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Biomedical subjects

M T Jennings

Publications and source records attributed to M T Jennings.

At least 19 recordsLinked to original sources
PubMed2001

Oligodendroglial ganglioglioma with anaplastic features arising from the thalamus.

Anaplastic gangliogliomas with an oligodendroglial component are exceedingly rare tumors of uncertain growth potential. We report a 17-year-old female with a massive ganglioglioma containing anaplastic oligodendroglioma apparently arising from the thalamus. Two weeks after partial resection, she was started on a regimen including escalated doses of topotecan in combination with a fixed-dosage intensification regimen of cisplatin, cyclophosphamide and vincristine with subsequent hyperfractionated external beam radiotherapy. She currently has stable disease.

Adolescent↗
PubMed2001

Pharmacotherapy of malignant astrocytomas of children and adults: current strategies and future trends.

This article reviews the conceptual progression in the pharmacological therapy of malignant astrocytoma (MA) over the past decade, and its future trends. It is a selective rather than an exhaustive inventory of literature citations. The experience of the Brain Tumour Cooperative Group (BTCG) and earlier phase III trials are summarised to place subsequent phase II and I studies of single and combination agent chemotherapy in perspective. The BTCG experience of the 1970s to 1980s may be summarised to indicate that external beam radiotherapy (EBRT) is therapeutic, although not curative, and not further improved upon by altering fractionation schedules, or the addition of radioenhancers. Whole brain and reduced whole brain EBRT with focal boost were comparable regimens. Nitrosourea-based, adjuvant chemotherapy provided a modest improvement in survival among adult patients, which was comparable with that of other single drugs or multidrug regimes. The multiagent schedules, however, had a correspondingly higher toxicity rate. Intra-arterial administration was associated with significant risk, which conferred no therapeutic advantage. The trend of the past decade has been towards multiagent chemotherapy although its benefit cannot be predicted from the classic prognostic factors. Published experience with investigational trials utilising myeloablative chemotherapy with autologous bone marrow or peripheral blood stem cell haemopoietic support, drug delivery enhancement methods and radiosensitisers is critically reviewed. None of these approaches have achieved wide-spread acceptance in the treatment of adult patients with MA. Greater attention is placed on recent 'chemoradiotherapy' trials, which attempt to integrate and maximise the cytoreductive potential of both modalities. This approach holds promise as an effective means to delay or overcome the evolution of tumour resistance, which is probably one of the dominant determinants of prognosis. However, the efficacy of this approach remains unproven. New chemotherapeutic agents as well as biological response modifiers, protein kinase inhibitors, angiogenesis inhibitors and gene therapy are also discussed; their role in the therapeutic armamentarium has not been defined.

Adult↗
PubMed2001

The molecular genetics of therapeutic resistance in malignant astrocytomas.

The adverse prognosis associated with malignant astrocytomas (MA) is due in part to the development of resistance by the tumor to chemo- and radiotherapy-induced cytotoxic damage. The mechanisms of resistance are poorly understood but function at the level of the endothelial cell, the blood-brain barrier and the neoplastic cell itself. The classic examples of drug resistance proteins, such as the p-glycoprotein/multidrug resistance protein 1, have been identified within MA biopsy specimens. However, it is questionable to what degree, if at all, these proteins contribute directly to the evolution and prognosis of the MA. Surprisingly, there are specific genes, not traditionally associated with resistance, which appear increasingly relevant to both tumor progression and insensitivity to cytotoxic damage. These genes are involved in cell cycle regulation, and include the retinoblastoma susceptibility gene (Rb), the tumor suppressor gene p53, as well as those encoding the cyclins, their kinases and inhibitors. The interaction between the products of these genes and intratumoral environmental factors appears to involve a dynamic and prognostically adverse selection process. It is from this perspective that the mechanism(s) of hypoxic-ischaemic selection for resistance and its therapeutic repercussions will be analyzed.

Animals↗
PubMed2001

December 2000: 6 month old boy with 2 week history of progressive lethargy.

