Biomedical subjects

Robert J Korst

Publications and source records attributed to Robert J Korst.

33 records · Page 2Linked to original sources

PubMed2003

High grade dysplasia: surveillance, mucosal ablation, or resection?

Barrett's esophagus is a common premalignant condition that results from chronic gastroesophageal reflux. High grade dysplasia in the metaplastic esophagus is thought to be the last step in the metaplasia-to-carcinoma sequence that characterizes this disease. The management of high grade dysplasia in Barrett's esophagus is controversial. Some investigators advocate a rigorous endoscopic surveillance program with biopsies, but this approach has been questioned because of its clinical impracticality, high cost, possibility of sampling errors, and difficulty demonstrating effectiveness on a reproducible basis. Others advocate mucosal ablative therapy to eradicate the dysplastic and metaplastic epithelium. This approach, still in its infancy, cannot be accepted as standard therapy at the present time because of limited follow-up, its questionable ability to completely eradicate the abnormal mucosa, the phenomenon of pseudoregression, and the patients require continued rigorous endoscopic surveillance. Esophagectomy, on the other hand, can be accomplished with a low mortality rate in these patients. We advocate this approach because a large number of them have invasive cancer in the esophagus despite a preoperative diagnosis of only high grade dysplasia. In addition, the 5-year survival is excellent even if invasive cancer is present, and these patients are liberated from rigorous endoscopic surveillance for the rest of their lives. For patients with high grade dysplasia in Barrett's esophagus who are poor operative risks, less invasive approaches such as mucosal ablation may play a role, but longer follow-up information is needed before this technique can be accepted even in this setting.

Barrett Esophagus↗

PubMed2003

Thoracic esophageal perforations: a decade of experience.

BACKGROUND: Perforation of the thoracic esophagus is a formidable challenge. Treatment and outcome are largely determined by the time to presentation. We reviewed our experience with esophageal perforations to determine the overall mortality and whether the time to presentation should influence management strategy. METHODS: A retrospective chart review was performed on all patients treated for perforation of the thoracic esophagus from 1990 to 2001. There were 26 patients (14 men and 12 women; median age, 62 years; range, 36 to 89 years). Fourteen patients presented within 24 hours (early), and 12 patients presented after 24 hours (delayed). Nine of the 12 patients in the delayed group presented after 72 hours. The causes of the perforations were as follows: instrumentation (19 patients), Boerhaave's syndrome (2 patients), intraoperative injury (1 patient), and other (4 patients). In the early group, 3 patients were treated conservatively, 10 patients underwent primary repair, and 1 patient required esophagectomy for carcinoma. In the delayed group, 3 patients were treated conservatively, 6 underwent successful repair of the perforation, 1 had a T-tube placement through the perforation and eventually required an esophagectomy, and 2 had an esophagectomy as primary surgical treatment. RESULTS: Hospital mortality was 3.8% (1 of 26) and morbidity was 38% (10 of 26). Persistent leaks occurred in 3 patients, 2 after primary repair and 1 after T-tube drainage. All patients selected for conservative management successfully healed their perforation. CONCLUSIONS: Primary repair can be carried out in most cases of thoracic esophageal perforation regardless of time to presentation, with a low mortality rate. A small but carefully selected group of patients may be treated successfully without operation. Esophagectomy should be reserved for patients with carcinoma or extensive necrosis of the esophagus.

Adult↗

PubMed2003

Resection of a symptomatic pericardial cyst using the computer-enhanced da Vinci Surgical System.

Traditionally, symptomatic pericardial cysts have been treated with thoracotomy and resection. More recently, video-assisted thoracoscopic procedures for pericardial cysts have been reported. We present the case of a 43-year-old man who was suffering from a symptomatic pericardial cyst. He underwent successful resection using a computer-enhanced robotic surgical system. This case is an example of the continued extension of robotic-assisted thoracic surgery.

Adult↗

PubMed2003

Active, specific immunotherapy for lung cancer: hurdles and strategies using genetic modification.

Active immunotherapy for lung cancer has been a challenge because of the poor antigenic characterization of these tumors and their ability to escape the immune response. However, knowledge of the mechanisms of anti-tumor immunity has expanded significantly over the past decade, leading to the development of more novel, specific strategies for augmenting the immune response. Genetic manipulation of tumor cells, immune cells, or both, may help overcome some of the previously encountered difficulties of immunotherapy. Laboratory and clinical investigations are currently ongoing to evaluate the feasibility and potential benefit of these novel approaches.

