Rebecca Kuo, MD JD
University of Chicago · Pharmacology
Active 1957–1994
About
Rebecca Kuo, MD, JD, is a highly skilled orthopaedic surgeon specializing in spine surgery. She treats a wide range of complex conditions, including spinal stenosis, cervical and thoracic myelopathy, cervical and lumbar disk disease, degenerative spine disorders, adult and adolescent spinal deformity, spinal tumors and infections, and spinal trauma. With advanced training and many years of experience, Dr. Kuo performs both minimally invasive and traditional spinal procedures, such as deformity treatment for both adults and children, and motion-preserving spinal techniques for cervical and lumbar disk replacement. She is committed to offering personalized care that addresses each patient’s unique needs, symptoms, and lifestyle, aiming to help manage chronic pain or complicated conditions and improve quality of life. Dr. Kuo emphasizes patient education about diagnosis and treatment options, fostering a supportive and collaborative environment to ensure patients feel informed and confident throughout their healthcare journey.
Research topics
- Biology
- Genetics
- Medicine
- Cancer research
- Psychology
Selected publications
1993 Robert R. deVilliers Lecture. Chromosome translocations: dangerous liaisons.
PubMed · 1994-04-01 · 10 citations
article1st authorCorrespondingRearrangements involving chromosome band 11q23 are very common in acute leukemia, both lymphoblastic and myeloid (monoblastic), and are less common in lymphoma. Although several different genes have been cloned from 11q23 translocation breakpoints, the great majority involve the MLL (myeloid-lymphoid leukemia) gene. The MLL gene has several different names, ALL1, Htrx, HRX; the central part of the gene codes for multiple zinc fingers which show strong homology to the Drosophila trithorax gene. MLL is involved in four common translocations as well as in 25 uncommon or rare translocations, insertions and deletions. The translocation breakpoints occur within an 8.3kb region which can be detected with a 0.7 kb cDNA probe. Twenty-five percent of patients have a deletion 3' of the breakpoint which includes the zinc finger region. Patients who previously received drugs that inhibit topoisomerase II often develop acute leukemia with translocations involving 11q23. These translocations break MLL in the same 8.3kb region. In the four breakpoints cloned to date, the translocation has led to a fusion gene on the derivative 11 chromosome with a chimeric transcript, consisting of 5' MLL and the 3' segment of the other gene. Although transcripts were also cloned from the other derivative chromosome, all the evidence indicates that the critical fusion gene is on the derivative 11 chromosome. The molecular dissection of these rearrangements will provide insights into the biology of MLL and into the interaction of MLL with topoisomerase II inhibitors. In addition, this research has provided DNA probes that will be important for diagnosis and for monitoring patients during the course of their disease.
PubMed · 1994-12-01
article1st authorCorrespondingRecurring chromosome abnormalities in leukemia and lymphoma.
PubMed · 1990-04-01 · 178 citations
article1st authorCorrespondingChromosome abnormalities in human leukemia as indicators of mutagenic exposure.
PubMed · 1985-01-01 · 5 citations
article1st authorCorrespondingIt is from an analysis of these data that I proposed that losses of all or part of the long arm of chromosomes 5 and/or 7 may be indicators of exposure to mutagenic agents (8). Moreover, our analysis of the regions of chromosomes 5 and 7 that are consistently missing can define the critical region of each chromosome with some precision. Looked at from another perspective, the frequency of losses of chromosomes 5 and/or 7 may be an indicator of the proportion of ANLL in each particular population that is related to some mutagenic exposure. These aberrations are most frequent in cells of patients who were previously exposed to various cytotoxic regimens for treatment of a primary (usually malignant) disease; these patients are considered to have 2 degrees ANLL. Among patients with ANLL de novo, abnormalities of chromosomes 5 and 7 are much more frequent in older than younger patients. Finally, among adult patients with ANLL de novo, -5 and -7 are more common in those whose occupations could potentially expose them to mutagenic agents such as chemicals, pesticides, or petroleum products. With regard to chromosome 5, most of these deletions are interstitial and always include 5q23 through q31, which I have called the critical region. Although I am less certain with regard to chromosome 7, it appears that the critical region that is consistently deleted may be 7q32 or 7q34-35.
Chromosome abnormalities in leukemia and lymphoma.