This 6-month-old Caucasian boy presented with a 10-day history of lethargy, obtundation, inability to hold his head up and mild torticollis. MRI and CT scans showed a large solid and cystic mass involving the right temporal, parietal and occipital lobes, pineal, superior pons, mesencephalon and posterior right thalamus. He underwent craniotomy initially for a partial tumor resection with an intraoperative diagnosis of desmoplastic astrocytoma. With immunohistochemistry and special stains the diagnosis of desmoplastic infantile ganglioglioma (DIG) was made. A near total resection was performed a week after initial resection.The patient then was treated with chemotherapy. Two months later an MRI showed tumor growth. Following additional aggressive chemotherapy, an MRI at 5 months post-resection indicated further tumor progression. This case illustrates that some DIGs may behave more aggressively than typical WHO grade I lesions.

Brain↗
PubMed1998

The role of transforming growth factor beta in glioma progression.

This review examines the apparently paradoxical conversion of transforming growth factor beta's (TGFbeta) regulatory role as a growth inhibitor among normal glial cells to that of a progression factor among glioblastomas (GM). In vitro, TGFbeta functions as an autocrine growth inhibitor of near-diploid gliomas of any grade. In contrast, hyperdiploid glioblastoma multiforme (HD-GM) cultures proliferate in response to TGFbeta, which is mediated by induction of platelet-derived growth factor B chain (PDGF-BB). The dominant hypothesis of TGFbeta's pathogenetic association with malignant transformation has been predicated upon acquisition of resistance to its growth inhibitory effects. However, the lack of obvious correlation with TGFbeta receptor (TbetaR) expression (or loss) between the HD-GM and the TGFbeta-inhibited GM cultures suggests the existence of intrinsically opposed regulatory mechanisms influenced by TGFbeta. The mechanism of conversion might be explained either by the loss of a putative tumor suppressor gene (TSG) which mediates TGFbeta's inhibition of growth or by enhancement of an active oncogenic pathway among the HD-GM. The frequency of mutations within glioma-associated TSG, such as TP53 and RB, suggests that defects in TGFbeta's inhibitory signaling pathway may have analogous effects in the progression to HD-GM, and TGFbeta's conversion to a mitogen. Alternative sites of inactivation which might explain the loss of TGFbeta's inhibitory effect include inactivating mutation/loss of the TbetaR type II, alterations in post-receptor signal transmission or the cyclin/cyclin dependent kinase system which regulates the phosphorylation of pRB. Loss or inactivation of a glial TSG with a consequent failure of inhibition appears to allow TGFbeta's other constitutive effects, such as induction of c-sis, to become functionally dominant. Mechanistically, TGFbeta's conversion from autocrine inhibitor to mitogen promotes 'clonal dominance' by conferring a Darwinian advantage to the hyperdiploid subpopulations through qualitative and quantitative differences in its modulation of PDGF-A and c-sis, with concomitant paracrine inhibition of competing, near-diploid elements.

Animals↗
PubMed1997

Transforming growth factor beta as a potential tumor progression factor among hyperdiploid glioblastoma cultures: evidence for the role of platelet-derived growth factor.

Among early-passage, near-diploid gliomas in vitro, transforming growth factor type beta (TGF beta) has been previously shown to be an autocrine growth inhibitor. In contrast, hyperdiploid (> or = 57 chromosomes/metaphase) glioblastoma multiforme (HD-GM) cultures were autocrinely stimulated by the TGF beta. The mechanism of this 'conversion' from autocrine inhibitor to mitogen is not understood; previous studies have suggested that platelet-derived growth factor (PDGF) might be modulated by TGF beta. The similar expression of TGF beta types 1-3, PDGF-AA; -BB, as well as the PDGF receptor alpha and beta subunits (a/beta PDGFR) between biopsies of the HD-GM and near-diploid, TGF beta-inhibited glioblastomas (GM) by immunohistochemistry did not explain the discrepancy in their regulatory responses. Flow cytometry demonstrated that TGF beta's mitogenic effect was selective for the aneuploid subpopulations of two of three selected HD-GM cultures, while the diploid cells were inhibited. Among the HD-GM, TGF beta 1 induced the RNA of PDGF-A, c-sis and TGF beta 1. The amount of PDGF-AA secreted following TGF beta treatment was sufficient to stimulate the proliferation of a HD-GM culture. Antibodies against PDGF-AA, -BB, -AB, alpha PDGFR and/or beta PDGFR subunits effectively neutralized TGF beta's induction of DNA synthesis among the HD-GM cell lines, indicating that PDGF served as the principal mediator of TGF beta's growth stimulatory effect. By comparison, TGF beta induced only the RNA of PDGF-A and TGF beta 1 among the near-diploid GM, c-sis was not expressed at all. However, the amount of PDGF-A which was secreted in response to TGF beta 1 was insufficient to prevent TGF beta's arrest of the near-diploid cultures in G1 phase. Thus, the emergence of hyperdiploidy was associated with qualitative and quantitative differences in TGF beta's modulation of PDGF-A and c-sis, which provided a mechanism by which the aneuploid glioma cells might achieve 'clonal dominance'. We hypothesize that TGF beta may serve as an autocrine promoter of GM progression by providing a selective advantage to the hyperdiploid subpopulation through the loss of a tumor suppressor gene which mediates TGF beta's inhibitory effect.