Animals↗

PubMed2003

In vivo gene transfer of pigment epithelium-derived factor inhibits tumor growth in syngeneic murine models of thoracic malignancies.

OBJECTIVE: Pigment epithelium-derived factor is known to be an inhibitor of angiogenesis. We hypothesized that in vivo gene transfer of pigment epithelium-derived factor may inhibit tumor angiogenesis and growth in syngeneic models of thoracic malignancies. METHODS: An adenovirus vector encoding the human pigment epithelium-derived factor cDNA (AdPEDF) was used to transduce human lung cancer cells in vitro. Transgene expression was assessed using Western analysis. Three different murine flank tumors (2 lung, 1 colon) were then established in syngeneic mice and treated intratumorally with phosphate-buffered saline, AdPEDF, or an empty vector (AdNull). Endpoints measured included transgene expression, tumor size, and animal survival, as well as microvessel density within the tumor. Additionally, a murine pulmonary metastasis model was established by intravenous injection of a syngeneic colon adenocarcinoma cell line expressing a marker gene (beta-galactosidase). One day later, treatment (phosphate-buffered saline, AdNull, or AdPEDF) was administered intrapleurally. Tumor burden (gross and histologic inspection, lung weight, and beta-galactosidase expression) was then evaluated 13 days after vector dosing, and survival was recorded. RESULTS: AdPEDF-derived expression of pigment epithelium-derived factor was demonstrated in vitro and in vivo. In syngeneic murine lung cancer flank tumors, intratumoral administration of AdPEDF significantly inhibited tumor growth (P <.01), prolonged mouse survival (P <.01), and decreased microvessel density (P <.01) compared with control groups. In the pulmonary metastasis model, AdPEDF-treated mice exhibited significantly reduced lung lesions, lung weight (P <.0005), beta-galactosidase expression (P <.05), and animal survival was prolonged (P <.05). CONCLUSION: Gene transfer of pigment epithelium-derived factor suppresses tumor vascularization and growth, while prolonging survival in syngeneic murine models of thoracic malignancies.

Adenoviruses, Human↗

PubMed2003

Cisplatin augments cytotoxic T-lymphocyte-mediated antitumor immunity in poorly immunogenic murine lung cancer.

OBJECTIVE: Many tumors are poorly immunogenic and resistant to cytotoxic T-lymphocyte-mediated cell lysis. Because cisplatin has been demonstrated to increase tumor cell Fas receptor expression, we hypothesized that cisplatin will enhance cytotoxic T-lymphocyte tumor cell killing and augment the antitumor effect of an active immunotherapy strategy in a poorly immunogenic murine lung cancer model. METHODS: Lewis lung carcinoma cells were exposed to cisplatin in vitro, and Fas receptor expression and apoptosis in response to an agonistic anti-Fas antibody were quantified using flow cytometry. Wild-type and Fas ligand-deficient mice bearing Lewis lung carcinoma flank tumors were then treated with intraperitoneal cisplatin as well as an intratumoral injection of an adenovirus gene transfer vector encoding CD40 ligand. End points included tumor size, animal survival, and Fas expression (determined using immunofluorescence). Cytotoxicity assays were performed using splenocytes from adenovirus gene transfer vector encoding CD40 ligand-treated animals as effectors and cisplatin-treated Lewis lung carcinoma cells as targets. RESULTS: Cisplatin induced heightened expression of Fas receptor on Lewis lung carcinoma cells in vitro and in vivo and enhanced apoptosis in cells exposed to an agonistic anti-Fas antibody. In vivo, the combination of 1 dose of intraperitoneal cisplatin and intratumoral adenovirus gene transfer vector encoding CD40 ligand inhibited tumor growth and prolonged survival compared with adenovirus gene transfer vector encoding CD40 ligand alone, resulting in a higher cure rate. This effect was lost in Fas ligand-deficient mice. Splenocytes from adenovirus gene transfer vector encoding CD40 ligand-treated wild-type mice lysed cisplatin-treated Lewis lung carcinoma cells more efficiently than untreated Lewis lung carcinoma cells, an effect lost in splenocytes from Fas ligand-deficient mice. CONCLUSION: Cisplatin augments the antitumor effect of a cytotoxic T-lymphocyte-mediated immunotherapy strategy, resulting in a higher cure rate than seen with immunotherapy alone. This effect is associated with the enhanced ability of cytotoxic T lymphocytes to lyse tumor cells that have been exposed to cisplatin through Fas/Fas ligand interactions.

