effects of chemotherapy. Participants received eight 21-day cycles of intravenous camrelizumab at 200 milligrams, or 3 milligrams per kilogram for patients weighing under 50 kilograms, combined with daily oral apatinib at 250 milligrams. The primary endpoint was the pathological complete response rate, the proportion of patients in whom no residual invasive cancer could be detected in the breast and lymph nodes at the time of surgery.

The efficacy results were modest but meaningful for a chemotherapy-free regimen. Of the 14 patients treated, 13 were evaluable for efficacy and 11 proceeded to surgery. Three of the 11 surgical patients, or 27.3 percent, achieved a pathological complete response, and the objective response rate, measured by radiographic tumor shrinkage according to RECIST criteria, was 46.2 percent among the 13 evaluable patients. Perhaps most striking was the durability of benefit: the 24-month disease-free survival rate reached 90.9 percent. Pathological complete response is a well-validated surrogate for long-term outcomes in triple-negative breast cancer, established by the landmark CTNeoBC pooled analysis, and a 27.3 percent rate falls below what is typically achieved with modern chemoimmunotherapy, but the near-complete absence of relapse among surviving patients during follow-up suggests that responders derive substantial protection.

Safety data provided some of the most encouraging findings. Treatment-related adverse events were predominantly grade 1 to 2, meaning mild to moderate in severity, and grade 3 or higher events occurred in 28.6 percent of patients. This toxicity profile compares favorably with standard neoadjuvant chemotherapy for triple-negative disease, which routinely causes severe neutropenia, hair loss, nausea, and peripheral neuropathy, and which is frequently combined with immune checkpoint inhibitors in current practice, compounding the burden. The absence of anthracyclines and taxanes also eliminates the risk of chemotherapy-related cardiac injury and secondary leukemias, long-term concerns for young breast cancer survivors. The trial’s quality-of-life assessments, using validated instruments including the EORTC QLQ-BR23 breast cancer module and the EQ-5D-5L questionnaire, reinforced the tolerability advantage of the regimen.

Context matters when interpreting these numbers. The current standard of care for high-risk early-stage triple-negative breast cancer, established by the KEYNOTE-522 trial, combines pembrolizumab with chemotherapy and has demonstrated pathological complete response rates above 60 percent along with improved event-free and overall survival, leading to guideline endorsements from both the National Comprehensive Cancer Network and the American Society of Clinical Oncology. The CamRelief trial further confirmed that camrelizumab added to neoadjuvant chemotherapy improves pathological complete response rates in Chinese patients. Against this benchmark, a 27.3 percent pathological complete response rate from immunotherapy and anti-angiogenic therapy alone is clearly not ready to replace chemoimmunotherapy for the general population. However, the trial’s TIL-enrichment strategy hints at a precision-oncology approach: if biomarkers can reliably identify the minority of patients whose tumors are already immunologically primed, a substantial fraction might avoid chemotherapy without sacrificing cure.

The exploratory biomarker work in the study adds scientific depth to the clinical findings. Transcriptomic analysis of tumor samples identified differential expression of genes involved in extracellular matrix remodeling and immune regulation between responding and non-responding patients. The extracellular matrix, the dense protein scaffold surrounding tumor cells, can physically exclude T cells and promote immunosuppression, and genes such as MMP-11 and SPP1 have been linked to macrophage polarization and poor prognosis in triple-negative breast cancer. Other work has shown that tumor-derived cytokines like Chi3l1 can induce neutrophil extracellular traps that wall off T cells. These molecular signatures may eventually serve as predictive biomarkers, allowing clinicians to determine before treatment begins which patients are likely to respond to the camrelizumab-apatinib combination and which require chemotherapy from the outset.

The study’s limitations are considerable and the authors are candid about them. With only 14 patients treated and 11 undergoing surgery, the trial was small, single-arm, and without a randomized comparator, making it impossible to exclude selection effects or to compare outcomes directly against standard therapy. The TIL threshold of greater than 10 percent, while grounded in international consensus guidelines for TIL assessment, defines a subgroup that represents only a portion of triple-negative breast cancer patients. Confidence intervals around the response estimates are correspondingly wide. Furthermore, pathological complete response, although a validated surrogate endpoint, is not identical to survival benefit, and ongoing debates in the oncology community about the adequacy of pathological response as a surrogate in immunotherapy trials, highlighted in recent analyses of distant disease-free survival data from large neoadjuvant trials, apply here as well.

Nevertheless, the trial, registered as NCT05556200, occupies an important position in a broader research movement toward chemotherapy-free treatment of immunologically hot tumors. Parallel efforts include neoadjuvant nivolumab-based dual checkpoint blockade in TIL-high triple-negative breast cancer presented at recent European oncology meetings, and the successful application of the same camrelizumab-apatinib combination in resectable non-small cell lung cancer. The convergence of these studies suggests that the chemotherapy-free paradigm is not a one-off experiment but a reproducible strategy built on a coherent biological principle: that tumors rich in infiltrating lymphocytes can be reactivated against themselves by removing immunosuppressive signals and normalizing the tumor microenvironment, without the need for cytotoxic drugs.