Aneuploidy↗
PubMed1995

Optimal cutoff levels of F-18 fluorodeoxyglucose uptake in the differentiation of low-grade from high-grade brain tumors with PET.

PURPOSE: To determine the optimal cutoff level of fluorine-18-labeled fluorodeoxyglucose (FDG) uptake in the differentiation of low-grade from high-grade cerebral tumors at position emission tomography (PET). MATERIALS AND METHODS: The authors retrospectively reviewed images from PET, magnetic resonance imaging, and computed tomography performed in 58 consecutive patients with histologically proved brain tumors. There were 32 high-grade tumors (20 gliomas) and 26 low-grade tumors (18 gliomas). RESULTS: The best cutoff level of FDG uptake ratios in the differentiation of high-grade from low-grade tumors was 1.5 for tumor-to-white matter (T/WM) ratios and 0.6 for tumor-to-cortex (T/C) ratios. These levels were the same when only gliomas were analyzed and when all tumors were analyzed. When a T/WM ratio of more than 1.5 was considered indicative of a high-grade tumor, the sensitivity and specificity were 94% and 77%, respectively. The results were similar for the T/C ratio. CONCLUSION: Cutoff levels of 1.5 for the T/WM FDG uptake ratio and 0.6 for the T/C ratio are useful in the differentiation of low-grade from high-grade gliomas with PET.

Adult↗
PubMed1995

Gliomatosis cerebri presenting as intractable epilepsy during early childhood.

We review 160 cases of gliomatosis cerebri from the literature and report an additional three infants and young children who presented with intractable epilepsy, corticospinal tract deficits, and developmental delay in whom a pathologic diagnosis was made. The progressive nature of the encephalopathy in our cases was documented by serial clinical examination, electroencephalograms, magnetic resonance imaging, and positron emission tomographic scans. The natural history of gliomatosis cerebri was determined by a retrospective review of the literature of 160 cases in 85 reports. The most common neurologic symptoms and signs included corticospinal tract deficits (58%), dementia/mental retardation (44%), headache (39%), seizures (38%), cranioneuropathies (37%), increased intracranial pressure (34%), and spinocerebellar deficits (33%). The most commonly involved central nervous system structures were the centrum semiovale and cerebrum (76%), mesencephalon (52%), pons (52%), thalamus (43%), basal ganglia (34%), and the cerebellum (29%). Fifty-two percent of patients were dead within 12 months of onset. Different grades of glial neoplasm may also coexist within gliomatosis cerebri such as astrocytoma with anaplastic astrocytoma, atypical or anaplastic oligodendroglioma, and glioblastoma multiforme. Hypotheses regarding the pathogenesis of gliomatosis cerebri include blastomatous dysgenesis, diffuse infiltration, multicentric origin, in situ proliferation, and "field transformation." The biologic determinants of whether a transformed glial cell behaves as a relatively localized tumor mass or truly loses anchorage dependence to become migratory as well as proliferative are not understood.

Brain↗
PubMed1994

TGF beta 1 and TGF beta 2 are potential growth regulators for medulloblastomas, primitive neuroectodermal tumors, and ependymomas: evidence in support of an autocrine hypothesis.