Adenoviridae↗

PubMed2003

Tumor size predicts survival within stage IA non-small cell lung cancer.

STUDY OBJECTIVES: The basic premise of CT screening is that size is an important determinant of survival in lung cancer. We sought to examine this hypothesis within stage IA non-small cell lung cancer (NSCLC). METHODS: A retrospective analysis of all patients with pathologically confirmed stage IA NSCLC resected from 1991 to 2001 was conducted. All but seven patients underwent anatomic lung resection and mediastinal lymph node dissection. Kaplan-Meier survival analysis was performed to estimate the 5-year overall and disease-specific survival probability stratified by tumor size. The influence of age, gender, histology, and tumor size on survival was also analyzed using a Cox proportional hazards regression model. RESULTS: There were 244 patients (mean age, 66.7 years; 45.1% were men). Lobectomy was performed in 229 patients, segmentectomy in 8 patients, and wedge resection in 7 patients. Operative mortality was 0.4%. Histologic breakdown was as follows: adenocarcinoma (59.4%), squamous (18.9%), bronchoalveolar (15.2%), large cell (4.5%), and poorly differentiated (2.0%). The median follow-up time for all patients was 2.6 years. The 5-year survival probability for all patients was 71.1% (95% confidence interval [CI], 63.6 to 78.6%). For 161 patients with tumor sizes < or = 2.0 cm, the 5-year survival probability was 77.2% (95% CI, 68.6 to 85.8%) in comparison with 60.3% (95% CI, 46.7 to 73.8%) in 83 patients with tumor size > 2.0 cm (p = 0.03 by log-rank test). The overall 5-year disease-specific survival was 74.9% (95% CI, 67.6 to 82.2%). Disease-specific survival was 81.4% (95% CI, 73.3 to 89.4%) for patients with tumors < or = 2.0 cm and 63.4% (95% CI, 49.6 to 77.1%) for patients with tumors > 2.0 cm. CONCLUSIONS: These data suggest that size within stage IA is an important predictor of survival and that further substaging should be considered.

Aged↗

PubMed2002

Long-term results of combined-modality therapy in resectable non-small-cell lung cancer.

PURPOSE: Assessment of long-term results of combined-modality therapy for resectable non-small-cell lung cancer is hampered by insufficient follow-up and small patient numbers. To evaluate this, we reviewed our collective experience. PATIENTS AND METHODS: This study was a retrospective chart review recording demographics, tumor stage, treatment, and outcome of consecutive patients undergoing surgery. Survival was analyzed by Kaplan-Meier, and prognostic factors were analyzed by log-rank and Cox regression. RESULTS: From January 1993 to December 1999, 470 patients were treated, with follow-up in 446: 27 stage I, 55 stage II, 316 stage III, 43 stage IV (solitary M1), and five uncertain. Chemotherapy was mitomycin/vinblastine/cisplatin (174 patients [39.0%]), carboplatin/paclitaxel (148 [33.2%]), and other combination (124 [27.8%]); 75 patients (16.8%) received induction radiation. Resection was complete in 77.4%, incomplete in 8.3%, attempted but with gross residual disease afterward in 1.8%, and not performed in 12.6%. Pathologic complete response occurred in 20 patients (4.5%). With median follow-up of 31.0 months for patients still alive, median and 3-year survival for pathologic stages 0, I, II, III, and IV were more than 90 months, 73%; 42 months, 52%; 23 months, 35%; 16 months, 28%; and 16 months, 23% (P <.001). In a multivariate analysis, age, complete resection, pathologic stage, and pneumonectomy, but not induction regimen, significantly influenced survival. CONCLUSION: Although pathologic complete response outside the protocol setting is low, survival of this large patient cohort is comparable to that of patients in published combined-modality trials. Survival is significantly influenced by patient age, complete resection, pathologic stage, and pneumonectomy. These results can help guide standard clinical practice and emphasize the need for novel induction regimens.

Adult↗

PubMed2002

Effect of adenovirus gene transfer vectors on the immunologic functions of mouse dendritic cells.