For patients, the immediate takeaway is one of cautious optimism rather than changed practice. Chemotherapy combined with immunotherapy remains the standard for early-stage triple-negative breast cancer, and no patient should alter treatment based on a 14-patient phase II study. But the trial demonstrates feasibility, manageable toxicity, preliminary activity, and a 90.9 percent two-year disease-free survival rate in a biomarker-selected population, providing the justification for larger, randomized studies that could ultimately define which patients qualify for chemotherapy-free care. If subsequent trials confirm these findings and validate the transcriptomic biomarkers identified by the researchers, the era in which every triple-negative breast cancer patient automatically receives chemotherapy may gradually give way to one in which treatment is tailored to the immunological fingerprint of each tumor, sparing many women the harshest burdens of cancer therapy while preserving, and perhaps improving, their chances of long-term cure.

Subject of Research: Neoadjuvant camrelizumab plus apatinib as a chemotherapy-free treatment for early-stage triple-negative breast cancer

Article Title: Efficacy, safety, and biomarker analysis of neoadjuvant camrelizumab plus apatinib as a chemotherapy-free strategy for early-stage triple-negative breast cancer: a phase II study

Article References: Tian, Z., Li, H., Deng, Y., Yao, H., Wang, Y., Jin, L., Deng, H., Chen, N., & Liu, J. (2026). Efficacy, safety, and biomarker analysis of neoadjuvant camrelizumab plus apatinib as a chemotherapy-free strategy for early-stage triple-negative breast cancer: a phase II study. Breast Cancer Research and Treatment, 219(2), Article 3. https://doi.org/10.1007/s10549-026-08066-5

Image Credits: AI Generated

DOI: 10.1007/s10549-026-08066-5

Keywords: triple-negative breast cancer, camrelizumab, apatinib, neoadjuvant therapy, immunotherapy, PD-1 inhibitor, anti-angiogenic therapy, tumor-infiltrating lymphocytes, pathological complete response, phase II trial, biomarkers, tumor microenvironment

The study, published in Breast Cancer Research and Treatment, retrospectively analyzed 87 women with metastatic triple-negative breast cancer who received Trop-2 antibody-drug conjugates between April 2020 and December 2025. Nearly all patients were treated with sacituzumab govitecan, an antibody-drug conjugate that links a topoisomerase I inhibitor payload to an antibody targeting Trop-2, a cell-surface protein abundantly expressed in triple-negative tumors. Two patients received sacituzumab tirumotecan, a related agent. Patients were divided into three groups: 60 received the antibody-drug conjugate alone, 13 received it together with the PD-1 inhibitor pembrolizumab, and 14 received a triple-agent regimen combining the antibody-drug conjugate, pembrolizumab, and the oral anti-angiogenic drug apatinib. All patients received at least two cycles of therapy in the second-line or later setting.

The results describe a clear stepwise gradient of activity. The objective response rate was 31.7 percent with monotherapy, 38.5 percent with the dual combination, and 57.1 percent with the triple-agent regimen. Disease control rates followed the same pattern, rising from 78.3 percent to 84.6 percent and then to 92.9 percent. More consequential still were the survival figures. Median progression-free survival was 3.8 months with monotherapy, 10.0 months with the dual combination, and 15.4 months with the triple-agent combination, over a median follow-up of 15.2 months. In pooled analysis, any combination therapy was associated with a hazard ratio of 0.387 for progression or death compared with monotherapy, and the benefit persisted after propensity-score-based overlap weighting, with an adjusted hazard ratio of 0.49.

The biological logic underlying the triplet is rooted in the interplay between tumor vasculature and antitumor immunity. Low-dose VEGF pathway inhibition is known to promote vascular normalization within tumors, reversing the hypoxic, immunosuppressive microenvironment that blunts immune checkpoint blockade. Preclinical work has shown that anti-angiogenic therapy enhances CD8-positive T cell activity, and that the OPN-TGF-beta pathway upregulates PD-1 on these T cells, increasing their sensitivity to PD-1 blockade. Clinical evidence has been accumulating in parallel: the ATRACTIB trial suggested that adding bevacizumab to atezolizumab and paclitaxel improved outcomes including in PD-L1-negative disease, and a multicenter phase II trial of camrelizumab, apatinib, and eribulin achieved a 37 percent response rate in heavily pretreated patients regardless of PD-L1 status. The new study extends this concept to an antibody-drug conjugate backbone.

Importantly, the exploratory subgroup analyses suggested that the activity of the triple-agent combination may not be confined to PD-L1-positive tumors. The interaction P-value between treatment effect and PD-L1 status was 0.098, and among the 39 patients with confirmed PD-L1-positive disease, median progression-free survival had not been reached in the triplet group compared with 5.0 months on monotherapy, a statistically significant difference. Prior treatment with a PD-1 inhibitor, documented in roughly half of the cohort, also did not appear to diminish the benefit of the triplet, with an interaction P-value of 0.828. This is clinically meaningful because primary resistance to checkpoint inhibitors occurs in approximately 60 percent of PD-L1-negative triple-negative breast cancers, and immunotherapy rechallenge after progression is often viewed with skepticism.

