Peter W. Nichols

University of Southern California

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Peter A. Jones

Van Andel Institute

116

Hui Shen

The University of Texas MD Anderson Cancer Center

Jean–Pierre J. Issa

Coriell Institute For Medical Research

David I. Quinn

University of Southern California

Woonbok Chung

Coriell Institute For Medical Research

H. Josh Jang

Washington University in St. Louis

Noah M. Hahn

Johns Hopkins University

Toshinori Hinoue

Van Andel Institute

Elizabeth R. Plimack

Fox Chase Cancer Center

Stephen B. Baylin

Johns Hopkins University

Cooperative Institutions

University of Southern California

538

Northwestern University

356

USC Norris Comprehensive Cancer Center

Southern California University for Professional Studies

Keck Hospital of USC

Los Angeles Medical Center

LAC+USC Medical Center

University of California, Los Angeles

Stanford University

National Cancer Institute

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Analysis of Somatic Changes in Human Tumor DNA Using Synthetic Oligonucleotide Probes

Cancer Communications (1989)

Satish Parimoo B A Bachman Dinesh Kumar Peter W. Nichols R B Wallace

Like most hematologic malignancies, solid cancers may be associated with non-random chromosomal abnormalities. Heterogeneity in the cell population in solid cancers and the chromosomal variations occurring among primary, explant, and passaged cells of a given tumor, however, present a major difficulty in assessment of their cytogenetic changes. Alternative approaches to identifying specific somatic changes in subtypes of solid cancers, without cell culture manipulations, must be developed. This report describes preliminary evidence indicating that oligonucleotide probes, homologous to short tandem repeats, that can determine individual identity, may also be useful tools with which to examine somatic changes in DNA which has been isolated directly from a tumor mass. Two, of the four, bladder tumors (transitional cell carcinomas) analyzed, exhibited oligonucleotide-based DNA fingerprint patterns that differed from those of corresponding constitutive or uninvolved tissue DNA. The changes that were observed included gain or loss of hypervariable DNA fragments or shifts in band intensities.

10.3727/095535489820874832

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Citations (2)

Two molecular pathways to transitional cell carcinoma of the bladder.

PubMed (1994)

Charles Spruck Petra F. Ohneseit Mirella Gonzalez‐Zulueta David Esrig Noriomi Miyao

Noninvasive transitional cell carcinomas of the bladder can have two distinct morphologies suggesting they contain different genetic alterations. Papillary transitional cell carcinomas (T(a) tumors) are often multifocal and only occasionally progress, whereas flat tumors (carcinomas in situ, CIS), frequently progress to invasive disease. We examined 216 bladder tumors of various stages and histopathologies for two genetic alterations previously described to be of importance in bladder tumorigenesis. Loss of heterozygosity of chromosome 9 was observed in 24 of 70 (34%) T(a) tumors but was present in only 3 of 24 (12%) CIS and dysplasia lesions (P = 0.04). In contrast, only 1 of 36 (3%) T(a) tumors contained a p53 gene mutation compared to 15 of 23 (65%) CIS and dysplasias (P < 0.001), a frequency comparable to that observed in muscle invasive tumors (25 of 49; 51%). The presence of p53 mutations in CIS and dysplasia could explain their propensities to progress since these mutations are known to destabilize the genome. Analysis of several tumor pairs involving a CIS and an invasive cancer provided evidence that the chromosome 9 alteration may in some cases be involved in the progression of CIS to more invasive tumors, in addition to its role in the initiation of T(a) tumors. However, the CIS and secondary tumor were found to contain different genetic alterations in some patients suggesting divergent progression pathways. Bladder carcinogenesis may therefore proceed through two distinct genetic alteration pathways responsible for generating superficial tumors with differing morphologies and pathologies.

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Relationship of tumor angiogenesis and nuclear p53 accumulation in invasive bladder cancer.

PubMed (1997)

Bernard H. Bochner David Esrig Susan Groshen Ming G. Dickinson Noel Weidner

The purpose of this investigation was to evaluate the relationship between tumor angiogenesis and nuclear p53 accumulation in invasive bladder cancer. We studied 161 patients with invasive transitional cell carcinoma of the bladder who had previously undergone radical cystectomy. Analysis was performed to determine the presence of p53 nuclear accumulation and extent of tumor-associated angiogenesis. p53 status identified a group of patients at high risk for tumor progression (p53-altered tumors), and microvessel density determinations added additional prognostic information by identifying a subset of aggressive tumors within the wild-type p53 subgroup. At 5 years, patients with tumors exhibiting no evidence of p53 alterations and low microvessel counts demonstrated 3% recurrence and 88% survival, compared to 43% recurrence and 59% overall survival for patients with intermediate vessel counts and 61% recurrence and 43% overall survival for patients with the highest vessel counts (P < 0.001 and P = 0.003, respectively). Angiogenesis also provides additional prognostic information to patients with tumors that demonstrate p53 alterations. An association between angiogenesis and p53 status did exist (P = 0. 05); however, 27% of the tumors that showed no evidence of p53 alterations exhibited high microvessel counts, and 26% of tumors with evidence of p53 alterations had low microvessel counts. Tumor-associated angiogenesis adds additional useful prognostic information to that which is obtained from p53 status in patients with invasive transitional cell carcinoma of the bladder. Although an association between p53 status and the degree of angiogenesis was identified, other factors appear to play a role in the regulation of tumor-induced neovasularization.