To address the effect of adenovirus (Ad) gene transfer vector transduction on the diverse functions of dendritic cells, we used an Ad vector encoding no transgene (AdNull) to transduce mouse bone-marrow-derived dendritic cells (BMDC). Initial experiments using an Ad vector encoding a marker gene (AdGFP, jellyfish green fluorescent protein) showed that the optimal ratio of infectious Ad particles to each cell was 100, when both transgene expression and resultant BMDC viability were taken into account. Exposure to AdNull resulted in upregulation of both surface activation markers (CD40, MHC class II, B7.1, B7.2, ICAM-1) and IL-12 expression by BMDC. AdNull activation of BMDC was observed in multiple strains of mice. Despite this, AdNull-transduced BMDC displayed only modestly impaired antigen uptake ability, as demonstrated in macropinocytosis and phagocytosis assays, in vitro. However, Ad-modified BMDC migrated to regional lymph nodes five times more efficiently than sham-transduced BMDC in vivo. In addition, Ad transduction significantly enhanced the ability of BMDC to present a model peptide antigen to T-lymphocyte hybridoma cells at low BMDC:T cell ratios. We conclude that Ad modification, in and of itself, induces a state of activation in mouse BMDC. This activation, albeit mild compared with that induced by other stimuli, produces measurable effects of the specific immunological functions of these antigen-presenting cells.

Adenoviridae↗

PubMed2002

Clinical pattern and pathologic stage but not histologic features predict outcome for bronchioloalveolar carcinoma.

BACKGROUND: The histologic criteria defining bronchioloalveolar carcinoma (BAC) were recently revised, but it is unclear whether these criteria predict clinical behavior. This study determined the outcome of resected BAC in relationship to clinical and radiologic disease pattern, and pathologic features. METHODS: Between 1989 and 2000, 100 consecutive surgically treated patients with adenocarcinomas exhibiting various degrees of BAC features were retrospectively studied. Histology was reviewed; tumors were classified as pure BAC, BAC with focal invasion, and adenocarcinoma with BAC features. Clinical and radiologic pattern were classified as unifocal, multifocal, or pneumonic. Demographic data, tumor stage, and outcome were recorded. Survival was analyzed by the Kaplan-Meier method, and prognostic factors were determined by the log-rank test. RESULTS: Patient median age was 65, and 74% of the patients were female. Pure BAC, BAC with focal invasion, and adenocarcinoma with BAC features occurred in 47, 21, and 32 patients, respectively. Unifocal disease occurred in 64 patients, multifocal in 29, and pneumonic in 7. Seventy-one patients had stage I/II tumors, 22 had stage III/IV, and 7 patients had Stage X tumors. Overall 5-year survival was 74%. There was no significant difference in survival among the three histologic subtypes. The pneumonic pattern had significantly worse survival compared with unifocal and multifocal patterns. Pathologic stage predicted survival, with 5-year survivals for I/II and III/IV of 83.7% and 59.6%, respectively. CONCLUSIONS: Clinical pattern and pathologic stage, but not the degree of invasion on histologic examination predict survival. Multifocal disease is associated with excellent long-term survival after resection. The favorable survival of stage III/IV BAC indicates that the current staging system does not fully describe this disease in patients undergoing resection because of its distinct tumor behavior.

Adenocarcinoma, Bronchiolo-Alveolar↗

PubMed2002

Adenovirus vector-mediated transfer of the vascular endothelial growth factor cDNA to healing abdominal fascia enhances vascularity and bursting strength in mice with normal and impaired wound healing.