One of the most intriguing findings emerged from an interaction test involving prior platinum exposure. Among patients who had previously received platinum chemotherapy, the hazard ratio for the triple-agent regimen versus monotherapy was 0.19, a dramatic reduction in the risk of progression or death, whereas among platinum-naive patients the hazard ratio was 1.11, showing essentially no difference. The interaction P-value of 0.039 suggests that platinum-pretreated patients may represent a subgroup particularly likely to benefit from the triplet, possibly because platinum sensitivity reflects underlying DNA damage repair deficiencies that also influence antibody-drug conjugate efficacy. The authors caution that this observation is exploratory and requires prospective validation, but it provides a concrete hypothesis for patient selection in future trials.

Safety data were reassuring. With prophylactic measures applied across the entire cohort, grade 3 or higher treatment-related adverse events occurred in 20.0 percent of monotherapy patients, 15.4 percent of the dual-combination group, and 14.3 percent of the triple-agent group, a difference that was not statistically significant. The most common severe toxicities were leukopenia and neutropenia across all groups. No treatment-related deaths were recorded, and no grade 3 or higher febrile neutropenia, hyperbilirubinemia, rash, or oral ulceration was reported. The starting dose of the antibody-drug conjugate was individualized according to performance status, with patients scoring 2 on the Eastern Cooperative Oncology Group scale receiving reduced starting doses below 80 percent of the standard level. Notably, an antibody-drug conjugate starting dose of at least 80 percent was associated with improved progression-free survival, underscoring the importance of maintaining dose intensity where tolerable.

Beyond the clinical outcomes, the research team developed an exploratory genomic scoring system aimed at identifying which patients are most likely to respond to the triple-agent strategy. The system incorporates mutations in 17 genes connected to Trop-2 antibody-drug conjugate sensitivity, homologous recombination repair, and angiogenesis pathways. Genes promoting therapeutic response, such as ATR, which may sensitize tumors to topoisomerase I inhibition and correlate with higher mutational burden and immunotherapy benefit, received positive weighted scores, while resistance-associated genes received negative scores. Patients whose total score exceeded zero were classified as likely to benefit from the triplet, and Fisher’s exact testing showed the classification was statistically significant. Genes such as VEGFRA and VEGFRB, tied to angiogenesis signaling, may indicate sensitivity to the anti-angiogenic component. The authors emphasize that the model’s principal value at this stage is hypothesis generation rather than clinical deployment.

The study also confirmed several prognostic patterns familiar from earlier research. Patients who initiated antibody-drug conjugate therapy in the second or third line had significantly longer progression-free survival than those treated later, at 5.8 versus 3.0 months. The presence of liver metastases, brain metastases, or visceral disease more broadly each independently predicted shorter progression-free survival after multivariable adjustment, with hazard ratios of 2.38, 2.51, and elevated risk for visceral involvement overall. These findings reinforce that disease biology and metastatic pattern remain dominant determinants of outcome even in the era of antibody-drug conjugates, and they highlight the need for improved risk stratification in biologically aggressive disease.

The investigators are transparent about the limitations inherent in a retrospective, single-center, non-randomized design. Selection bias and residual confounding cannot be excluded, baseline characteristics such as treatment line and PD-L1 status differed descriptively across groups, and the small size of the combination cohorts, 13 and 14 patients respectively, limits statistical power. Sensitivity analyses restricted to second- or third-line patients yielded directionally consistent but non-significant results, likely reflecting reduced sample size. To address these constraints, the team has launched a prospective randomized controlled trial, registered as NCT06851299, designed to rigorously test the efficacy and safety of Trop-2 antibody-drug conjugate-based combination regimens and to validate the genomic risk score. If those results confirm the signals described here, a triplet regimen combining a Trop-2 antibody-drug conjugate, PD-1 blockade, and anti-angiogenic therapy could reshape the treatment algorithm for one of breast cancer’s most lethal forms, extending meaningful survival to patients who currently have few good options.

Subject of Research: Trop-2-directed antibody-drug conjugate monotherapy and combination therapy for pretreated metastatic triple-negative breast cancer

Article Title: Exploring trop-2-directed ADCs monotherapy and combination therapy in pretreated mTNBC: a real-world study

Article References: Liu, J., Ding, L., Wang, J., Chen, T., Long, T., Li, Q., Chai, J., Yao, H., Wang, Y., & Zhao, J. (2026). Exploring trop-2-directed ADCs monotherapy and combination therapy in pretreated mTNBC: a real-world study. Breast Cancer Research and Treatment, 219(2), Article 10. https://doi.org/10.1007/s10549-026-08070-9

Image Credits: AI Generated

DOI: 10.1007/s10549-026-08070-9

Keywords: Trop-2 antibody-drug conjugates, metastatic triple-negative breast cancer, sacituzumab govitecan, PD-1 inhibitors, anti-angiogenic therapy, triple-agent combination therapy, pembrolizumab, apatinib, progression-free survival, biomarker-guided therapy, real-world study, immune checkpoint inhibitors