Our previous investigations of transforming growth factor types beta 1 and beta 2 (TGF beta s) showed negative or positive autocrine growth regulation of gliomas in vitro. Near-diploid gliomas were inhibited by the TGF beta s, whereas a stimulatory response correlated with progressive anaplasia and karyotypic divergence. We have tested the hypothesis that cytogenetic aberrations may be associated with conversion of TGF beta autoregulation from inhibitory to stimulatory among other cultured neuroectodermal tumors. Anchorage-independent growth and karyotypic aberrations supported the malignant nature in vitro of two medulloblastoma (MBL), two primitive neuroectodermal tumor (PNET), and two ependymoma (EPD) cultures. Transforming growth factor type beta 1 and/or TGF beta 2 RNA was evident by Northern blot analysis among these cell cultures. By radioreceptor assay active TGF beta was present in conditioned medium in concentrations of 0 to 14 ng/mL, whereas the total amount of active and latent TGF beta secreted was in the range of 3 to 118 ng/mL. Expression of the TGF beta radioreceptor (TGF beta-R) types I and II was shown by cross-linking assay. Responses to exogenous TGF beta were determined by [3H]-thymidine incorporation, cell counts, and anchorage-independent clonogenicity. Exogenous TGF beta was growth inhibitory for the near-diploid MBL, PNET, and EPD in vitro, as well as antagonistic to the mitogenic effect of epidermal growth factor (EGF) and insulin. In contrast, MBL, PNET, and EPD with a hyperdiploid subpopulation were stimulated to proliferate in monolayer culture or soft agar by TGF beta 1 and TGF beta 2. The growth response did not correlate with TGF beta-R type. Autocrine regulation was supported by antibody neutralization experiments performed with quiescent cells in the absence of exogenous TGF beta. Anti-TGF beta antisera enhanced the growth of TGF beta-inhibited cultures, whereas the TGF beta-stimulated cultures were inhibited by the antisera. Karyotypic divergence seemed to predict response as MBL, PNET, and EPD with hyperdiploid elements exhibited autocrine TGF beta-stimulation. In contrast, the near-diploid cultures were inhibited by the TGF beta s. By analogy with the gliomas, conversion of TGF beta autocrine regulation from inhibition to stimulation may be a late progression marker of anaplasia among MBL, PNET, and EPD. Secretion of this TGF, which serves both as a mitogen and immunosuppressive agent may contribute to the adverse prognosis of hyperdiploid neuroectodermal neoplasms of the central nervous system (CNS).

Antibodies↗
PubMed1993

Transforming growth factor-beta in neural embryogenesis and neoplasia.

The transforming growth factor-beta (TGF-beta) family of polypeptides includes three structurally and functionally related mammalian isoforms that influence cell proliferation, differentiation, and extracellular matrix production. Recent identification of these isoforms in the embryonic murine central nervous system suggests that these factors may regulate proliferation and differentiation of meningeal and neuroepithelial cells during development. Predominant expression of TGF-beta 1 in the leptomeninges compared with the brain of the murine and human central nervous system implicates this isoform in regulation of that mesodermal tissue. Thus, defective TGF-beta regulation may contribute to neoplastic transformation. Failure to activate latent TGF-beta s may contribute to the loss of autocrine regulation seen in meningiomas. Expression of TGF-beta 2 and TGF-beta 3 primarily in embryonic murine radial glia and adult human astrocytes suggests other roles for these isoforms, including glioblast differentiation and guidance of neuroblast migration. Although inhibitory to "normal" astrocyte proliferation, TGF-beta s demonstrate autocrine growth stimulation in vitro among hyperdiploid malignant gliomas, medulloblastomas, primitive neuroectodermal tumors, and anaplastic ependymomas. Hence, synthesis and release of active TGF-beta s by malignant brain tumors may create aberrant stimulatory autocrine loops. The mechanism of TGF-beta-induced growth stimulation is poorly understood. Future studies will likely clarify and identify additional roles for the TGF-beta isoforms in neuro-embryogenesis and neoplasia.

Animals↗
PubMed1993

Neoplastic meningitis as the presentation of occult primitive neuroectodermal tumors.

Seven children and young adults initially presented with subacute meningitis and/or increased intracranial pressure. The diagnosis of neoplastic meningitis secondary to a primitive neuroectodermal neoplasm was delayed by the absence of an obvious primary tumor. The neuroradiologic appearance was that of a basimeningeal infiltrative process, complicated by communicating hydrocephalus or "pseudotumor cerebri." Myelography was important in the diagnosis of disseminated meningeal malignancy in four cases. Cerebrospinal fluid cytologic diagnosis was insensitive but ultimately confirmed in five cases. All seven patients experienced progressive disease despite neuraxis radiotherapy and intensive chemotherapy; six have died. Systemic dissemination to bone and/or peritoneum occurred in three patients while on therapy. In two, a primary parenchymal brain or spinal cord tumor could not be identified at postmortem examination. The presentation of a primitive neuroectodermal tumor as subacute meningitis without an evident primary tumor heralds an aggressive and refractory neoplasm.