BACKGROUND: We hypothesized that adenovirus-mediated transfer of the vascular endothelial growth factor (VEGF121) complementary DNA (cDNA) to murine laparotomy fascial wounds would enhance vascularity and bursting strength. METHODS: Microfibrillar collagen sponges saturated with adenovirus (Ad) vectors encoding for the human VEGF121 cDNA (Ad(CU)VEGF121.1), a control marker gene (Ad beta gal, AdLuc) or no transgene (AdNull) were sutured to fascial edges during laparotomy closure in normal mice and mice treated with dexamethasone. Endpoints addressed included transgene expression in the fascia and surrounding tissue, the number of blood vessels in the healing wound determined using immunostaining, and wound bursting strength using a calibrated tensinometer. RESULTS: Transgene expression was detected readily in the fascial edges, but only marginally detectable in neighboring tissues. In normal mice and mice treated with dexamethasone, no differences were observed at 7 days. Strikingly, however, 21 days after wound closure/therapy, significantly more blood vessels were present in the wounds that received the VEGF121 vector compared with controls (normal: AdNull: 4.2 +/- 1.8; Ad(CU)VEGF121.1: 11.2 +/- 1.2; P <.05; dexamethasone: AdNull: 1.4 +/- 0.8; Ad(CU)VEGF121.1: 5.4 +/- 1.2; P <.05), and bursting strength was significantly higher in VEGF121-treated wounds (normal: AdNull: 665 +/- 68 mN/mm; Ad(CU)VEGF121.1: 956 +/- 82 mN/mm; P <.0005; dexamethasone: AdNull: 234 +/- 111 mN/mm; Ad(CU)VEGF121.1: 592 +/- 121 mN/mm; P <.03). CONCLUSIONS: Adenovirus-mediated gene transfer to healing fascial wounds is achieved readily using a microfibrillar collagen sponge, with transfer of the human VEGF121 cDNA significantly enhancing wound vascularity and bursting strength in normal mice, as well as in mice treated with dexamethasone.

Adenoviridae↗

PubMed2002

The effects of advanced age on the incidence of supraventricular arrhythmias after pneumonectomy in dogs.

UNLABELLED: Because advanced age is the strongest independent risk factor for the development of supraventricular arrhythmias after lung resection, we compared the incidence and premorbid events of supraventricular arrhythmias after pneumonectomy in young and elderly dogs with the aim of better understanding potential age-related arrhythmogenic mechanisms. Right pneumonectomy was performed in 15 male mongrel dogs ("old" > or =8 yr [n = 8], "young" <4 yr [n = 7]) and the electrocardiogram continuously recorded by an implantable telemetry system for 1 wk before euthanizing. After surgery, 7 of 8 older animals (88%) developed a total of 23 episodes of sustained (>30 s) paroxysmal supraventricular tachycardia (SVT), compared with 0 of 7 (0%) young dogs, P = 0.0014. Analysis of heart rate over the 60 min preceding the onset of SVT revealed a progressive increase in sinus rhythm beginning 15 min before the arrhythmia. Comparison of the heart rate and rhythm obtained in younger animals from the corresponding postoperative hour demonstrated that although older animals developed more atrial (P = 0.03) and ventricular premature contractions (P = 0.056) and episodes of nonsustained ventricular tachycardia (P = 0.01), heart rate was similar for both groups until the increase in elderly dogs preceding the onset of SVT. Histologic examination of the atria showed interstitial fibrosis in old but not young animals. In addition, 4 of 8 (50%) elderly animals exhibited an inflammatory response within the atria consistent with acute myo- and epicarditis. We conclude that elderly dogs have an increased supraventricular arrhythmogenic potential within the first week after pneumonectomy than younger animals, perhaps because of increased atrial fibrosis and inflammation. Heart rate analysis before SVT onset suggests that adrenergic predominance was a probable responsible trigger. IMPLICATIONS: In this canine pneumonectomy model, advanced age was associated with an increased incidence of supraventricular arrhythmias, perhaps because of increased atrial fibrosis and inflammation.

Age Factors↗

PubMed2002

Type I thyroplasty for acute unilateral vocal fold paralysis following intrathoracic surgery.

Patients who undergo intrathoracic operative procedures for malignancy may require sacrifice of a recurrent laryngeal nerve. Postoperative vocal fold paralysis may lead to diminished cough with secretion retention, aspiration, and life-endangering pneumonia. This study retrospectively reviews our institution's experience of 23 patients who underwent type I thyroplasty within the 2-week (acute) period after thoracic surgery. Primary lung cancer (n = 16) was the most common disease. Upper lobectomy (n = 9) and pneumonectomy (n = 7) were the most frequent surgical procedures. Silicone medialization alone (n = 11) or with arytenoid adduction (n = 12) was performed. There were no significant postoperative complications. Improvements in hoarseness (86%), dyspnea (72%), dysphagia (50%), and aspiration (79%) were noted. Pulmonary status improved after vocal fold medialization, as reflected by decreased need for therapeutic bronchoscopy in the majority of patients in the postoperative period. Type I thyroplasty for vocal fold paralysis in the acute phase following thoracic surgery is well tolerated and is associated with improved patient outcome with no postoperative deaths in this high-risk patient population.