PubMed · 1983-07-08 · 13 citations
article1st authorCorrespondingNonrandom chromosome changes have been identified in a number of malignant human tumors. The leukemias are among the best studied malignant cells and they provide the largest body of relevant cytogenetic data. In chronic myeloid leukemia, a reasonably consistent translocation [t(9;22) (q34;q11)] is observed in 93 percent of all Ph1 positive patients. In the other patients, translocations are either two-way, involving No. 22 with some other chromosome or complex translocations involving Nos. 9 and 22 and another chromosome. In acute nonlymphocytic leukemia, two translocations are each specifically associated with leukemic cells arrested at two different stages of maturation. One of these, t(8;21)(q22;q22), is found mainly in patients with acute myeloblastic leukemia with maturation (AML-M2). The other, t(15;17)(q22?;q21?), is seen only in patients with acute promyelocytic leukemia (APL-M3). Various translocations have been observed in B-cell acute lymphoblastic leukemia or in Burkitt lymphoma. The most common is t(8;14)(q24;q32), but variants of this, namely t(2;8)(p13?;q24) and t(8;22)(q24;q11), have also been observed; in all of these, the consistent change involves 8q24. The various immunoglobulin loci are located on chromosomes 2, 14, and 22 in the same chromosome band affected by the translocations in B-cell leukemia. These translocations may occur randomly. If a specific translocation provides a particular cell type with a growth advantage, then selection could act to cause the proliferation of this aneuploid cell line vis-a-vis cells with a normal karyotype. In this view, the chromosome change could be the fundamental event leading to the leukemic transformation of an otherwise normal cell. The challenge for the future is to define the genes located at the sites of consistent translocations in myeloid leukemias and to determine the alterations in gene function that are associated with the translocation.
PubMed · 1982-01-01 · 5 citations
article1st authorCorrespondingNonrandom chromosome changes have been observed in human acute nonlymphocytic leukemia (ANLL). Two specific translocations have been detected only in ANLL arrested in a particular stage in myeloid maturation, i.e., t(8;21) associated with acute myeloblastic leukemia (AML) with maturation (M2) and t(15;17) associated with acute promyelocytic leukemia (M3). Patients with these translocations are substantially younger then patients with the same type of leukemia who have either a normal karyotype or other chromosome abnormalities. Patients who have ANLL secondary to treatment for a prior malignant disease tend to have AML (M1 or M2) and an abnormal karyotype with losses of chromosome #5 and/or #7. A similar high incidence of AML and aneuploidy affecting particularly #5, 7, 8, and 21 was seen in patients with ANLL who were exposed to chemicals and pesticides. Complete unselected data are available for 239 patients with ANLL; 128 of these were classified as having AML (M1 or M2). Within the AML group, 65% of the patients were chromosomally abnormal. Except for 16 patients with a t(8;21), the percentage of those with an abnormal karyotype increased with age, particularly above the age of 50 years. In regard to abnormalities other than t(8;21), 29 patients had loss of part of all of #5 and/or #7, 11 had +8, and 27 had other abnormalities. On the other hand, of 70 patients with acute myelomonocytic leukemia (M4), 42 were normal, only 3 had loss of #5 or 7, 1 was -7, +8, and 4 were +8, whereas 20 had other abnormalities. This difference in karyotype may reflect different etiologic factors in these two types of leukemia.
Consistent translocations in human leukemia.
PubMed · 1982-01-01
article1st authorCorrespondingChromosomes in leukemia and lymphoma.
PubMed · 1978-07-01 · 92 citations
article1st authorCorrespondingIdentificaton of a translocation with quinacrine fluorescence in a patient with acute leukemia.
PubMed · 1973-06-01 · 366 citations
article1st authorCorrespondingPossible non random selection of D group chromosomes involved in centric-fusion translocations.
PubMed · 1969-09-01 · 22 citations
article1st authorCorresponding
Frequent coauthors
- 2 shared
Schwartz Ml
Brown University
- 1 shared
Eugene Pergament
- 1 shared
Kaplitz Se
Labs
- Resume-aware match score
- Save to shortlist
- AI-drafted outreach
See your match with Rebecca Kuo, MD JD
PhdFit ranks faculty by your research interests, methods, and publications — grounded in their actual work, not templates.
- Free to start
- No credit card
- 30-second signup