Microvessel

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Supplementary Tables 1 from A Phase II Trial of Guadecitabine plus Atezolizumab in Metastatic Urothelial Carcinoma Progressing after Initial Immune Checkpoint Inhibitor Therapy

H. Josh Jang Galen Hostetter Alexander W. MacFarlane Zachary Madaj Eric A. Ross

Supplementary Tables Supplementary Table 1: Patient and tumor sample information Supplementary Table 2: Tumor mutation burden Supplementary Table 3: Unfiltered whole exome sequencing mutation analysis Supplementary Table 4: Filtered whole exome sequencing mutation analysis Supplementary Table 5: Immunohistochemistry scores of tumors Supplementary Table 6: FACS panel for PBMC analysis Supplementary Table 7: Geometric mean fluorescence intensity (GMFI) from PBMC FACS Supplementary Table 8: Representativeness of Study Participants

Atezolizumab

Metastatic Urothelial Carcinoma

10.1158/1078-0432.27030415.v1

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Figure S9 from A Phase II Trial of Guadecitabine plus Atezolizumab in Metastatic Urothelial Carcinoma Progressing after Initial Immune Checkpoint Inhibitor Therapy

H. Josh Jang Galen Hostetter Alexander W. MacFarlane Zachary Madaj Eric A. Ross

Supplementary Figure 9: CD8 infiltration in tumor is associated with survival.

Atezolizumab

Metastatic Urothelial Carcinoma

10.1158/1078-0432.27030418.v1

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Figure S10 from A Phase II Trial of Guadecitabine plus Atezolizumab in Metastatic Urothelial Carcinoma Progressing after Initial Immune Checkpoint Inhibitor Therapy

H. Josh Jang Galen Hostetter Alexander W. MacFarlane Zachary Madaj Eric A. Ross

Supplementary Figure 10: Peripheral immune cell dynamics induced by combination therapy.

Atezolizumab

Metastatic Urothelial Carcinoma

Immune checkpoint

10.1158/1078-0432.27030448

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Figure S11 from A Phase II Trial of Guadecitabine plus Atezolizumab in Metastatic Urothelial Carcinoma Progressing after Initial Immune Checkpoint Inhibitor Therapy

H. Josh Jang Galen Hostetter Alexander W. MacFarlane Zachary Madaj Eric A. Ross

Supplementary Figure 11: Peripheral immune cells are activated mid-treatment cycle.

Atezolizumab

Metastatic Urothelial Carcinoma

10.1158/1078-0432.27030445.v1

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Stereotaxic Biopsy Diagnosis of Central Nervous System Lymphoma

American Journal of Clinical Pathology (1988)

Thomas Namiki Peter W. Nichols Terrance Young Sue Martin Para Chandrasoma

Twelve cases of central nervous system lymphoma diagnosed by stereotaxic brain biopsy are reviewed to determine the most effective method to establish the diagnosis given the small amount of tissue obtained by this technique. The stereotaxic biopsy material was examined cytologically, histologically, and immunocytochemically. The diagnosis was established by a smear made at the time of biopsy in eight cases. Histologic sections were diagnostic of lymphoma in 11 of 12 cases. Accurate classification according to the Working Formulation was possible in six cases, with diagnosis of diffuse small non-cleaved non-Burkitt's in three, large cell immunoblastic in two, and mixed small and large cell type in one. Five additional cases were diagnosed as high-grade lymphoma but could not be further subclassified because of the small biopsy size or formalin fixation. Immunocytochemical stains for lymphoid markers on paraffin-embedded material confirmed the diagnosis in ten cases, and, in one of these, the demonstration of monoclonality on air-dried cytospins identified an atypical polymorphous lymphocytic population as neoplastic.

Brain biopsy

10.1093/ajcp/90.1.40

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Citations (27)

Figure S8 from A Phase II Trial of Guadecitabine plus Atezolizumab in Metastatic Urothelial Carcinoma Progressing after Initial Immune Checkpoint Inhibitor Therapy

H. Josh Jang Galen Hostetter Alexander W. MacFarlane Zachary Madaj Eric A. Ross

Supplementary Figure 8: PD-L1 levels in tumor or tumor microenvironment does not associate with tumor progression or control.

Atezolizumab

Metastatic Urothelial Carcinoma

Immune checkpoint

10.1158/1078-0432.27030421.v1

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