Arytenoid Cartilage↗

PubMed2002

Adenovirus vector-mediated overexpression of a truncated form of the p65 nuclear factor kappa B cDNA in dendritic cells enhances their function resulting in immune-mediated suppression of preexisting murine tumors.

PURPOSE: The purpose of this study was to evaluate the effect of the Rel homology domain (RHD) of the transcription factor, nuclear factor kappa B (NF kappa B), on proinflammatory gene expression in bone marrow-derived dendritic cells (BMDCs). EXPERIMENTAL DESIGN: We used an adenovirus vector encoding only the RHD of the NF kappa B (p65 family member) cDNA (AdRHD) to transduce murine BMDCs ex vivo. Endpoints measured included BMDC expression of activation markers, cytokine secretion, peptide antigen presentation, and the ability of these transduced cells to induce antitumor immunity in vivo. RESULTS: AdRHD-transduced BMDCs secreted higher levels of the cytokines interleukin (IL) 1 beta, IL-6, and IL-12 (p40) compared with sham-transduced BMDCs or those transduced with an empty vector. AdRHD induced heightened surface expression of the activation markers CD40, B7.1, B7.2, and MHC class II on BMDCs, and these cells were able to present a peptide antigen to a T-lymphocyte hybridoma more efficiently than controls in vitro. Growth of syngeneic, established tumors (CT26 and B16.F10) was inhibited, and survival was prolonged in the mice that received intratumoral AdRHD-modified BMDCs compared with controls. Splenocytes from CT26 tumor-bearing animals that received intratumoral AdRHD-modified BMDCs were able to lyse CT26 target cells more efficiently than controls. Similar experiments using host mice harboring targeted mutations in CD4 and CD8, as well as BMDCs from mice lacking MHC class I, MHC class II, or IL-12 revealed that this tumor immunity was dependent on the presence of CD4+ and CD8+ cells in the tumor-bearing host, as well as MHC class I, MHC class II, and IL-12 expression by the administered BMDCs. Furthermore, induction of IL-12 (p40) expression by AdRHD was completely abrogated in BMDCs lacking the c-Rel NF kappa B family member. CONCLUSIONS: We made the following conclusions: (a) gene transfer-mediated overexpression of the RHD of NF kappa B activates BMDCs; (b) AdRHD-transduced BMDCs induce antitumor immunity when administered intratumorally, an effect mediated by both the CD4+ T cell/MHC class II and the CD8+ T cell/MHC class I pathways, as well as IL-12; and (c) IL-12 (p40) up-regulation by the RHD transgene in BMDCs is dependent on the presence of the c-Rel NF kappa B family member.

Adenoviridae↗

PubMedDate not supplied

Intratumoral expression of macrophage-derived chemokine induces CD4+ T cell-independent antitumor immunity in mice.

Macrophage-derived chemokine is chemotactic for a variety of leukocytes, and has been shown to be involved in T 2-mediated cellular immunity. To evaluate the role of this chemokine in tumor immunity in vivo, an adenovirus vector encoding the human macrophage-derived chemokine cDNA (AdMDC) was administered to established murine tumors. Gene transfer with AdMDC significantly inhibited tumor growth and prolonged animal survival. AdMDC was not directly cytotoxic to tumor cells, but splenocytes from animals that received intratumoral AdMDC were able to lyse syngeneic tumor cells, and purified splenic CD8 cells secreted interferon-gamma in a tumor-specific manner. The antitumor activity of AdMDC was lost in mice lacking CD8 T lymphocytes, but surprisingly, it was preserved in animals lacking CD4 cells, as was the systemic cytotoxic T lymphocyte response. Systemic NK cells did not play a role in the antitumor immune response induced by AdMDC. Experiments using knockout mice demonstrated that host expression of MHC Class I, but not Class II, IL-4, or IL-12, was necessary for AdMDC to exert its antitumor effect, and immunohistochemistry demonstrated infiltrates of CD8 and CD86 cells, but not CD4 cells in treated tumors. These studies highlight a new function for macrophage-derived chemokine by demonstrating that it possesses in vivo antitumor activity with CD8 T cells as the effector cells, and interestingly, that the CD4 cell/MHC II pathway of CD8 cell activation is not required for the antitumor effects of this chemokine.(H)

Adenocarcinoma↗