Adolescent↗
PubMed1992

In vitro karyotypic and immunophenotypic characterisation of primitive neuroectodermal tumours: similarities to malignant gliomas.

Monoclonal antibody (Mab) mediated immunotherapy of brain tumours requires the identification of tumour-restricted cell surface antigens. We have characterised four primitive neuroectodermal tumours, which included pineoblastoma, medulloblastoma and ependymoblastoma cultures, that demonstrated in vitro evidence of malignant behaviour (anchorage-independent growth and nu/nu xenograft tumour formation). The cytogenetic findings ranged from normal G-banded and Q-banded karyotypes through mixed near-diploid/hyperdiploid. These cultures resembled the cell surface immunophenotypic spectrum of malignant gliomas. They were distinguished from normal glia in vitro by the expression of restricted fetal mesenchymal, neuronal, myoblastic, melanocytic, epidermal, chondrocytic, lymphoid and epithelial antigens. Certain antigens appeared sufficiently represented among central nervous system (CNS) neoplasms to afford potential targets for Mab-mediated immunotherapy.

Adolescent↗
PubMed1992

Comparison of fecal occult blood tests for detection of gastrointestinal bleeding in pediatric patients.

To compare fecal occult blood tests (Hemoccult II, Hemoccult SENSA, HemeSelect) for detecting the presence of occult gastrointestinal bleeding in a pediatric population at high risk, we analyzed stool specimens from 100 children who followed a restricted diet. Forty-two children had upper and 58 lower gastrointestinal sources of bleeding. Positivity rates ranged from 10.8% to 26% dependent upon the occult blood test. Whereas Hemoccult II and Hemoccult SENSA slides detected several positive specimens in upper gastrointestinal bleeding sources, all HemeSelect slides were negative in these subjects. In lower gastrointestinal bleeding, HemeSelect slides were positive in 26.8% of samples as opposed to 15.9% and 17.5% positivity rates for Hemoccult II and Hemoccult SENSA, but this difference was not statistically significant. We conclude that fecal occult blood tests vary, depending upon the origin of bleeding. Our results favor use of Hemoccult SENSA slides for suspected upper gastrointestinal bleeding and HemeSelect slides for lower gastrointestinal bleeding in children. However, if only one all-purpose fecal occult blood test is to be utilized, then our data supports the use of Hemoccult SENSA slides for children.

Adolescent↗
PubMed1992

Serum delta bilirubin estimation by an automated method.

This study compares delta bilirubin values in 40 serum samples from patients with various diagnoses, as estimated by the automated Kodak Ektachem system and measured by a manual method. Regression analysis of the results yielded a slope = 0.832, intercept = 9.9 and r = 0.724. Within-run standard deviation was 1.7 mumol/l for the automated method. In samples with predominantly unconjugated bilirubin, the Ektachem system over-estimated delta bilirubin values. In specimens with conjugated hyperbilirubinaemia, the Ektachem system and manual method were in close agreement for delta bilirubin values. We conclude that samples with predominantly unconjugated bilirubin should have the presence of delta bilirubin confirmed by the manual assay. Since the Ektachem system currently provides the only automated means of estimating delta bilirubin values, its use appears warranted.

Autoanalysis↗
PubMed1991

TGF beta 1 and TGF beta 2 are potential growth regulators for low-grade and malignant gliomas in vitro: evidence in support of an autocrine hypothesis.

Low-grade astrocytomas, anaplastic astrocytomas and glioblastomas in vitro were found to ubiquitously produce the mRNA of transforming growth factor-beta (TGF beta). TGF beta 1 and TGF beta 2 mRNA were expressed to a lesser degree among the hyperdiploid malignant gliomas. By radioreceptor assay of conditioned medium, TGF beta was secreted predominantly in latent form, in both latent and active form, or only in active form within a panel of low-grade and malignant gliomas. The TGF beta receptor (types I, II, and III) was evident among the glioma lines. Many near-diploid gliomas were growth-inhibited by TGF beta 1 and TGF beta 2 in vitro. Most hyperdiploid glioblastomas showed a positive mitogenic response to exogenous TGF beta 1 and TGF beta 2. A synergistic or additive mitogenic interaction with epidermal growth factor and insulin was observed among some. Under serum-free conditions, anti-TGF beta antibody neutralized the expected growth-regulatory effect of endogenous TGF beta, thus establishing the specificity of the response in vitro. TGF beta 1 also enhanced the clonogenicity of certain gliomas which had been growth-stimulated in monolayer. Thus, basic elements in support of an autocrine hypothesis have been demonstrated: TGF beta mRNA was expressed among low-grade and malignant gliomas, TGF beta was secreted in latent and/or active form into conditioned media and appeared to serve as an endogenous regulator of glioma proliferation in vitro. The mitogenic response, either positive or negative, correlated with the degree of anaplasia and karyotypic divergence.

Blotting, Northern↗
PubMed1990

Factor analysis of the immunophenotypes of astrocytomas and malignant gliomas: correlations with tumor grade and patient survival.

Our previous investigations correlated the degree of cytogenetic and immunophenotypic heterogeneity of cultured normal glia, astrocytomas and malignant gliomas. The possible significance was suggested by the statistical correlation of individual antigens with diagnosis and patient survival. The present study has established the patterns of covariation of titers of monoclonal antibody reactivity with a panel of cell surface antigens among normal glia (8), astrocytomas (4), anaplastic astrocytomas (12), mixed malignant gliomas (8) and glioblastomas (21). A mean aggregate titer across 43 antigens was computed for each culture and then subtracted from the observed individual titers. Factor analysis was performed to determine a small number of Factors, derived as the weighted average of the 43 mean-adjusted antigens, which accounted for a significant proportion of the covariation of immunophenotypic expression in the sample of 53 cultures. Clusters of antigens were found to independently segregate in their deviation from the aggregate phenotype. Adjusting for age and diagnosis, Factors 1 and 4 correlated with patient survival among recurrent and primary neoplasms, respectively. Factor 2 additionally discriminated between primary and recurrent gliomas. Factor 3 was associated with age at diagnosis. Factors 1 and 2 correlated with the histopathologic grade of glial tumor. Scatter plots of Factor 1 vs. 2 revealed the minimal immunophenotypic diversity of the normal glia. Astrocytomas were similar but not identical. Progressive divergence was evident between the immunophenotypes of anaplastic astrocytomas, mixed gliomas and glioblastomas. These data suggest that qualitative and quantitative differences in antigenic heterogeneity may identify stages in glial tumor progression.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Monoclonal↗
PubMed1989

Five novel cell surface antigens of CNS neoplasms.

Optimal monoclonal antibody-mediated immunotherapy requires the identification of tumor-restricted cell surface antigens. We have identified and partially characterized 5 new monoclonal antibodies generated against malignant astrocytoma, medulloblastoma, neuroblastoma and melanoma which were used to define 5 neuroectodermal tumor antigenic systems. CNT/1 identifies a 57-kDa, heat-stable, trypsin-sensitive neuroblastoma surface antigen, which is expressed intracellularly in many malignant gliomas, medulloblastomas, ependymomas, breast and ovarian carcinomas. CNT/2 reacts with a 130-kDa, heat-labile, trypsin- and neuraminidase-resistant antigen restricted to low-grade astrocytomas and malignant gliomas. CNT/11 reacts with a 70-kDa, heat-labile, trypsin-sensitive antigen coded for by a gene on chromosome 12, and is restricted to astrocytomas, neuroblastomas and sarcomas. CNT/8 identifies a heat-labile, trypsin-sensitive antigen whose gene has been localized to chromosome 15 and is expressed by neuroectodermal and mesodermally derived tumors and few epithelial cancers. The B2.6 antigen is identified only in terms of serologic reactivity with a subset of cultured astrocytomas and melanomas. Neuroectodermal tumor-associated antigens may be categorized as lineage-consistent, lineage-independent and putatively tumor-restricted in their expression. These restricted antibodies may be potentially useful reagents to consider for monoclonal antibody-mediated immunotherapy of CNS neoplasms.

Antibodies, Monoclonal↗